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The definition of “hospitalist,” according to the SHM website, is a clinician “dedicated to delivering comprehensive medical care to hospitalized patients.” For years, the hospital setting was the specialties’ identifier. But as hospitalists’ scope has expanded, and post-acute care (PAC) in the United States has grown, more hospitalists are extending their roles into this space.
PAC today is more than the traditional nursing home, according to Manoj K. Mathew, MD, SFHM, national medical director of Agilon Health in Los Angeles.
Many of those expanded settings Dr. Mathew describes emerged as a result of the Affordable Care Act. Since its enactment in 2010, the ACA has heightened providers’ focus on the “Triple Aim” of improving the patient experience (including quality and satisfaction), improving the health of populations, and reducing the per capita cost of healthcare.1 Vishal Kuchaculla, MD, New England regional post-acute medical director of Knoxville,Tenn.-based TeamHealth, says new service lines also developed as Medicare clamped down on long-term inpatient hospital stays by giving financial impetus to discharge patients as soon as possible.
“Over the last few years, there’s been a major shift from fee-for-service to risk-based payment models,” Dr. Kuchaculla says. “The government’s financial incentives are driving outcomes to improve performance initiatives.”
“Today, LTACHs can be used as substitutes for short-term acute care,” says Sean R. Muldoon, MD, MPH, FCCP, chief medical officer of Kindred Healthcare in Louisville, Ky., and former chair of SHM’s Post-Acute Care Committee. “This means that a patient can be directly admitted from their home to an LTACH. In fact, many hospice and home-care patients are referred from physicians’ offices without a preceding hospitalization.”
Hospitalists can fill a need
More hospitalists are working in PACs for a number of reasons. Dr. Mathew says PAC facilities and services have “typically lacked the clinical structure and processes to obtain the results that patients and payors expect.
“These deficits needed to be quickly remedied as patients discharged from hospitals have increased acuity and higher disease burdens,” he adds. “Hospitalists were the natural choice to fill roles requiring their expertise and experience.”
Dr. Muldoon considers the expanded scope of practice into PACs an additional layer to hospital medicine’s value proposition to the healthcare system.
“As experts in the management of inpatient populations, it’s natural for hospitalists to expand to other facilities with inpatient-like populations,” he says, noting SNFs are the most popular choice, with IRFs and LTACHs also being common places to work. Few hospitalists work in home care or hospice.
PAC settings are designed to help patients who are transitioning from an inpatient setting back to their home or other setting.
“Many patients go home after a SNF stay, while others will move to a nursing home or other longer-term care setting for the first time,” says Tiffany Radcliff, PhD, a health economist in the department of health policy and management at Texas A&M University School of Public Health in College Station. “With this in mind, hospitalists working in PAC have the opportunity to address each patient’s ongoing care needs and prepare them for their next setting. Hospitalists can manage medication or other care regimen changes that resulted from an inpatient stay, reinforce discharge instructions to the patient and their caregivers, and identify any other issues with continuing care that need to be addressed before discharge to the next care setting.”
Transitioning Care
Even if a hospitalist is not employed at a PAC, it’s important that they know something about them.
“As patients are moved downstream earlier, hospitalists are being asked to help make a judgment regarding when and where an inpatient is transitioned,” Dr. Muldoon says. As organizations move toward becoming fully risk capable, it is necessary to develop referral networks of high-quality PAC providers to achieve the best clinical outcomes, reduce readmissions, and lower costs.2“Therefore, hospitalists should have a working knowledge of the different sites of service as well as some opinion on the suitability of available options in their community,” Dr. Muldoon says. “The hospitalist can also help to educate the hospitalized patient on what to expect at a PAC.”
If a patient is inappropriately prepared for the PAC setting, it could lead to incomplete management of their condition, which ultimately could lead to readmission.
“When hospitalists know how care is provided in a PAC setting, they are better able to ensure a smoother transition of care between settings,” says Tochi Iroku-Malize, MD, MPH, MBA, FAAFP, SFHM, chair of family medicine at Northwell Health in Long Island, N.Y. “This will ultimately prevent unnecessary readmissions.”
Further, the quality metrics that hospitals and thereby hospitalists are judged by no longer end at the hospital’s exit.
“The ownership of acute-care outcomes requires extending the accountability to outside of the institution’s four walls,” Dr. Mathew says. “The inpatient team needs to place great importance on the transition of care and the subsequent quality of that care when the patient is discharged.”
Robert W. Harrington Jr., MD, SFHM, chief medical officer of Plano, Texas–based Reliant Post-Acute Care Solutions and former SHM president, says the health system landscapes are pushing HM beyond the hospitals’ walls.
How PAC settings differ from hospitals
Practicing in PAC has some important nuances that hospitalists from short-term acute care need to get accustomed to, Dr. Muldoon says. Primarily, the diagnostic capabilities are much more limited, as is the presence of high-level staffing. Further, patients are less resilient to medication changes and interventions, so changes need to be done gradually.
“Hospitalists who try to practice acute-care medicine in a PAC setting may become frustrated by the length of time it takes to do a work-up, get a consultation, and respond to a patient’s change of condition,” Dr. Muldoon says. “Nonetheless, hospitalists can overcome this once recognizing this mind shift.”
According to Dr. Harrington, another challenge hospitalists may face is the inability of the hospital’s and PAC facility’s IT platforms to exchange electronic information.
“The major vendors on both sides need to figure out an interoperability strategy,” he says. “Currently, it often takes 1-3 days to receive a new patient’s discharge summary. The summary may consist of a stack of paper that takes significant time to sort through and requires the PAC facility to perform duplicate data entry. It’s a very highly inefficient process that opens up the doors to mistakes and errors of omission and commission that can result in bad patient outcomes.”
Arif Nazir, MD, CMD, FACP, AGSF, chief medical officer of Signature HealthCARE and president of SHC Medical Partners, both in Louisville, Ky., cites additional reasons the lack of seamless communication between a hospital and PAC facility is problematic. “I see physicians order laboratory tests and investigations that were already done in the hospital because they didn’t know they were already performed or never received the results,” he says. “Similarly, I see patients continue to take medications prescribed in the hospital long term even though they were only supposed to take them short term. I’ve also seen patients come to a PAC setting from a hospital without any formal understanding of their rehabilitative period and expectations for recovery.”
What’s ahead?
Looking to the future, Surafel Tsega, MD, clinical instructor at Mount Sinai Hospital in New York, says he thinks there will be a move toward greater collaboration among inpatient and PAC facilities, particularly in the discharge process, given that hospitals have an added incentive to ensure safe transitions because reimbursement from the Centers for Medicare & Medicaid Services is tied to readmissions and there are penalties for readmission. This involves more comprehensive planning regarding “warm handoffs” (e.g., real-time discussions with PAC providers about a patient’s hospital course and plan of care upon discharge), transferring of information, and so forth.
And while it can still be challenging to identify high-risk patients or determine the intensity and duration of their care, Dr. Mathew says risk-stratification tools and care pathways are continually being refined to maximize value with the limited resources available. In addition, with an increased emphasis on employing a team approach to care, there will be better integration of non-medical services to address the social determinants of health, which play significant roles in overall health and healing.
“Working with community-based organizations for this purpose will be a valuable tool for any of the population health–based initiatives,” he says.
Dr. Muldoon says he believes healthcare reform will increasingly view an inpatient admission as something to be avoided.
“If hospitalization can’t be avoided, then it should be shortened as much as possible,” he says. “This will shift inpatient care into LTACHs, SNFs, and IRFs. Hospitalists would be wise to follow patients into those settings as traditional inpatient census is reduced. This will take a few years, so hospitalists should start now in preparing for that downstream transition of individuals who were previously inpatients.”
The cost of care, and other PAC facts and figures
The amount of money that Medicare spends on post-acute care (PAC) has been increasing. In 2012, 12.6% of Medicare beneficiaries used some form of PAC, costing $62 billion.2 That amounts to the Centers for Medicare & Medicaid Services spending close to 25% of Medicare beneficiary expenses on PAC, a 133% increase from 2001 to 2012. Among the different types, $30.4 billion was spent on skilled nursing facilities (SNFs), $18.6 billion on home health, and $13.1 billion on long-term acute care (LTAC) and acute-care rehabilitation.2
It’s also been reported that after short-term acute-care hospitalization, about one in five Medicare beneficiaries requires continued specialized treatment in one of the three typical Medicare PAC settings: inpatient rehabilitation facilities (IRFs), LTAC hospitals, and SNFs.3
What’s more, hospital readmission nearly doubles the cost of an episode, so the financial implications for organizations operating in risk-bearing arrangements are significant. In 2013, 2,213 hospitals were charged $280 million in readmission penalties.2
References
1. The role of post-acute care in new care delivery models. American Hospital Association website. Available at: http://www.aha.org/research/reports/tw/15dec-tw-postacute.pdf. Accessed Nov. 7, 2016.
2. Post-acute care integration: Today and in the future. DHG Healthcare website. Available at: http://www2.dhgllp.com/res_pubs/HCG-Post-Acute-Care-Integration.pdf. Accessed Nov. 7, 2016.
3. Overview: Post-acute care transitions toolkit. Society for Hospital Medicine website. Available at: http://www.hospitalmedicine.org/Web/Quality___Innovation/Implementation_Toolkit/pact/Overview_PACT.aspx?hkey=dea3da3c-8620-46db-a00f-89f07f021958. Accessed Nov. 10, 2016.
The definition of “hospitalist,” according to the SHM website, is a clinician “dedicated to delivering comprehensive medical care to hospitalized patients.” For years, the hospital setting was the specialties’ identifier. But as hospitalists’ scope has expanded, and post-acute care (PAC) in the United States has grown, more hospitalists are extending their roles into this space.
PAC today is more than the traditional nursing home, according to Manoj K. Mathew, MD, SFHM, national medical director of Agilon Health in Los Angeles.
Many of those expanded settings Dr. Mathew describes emerged as a result of the Affordable Care Act. Since its enactment in 2010, the ACA has heightened providers’ focus on the “Triple Aim” of improving the patient experience (including quality and satisfaction), improving the health of populations, and reducing the per capita cost of healthcare.1 Vishal Kuchaculla, MD, New England regional post-acute medical director of Knoxville,Tenn.-based TeamHealth, says new service lines also developed as Medicare clamped down on long-term inpatient hospital stays by giving financial impetus to discharge patients as soon as possible.
“Over the last few years, there’s been a major shift from fee-for-service to risk-based payment models,” Dr. Kuchaculla says. “The government’s financial incentives are driving outcomes to improve performance initiatives.”
“Today, LTACHs can be used as substitutes for short-term acute care,” says Sean R. Muldoon, MD, MPH, FCCP, chief medical officer of Kindred Healthcare in Louisville, Ky., and former chair of SHM’s Post-Acute Care Committee. “This means that a patient can be directly admitted from their home to an LTACH. In fact, many hospice and home-care patients are referred from physicians’ offices without a preceding hospitalization.”
Hospitalists can fill a need
More hospitalists are working in PACs for a number of reasons. Dr. Mathew says PAC facilities and services have “typically lacked the clinical structure and processes to obtain the results that patients and payors expect.
“These deficits needed to be quickly remedied as patients discharged from hospitals have increased acuity and higher disease burdens,” he adds. “Hospitalists were the natural choice to fill roles requiring their expertise and experience.”
Dr. Muldoon considers the expanded scope of practice into PACs an additional layer to hospital medicine’s value proposition to the healthcare system.
“As experts in the management of inpatient populations, it’s natural for hospitalists to expand to other facilities with inpatient-like populations,” he says, noting SNFs are the most popular choice, with IRFs and LTACHs also being common places to work. Few hospitalists work in home care or hospice.
PAC settings are designed to help patients who are transitioning from an inpatient setting back to their home or other setting.
“Many patients go home after a SNF stay, while others will move to a nursing home or other longer-term care setting for the first time,” says Tiffany Radcliff, PhD, a health economist in the department of health policy and management at Texas A&M University School of Public Health in College Station. “With this in mind, hospitalists working in PAC have the opportunity to address each patient’s ongoing care needs and prepare them for their next setting. Hospitalists can manage medication or other care regimen changes that resulted from an inpatient stay, reinforce discharge instructions to the patient and their caregivers, and identify any other issues with continuing care that need to be addressed before discharge to the next care setting.”
Transitioning Care
Even if a hospitalist is not employed at a PAC, it’s important that they know something about them.
“As patients are moved downstream earlier, hospitalists are being asked to help make a judgment regarding when and where an inpatient is transitioned,” Dr. Muldoon says. As organizations move toward becoming fully risk capable, it is necessary to develop referral networks of high-quality PAC providers to achieve the best clinical outcomes, reduce readmissions, and lower costs.2“Therefore, hospitalists should have a working knowledge of the different sites of service as well as some opinion on the suitability of available options in their community,” Dr. Muldoon says. “The hospitalist can also help to educate the hospitalized patient on what to expect at a PAC.”
If a patient is inappropriately prepared for the PAC setting, it could lead to incomplete management of their condition, which ultimately could lead to readmission.
“When hospitalists know how care is provided in a PAC setting, they are better able to ensure a smoother transition of care between settings,” says Tochi Iroku-Malize, MD, MPH, MBA, FAAFP, SFHM, chair of family medicine at Northwell Health in Long Island, N.Y. “This will ultimately prevent unnecessary readmissions.”
Further, the quality metrics that hospitals and thereby hospitalists are judged by no longer end at the hospital’s exit.
“The ownership of acute-care outcomes requires extending the accountability to outside of the institution’s four walls,” Dr. Mathew says. “The inpatient team needs to place great importance on the transition of care and the subsequent quality of that care when the patient is discharged.”
Robert W. Harrington Jr., MD, SFHM, chief medical officer of Plano, Texas–based Reliant Post-Acute Care Solutions and former SHM president, says the health system landscapes are pushing HM beyond the hospitals’ walls.
How PAC settings differ from hospitals
Practicing in PAC has some important nuances that hospitalists from short-term acute care need to get accustomed to, Dr. Muldoon says. Primarily, the diagnostic capabilities are much more limited, as is the presence of high-level staffing. Further, patients are less resilient to medication changes and interventions, so changes need to be done gradually.
“Hospitalists who try to practice acute-care medicine in a PAC setting may become frustrated by the length of time it takes to do a work-up, get a consultation, and respond to a patient’s change of condition,” Dr. Muldoon says. “Nonetheless, hospitalists can overcome this once recognizing this mind shift.”
According to Dr. Harrington, another challenge hospitalists may face is the inability of the hospital’s and PAC facility’s IT platforms to exchange electronic information.
“The major vendors on both sides need to figure out an interoperability strategy,” he says. “Currently, it often takes 1-3 days to receive a new patient’s discharge summary. The summary may consist of a stack of paper that takes significant time to sort through and requires the PAC facility to perform duplicate data entry. It’s a very highly inefficient process that opens up the doors to mistakes and errors of omission and commission that can result in bad patient outcomes.”
Arif Nazir, MD, CMD, FACP, AGSF, chief medical officer of Signature HealthCARE and president of SHC Medical Partners, both in Louisville, Ky., cites additional reasons the lack of seamless communication between a hospital and PAC facility is problematic. “I see physicians order laboratory tests and investigations that were already done in the hospital because they didn’t know they were already performed or never received the results,” he says. “Similarly, I see patients continue to take medications prescribed in the hospital long term even though they were only supposed to take them short term. I’ve also seen patients come to a PAC setting from a hospital without any formal understanding of their rehabilitative period and expectations for recovery.”
What’s ahead?
Looking to the future, Surafel Tsega, MD, clinical instructor at Mount Sinai Hospital in New York, says he thinks there will be a move toward greater collaboration among inpatient and PAC facilities, particularly in the discharge process, given that hospitals have an added incentive to ensure safe transitions because reimbursement from the Centers for Medicare & Medicaid Services is tied to readmissions and there are penalties for readmission. This involves more comprehensive planning regarding “warm handoffs” (e.g., real-time discussions with PAC providers about a patient’s hospital course and plan of care upon discharge), transferring of information, and so forth.
And while it can still be challenging to identify high-risk patients or determine the intensity and duration of their care, Dr. Mathew says risk-stratification tools and care pathways are continually being refined to maximize value with the limited resources available. In addition, with an increased emphasis on employing a team approach to care, there will be better integration of non-medical services to address the social determinants of health, which play significant roles in overall health and healing.
“Working with community-based organizations for this purpose will be a valuable tool for any of the population health–based initiatives,” he says.
Dr. Muldoon says he believes healthcare reform will increasingly view an inpatient admission as something to be avoided.
“If hospitalization can’t be avoided, then it should be shortened as much as possible,” he says. “This will shift inpatient care into LTACHs, SNFs, and IRFs. Hospitalists would be wise to follow patients into those settings as traditional inpatient census is reduced. This will take a few years, so hospitalists should start now in preparing for that downstream transition of individuals who were previously inpatients.”
The cost of care, and other PAC facts and figures
The amount of money that Medicare spends on post-acute care (PAC) has been increasing. In 2012, 12.6% of Medicare beneficiaries used some form of PAC, costing $62 billion.2 That amounts to the Centers for Medicare & Medicaid Services spending close to 25% of Medicare beneficiary expenses on PAC, a 133% increase from 2001 to 2012. Among the different types, $30.4 billion was spent on skilled nursing facilities (SNFs), $18.6 billion on home health, and $13.1 billion on long-term acute care (LTAC) and acute-care rehabilitation.2
It’s also been reported that after short-term acute-care hospitalization, about one in five Medicare beneficiaries requires continued specialized treatment in one of the three typical Medicare PAC settings: inpatient rehabilitation facilities (IRFs), LTAC hospitals, and SNFs.3
What’s more, hospital readmission nearly doubles the cost of an episode, so the financial implications for organizations operating in risk-bearing arrangements are significant. In 2013, 2,213 hospitals were charged $280 million in readmission penalties.2
References
1. The role of post-acute care in new care delivery models. American Hospital Association website. Available at: http://www.aha.org/research/reports/tw/15dec-tw-postacute.pdf. Accessed Nov. 7, 2016.
2. Post-acute care integration: Today and in the future. DHG Healthcare website. Available at: http://www2.dhgllp.com/res_pubs/HCG-Post-Acute-Care-Integration.pdf. Accessed Nov. 7, 2016.
3. Overview: Post-acute care transitions toolkit. Society for Hospital Medicine website. Available at: http://www.hospitalmedicine.org/Web/Quality___Innovation/Implementation_Toolkit/pact/Overview_PACT.aspx?hkey=dea3da3c-8620-46db-a00f-89f07f021958. Accessed Nov. 10, 2016.
The definition of “hospitalist,” according to the SHM website, is a clinician “dedicated to delivering comprehensive medical care to hospitalized patients.” For years, the hospital setting was the specialties’ identifier. But as hospitalists’ scope has expanded, and post-acute care (PAC) in the United States has grown, more hospitalists are extending their roles into this space.
PAC today is more than the traditional nursing home, according to Manoj K. Mathew, MD, SFHM, national medical director of Agilon Health in Los Angeles.
Many of those expanded settings Dr. Mathew describes emerged as a result of the Affordable Care Act. Since its enactment in 2010, the ACA has heightened providers’ focus on the “Triple Aim” of improving the patient experience (including quality and satisfaction), improving the health of populations, and reducing the per capita cost of healthcare.1 Vishal Kuchaculla, MD, New England regional post-acute medical director of Knoxville,Tenn.-based TeamHealth, says new service lines also developed as Medicare clamped down on long-term inpatient hospital stays by giving financial impetus to discharge patients as soon as possible.
“Over the last few years, there’s been a major shift from fee-for-service to risk-based payment models,” Dr. Kuchaculla says. “The government’s financial incentives are driving outcomes to improve performance initiatives.”
“Today, LTACHs can be used as substitutes for short-term acute care,” says Sean R. Muldoon, MD, MPH, FCCP, chief medical officer of Kindred Healthcare in Louisville, Ky., and former chair of SHM’s Post-Acute Care Committee. “This means that a patient can be directly admitted from their home to an LTACH. In fact, many hospice and home-care patients are referred from physicians’ offices without a preceding hospitalization.”
Hospitalists can fill a need
More hospitalists are working in PACs for a number of reasons. Dr. Mathew says PAC facilities and services have “typically lacked the clinical structure and processes to obtain the results that patients and payors expect.
“These deficits needed to be quickly remedied as patients discharged from hospitals have increased acuity and higher disease burdens,” he adds. “Hospitalists were the natural choice to fill roles requiring their expertise and experience.”
Dr. Muldoon considers the expanded scope of practice into PACs an additional layer to hospital medicine’s value proposition to the healthcare system.
“As experts in the management of inpatient populations, it’s natural for hospitalists to expand to other facilities with inpatient-like populations,” he says, noting SNFs are the most popular choice, with IRFs and LTACHs also being common places to work. Few hospitalists work in home care or hospice.
PAC settings are designed to help patients who are transitioning from an inpatient setting back to their home or other setting.
“Many patients go home after a SNF stay, while others will move to a nursing home or other longer-term care setting for the first time,” says Tiffany Radcliff, PhD, a health economist in the department of health policy and management at Texas A&M University School of Public Health in College Station. “With this in mind, hospitalists working in PAC have the opportunity to address each patient’s ongoing care needs and prepare them for their next setting. Hospitalists can manage medication or other care regimen changes that resulted from an inpatient stay, reinforce discharge instructions to the patient and their caregivers, and identify any other issues with continuing care that need to be addressed before discharge to the next care setting.”
Transitioning Care
Even if a hospitalist is not employed at a PAC, it’s important that they know something about them.
“As patients are moved downstream earlier, hospitalists are being asked to help make a judgment regarding when and where an inpatient is transitioned,” Dr. Muldoon says. As organizations move toward becoming fully risk capable, it is necessary to develop referral networks of high-quality PAC providers to achieve the best clinical outcomes, reduce readmissions, and lower costs.2“Therefore, hospitalists should have a working knowledge of the different sites of service as well as some opinion on the suitability of available options in their community,” Dr. Muldoon says. “The hospitalist can also help to educate the hospitalized patient on what to expect at a PAC.”
If a patient is inappropriately prepared for the PAC setting, it could lead to incomplete management of their condition, which ultimately could lead to readmission.
“When hospitalists know how care is provided in a PAC setting, they are better able to ensure a smoother transition of care between settings,” says Tochi Iroku-Malize, MD, MPH, MBA, FAAFP, SFHM, chair of family medicine at Northwell Health in Long Island, N.Y. “This will ultimately prevent unnecessary readmissions.”
Further, the quality metrics that hospitals and thereby hospitalists are judged by no longer end at the hospital’s exit.
“The ownership of acute-care outcomes requires extending the accountability to outside of the institution’s four walls,” Dr. Mathew says. “The inpatient team needs to place great importance on the transition of care and the subsequent quality of that care when the patient is discharged.”
Robert W. Harrington Jr., MD, SFHM, chief medical officer of Plano, Texas–based Reliant Post-Acute Care Solutions and former SHM president, says the health system landscapes are pushing HM beyond the hospitals’ walls.
How PAC settings differ from hospitals
Practicing in PAC has some important nuances that hospitalists from short-term acute care need to get accustomed to, Dr. Muldoon says. Primarily, the diagnostic capabilities are much more limited, as is the presence of high-level staffing. Further, patients are less resilient to medication changes and interventions, so changes need to be done gradually.
“Hospitalists who try to practice acute-care medicine in a PAC setting may become frustrated by the length of time it takes to do a work-up, get a consultation, and respond to a patient’s change of condition,” Dr. Muldoon says. “Nonetheless, hospitalists can overcome this once recognizing this mind shift.”
According to Dr. Harrington, another challenge hospitalists may face is the inability of the hospital’s and PAC facility’s IT platforms to exchange electronic information.
“The major vendors on both sides need to figure out an interoperability strategy,” he says. “Currently, it often takes 1-3 days to receive a new patient’s discharge summary. The summary may consist of a stack of paper that takes significant time to sort through and requires the PAC facility to perform duplicate data entry. It’s a very highly inefficient process that opens up the doors to mistakes and errors of omission and commission that can result in bad patient outcomes.”
Arif Nazir, MD, CMD, FACP, AGSF, chief medical officer of Signature HealthCARE and president of SHC Medical Partners, both in Louisville, Ky., cites additional reasons the lack of seamless communication between a hospital and PAC facility is problematic. “I see physicians order laboratory tests and investigations that were already done in the hospital because they didn’t know they were already performed or never received the results,” he says. “Similarly, I see patients continue to take medications prescribed in the hospital long term even though they were only supposed to take them short term. I’ve also seen patients come to a PAC setting from a hospital without any formal understanding of their rehabilitative period and expectations for recovery.”
What’s ahead?
Looking to the future, Surafel Tsega, MD, clinical instructor at Mount Sinai Hospital in New York, says he thinks there will be a move toward greater collaboration among inpatient and PAC facilities, particularly in the discharge process, given that hospitals have an added incentive to ensure safe transitions because reimbursement from the Centers for Medicare & Medicaid Services is tied to readmissions and there are penalties for readmission. This involves more comprehensive planning regarding “warm handoffs” (e.g., real-time discussions with PAC providers about a patient’s hospital course and plan of care upon discharge), transferring of information, and so forth.
And while it can still be challenging to identify high-risk patients or determine the intensity and duration of their care, Dr. Mathew says risk-stratification tools and care pathways are continually being refined to maximize value with the limited resources available. In addition, with an increased emphasis on employing a team approach to care, there will be better integration of non-medical services to address the social determinants of health, which play significant roles in overall health and healing.
“Working with community-based organizations for this purpose will be a valuable tool for any of the population health–based initiatives,” he says.
Dr. Muldoon says he believes healthcare reform will increasingly view an inpatient admission as something to be avoided.
“If hospitalization can’t be avoided, then it should be shortened as much as possible,” he says. “This will shift inpatient care into LTACHs, SNFs, and IRFs. Hospitalists would be wise to follow patients into those settings as traditional inpatient census is reduced. This will take a few years, so hospitalists should start now in preparing for that downstream transition of individuals who were previously inpatients.”
The cost of care, and other PAC facts and figures
The amount of money that Medicare spends on post-acute care (PAC) has been increasing. In 2012, 12.6% of Medicare beneficiaries used some form of PAC, costing $62 billion.2 That amounts to the Centers for Medicare & Medicaid Services spending close to 25% of Medicare beneficiary expenses on PAC, a 133% increase from 2001 to 2012. Among the different types, $30.4 billion was spent on skilled nursing facilities (SNFs), $18.6 billion on home health, and $13.1 billion on long-term acute care (LTAC) and acute-care rehabilitation.2
It’s also been reported that after short-term acute-care hospitalization, about one in five Medicare beneficiaries requires continued specialized treatment in one of the three typical Medicare PAC settings: inpatient rehabilitation facilities (IRFs), LTAC hospitals, and SNFs.3
What’s more, hospital readmission nearly doubles the cost of an episode, so the financial implications for organizations operating in risk-bearing arrangements are significant. In 2013, 2,213 hospitals were charged $280 million in readmission penalties.2
References
1. The role of post-acute care in new care delivery models. American Hospital Association website. Available at: http://www.aha.org/research/reports/tw/15dec-tw-postacute.pdf. Accessed Nov. 7, 2016.
2. Post-acute care integration: Today and in the future. DHG Healthcare website. Available at: http://www2.dhgllp.com/res_pubs/HCG-Post-Acute-Care-Integration.pdf. Accessed Nov. 7, 2016.
3. Overview: Post-acute care transitions toolkit. Society for Hospital Medicine website. Available at: http://www.hospitalmedicine.org/Web/Quality___Innovation/Implementation_Toolkit/pact/Overview_PACT.aspx?hkey=dea3da3c-8620-46db-a00f-89f07f021958. Accessed Nov. 10, 2016.
Transplantation palliative care: The time is ripe
Over 10 years ago, a challenge was made in a surgical publication for increased collaboration between the fields of transplantation and palliative care.1
Since that time not much progress has been made bringing these fields together in a consistent way that would mutually benefit patients and the specialties. However, other progress has been made, particularly in the field of palliative care, which could brighten the prospects and broaden the opportunities to accomplish collaboration between palliative care and transplantation.
Growth of palliative services
During the past decade there has been a robust proliferation of hospital-based palliative care programs in the United States. In all, 67% of U.S. hospitals with 50 or more beds report palliative care teams, up from 63% in 2011 and 53% in 2008.
Only a decade ago, critical care and palliative care were generally considered mutually exclusive. Evidence is trickling in to suggest that this is no longer the case. Although palliative care was not an integral part of critical care at that time, patients, families, and even practitioners began to demand these services. Cook and Rocker have eloquently advocated the rightful place of palliative care in the ICU.2
Studies in recent years have shown that the integration of palliative care into critical care decreases in length of ICU and hospital stay, decreases costs, enhances patient/family satisfaction, and promotes a more rapid consensus about goals of care, without increasing mortality. The ICU experience to date could be considered a reassuring precedent for transplantation palliative care.
Integration of palliative care with transplantation
Early palliative care intervention has been shown to improve symptom burden and depression scores in end-stage liver disease patients awaiting transplant. In addition, early palliative care consultation in conjunction with cancer treatment has been associated with increased survival in non–small-cell lung cancer patients. It has been demonstrated that early integration of palliative care in the surgical ICU alongside disease-directed curative care can be accomplished without change in mortality, while improving end-of-life practice in liver transplant patients.3
What palliative care can do for transplant patients
What does palliative care mean for the person (and family) awaiting transplantation? For the cirrhotic patient with cachexia, ascites, and encephalopathy, it means access to the services of a team trained in the management of these symptoms. Palliative care teams can also provide psychosocial and spiritual support for patients and families who are intimidated by the complex navigation of the health care system and the existential threat that end-stage organ failure presents to them. Skilled palliative care and services can be the difference between failing and extended life with a higher quality of life for these very sick patients
Resuscitation of a patient, whether through restoration of organ function or interdicting the progression of disease, begins with resuscitation of hope. Nothing achieves this more quickly than amelioration of burdensome symptoms for the patient and family.
The barriers for transplant surgeons and teams referring and incorporating palliative care services in their practices are multiple and profound. The unique dilemma facing the transplant team is to balance the treatment of the failing organ, the treatment of the patient (and family and friends), and the best use of the graft, a precious gift of society.
Palliative surgery has been defined as any invasive procedure in which the main intention is to mitigate physical symptoms in patients with noncurable disease without causing premature death. The very success of transplantation over the past 3 decades has obscured our memory of transplantation as a type of palliative surgery. It is a well-known axiom of reconstructive surgery that the reconstructed site should be compared to what was there, not to “normal.” Even in the current era of improved immunosuppression and posttransplant support services, one could hardly describe even a successful transplant patient’s experience as “normal.” These patients’ lives may be extended and/or enhanced but they need palliative care before, during, and after transplantation. The growing availability of trained palliative care clinicians and teams, the increased familiarity of palliative and end-of-life care to surgical residents and fellows, and quality metrics measuring palliative care outcomes will provide reassurance and guidance to address reservations about the convergence of the two seemingly opposite realities.
A modest proposal
We propose that palliative care be presented to the entire spectrum of transplantation care: on the ward, in the ICU, and after transplantation. More specific “triggers” for palliative care for referral of transplant patients should be identified. Wentlandt et al.4 have described a promising model for an ambulatory clinic, which provides early, integrated palliative care to patients awaiting and receiving organ transplantation. In addition, we propose an application for grant funding for a conference and eventual formation of a work group of transplant surgeons and team members, palliative care clinicians, and patient/families who have experienced one of the aspects of the transplant spectrum. We await the subspecialty certification in hospice and palliative medicine of a transplant surgeon. Outside of transplantation, every other surgical specialty in the United States has diplomates certified in hospice and palliative medicine. We await the benefits that will accrue from research about the merging of these fields.
1. Molmenti EP, Dunn GP: Transplantation and palliative care: The convergence of two seemingly opposite realities. Surg Clin North Am. 2005;85:373-82.
2. Cook D, Rocker G. Dying with dignity in the intensive care unit. N Engl J Med. 2014;370:2506-14.
3. Lamba S, Murphy P, McVicker S, Smith JH, and Mosenthal AC. Changing end-of-life care practice for liver transplant patients: structured palliative care intervention in the surgical intensive care unit. J Pain Symptom Manage. 2012; 44(4):508-19.
4. Wentlandt, K., Dall’Osto, A., Freeman, N., Le, L. W., Kaya, E., Ross, H., Singer, L. G., Abbey, S., Clarke, H. and Zimmermann, C. (2016), The Transplant Palliative Care Clinic: An early palliative care model for patients in a transplant program. Clin Transplant. 2016 Nov 4; doi: 10.1111/ctr.12838.
Dr. Azoulay is a transplantation specialist of Assistance Publique – Hôpitaux de Paris, and the University of Paris. Dr. Dunn is medical director of the Palliative Care Consultation Service at the University of Pittsburgh Medical Center Hamot, and vice-chair of the ACS Committee on Surgical Palliative Care.
Over 10 years ago, a challenge was made in a surgical publication for increased collaboration between the fields of transplantation and palliative care.1
Since that time not much progress has been made bringing these fields together in a consistent way that would mutually benefit patients and the specialties. However, other progress has been made, particularly in the field of palliative care, which could brighten the prospects and broaden the opportunities to accomplish collaboration between palliative care and transplantation.
Growth of palliative services
During the past decade there has been a robust proliferation of hospital-based palliative care programs in the United States. In all, 67% of U.S. hospitals with 50 or more beds report palliative care teams, up from 63% in 2011 and 53% in 2008.
Only a decade ago, critical care and palliative care were generally considered mutually exclusive. Evidence is trickling in to suggest that this is no longer the case. Although palliative care was not an integral part of critical care at that time, patients, families, and even practitioners began to demand these services. Cook and Rocker have eloquently advocated the rightful place of palliative care in the ICU.2
Studies in recent years have shown that the integration of palliative care into critical care decreases in length of ICU and hospital stay, decreases costs, enhances patient/family satisfaction, and promotes a more rapid consensus about goals of care, without increasing mortality. The ICU experience to date could be considered a reassuring precedent for transplantation palliative care.
Integration of palliative care with transplantation
Early palliative care intervention has been shown to improve symptom burden and depression scores in end-stage liver disease patients awaiting transplant. In addition, early palliative care consultation in conjunction with cancer treatment has been associated with increased survival in non–small-cell lung cancer patients. It has been demonstrated that early integration of palliative care in the surgical ICU alongside disease-directed curative care can be accomplished without change in mortality, while improving end-of-life practice in liver transplant patients.3
What palliative care can do for transplant patients
What does palliative care mean for the person (and family) awaiting transplantation? For the cirrhotic patient with cachexia, ascites, and encephalopathy, it means access to the services of a team trained in the management of these symptoms. Palliative care teams can also provide psychosocial and spiritual support for patients and families who are intimidated by the complex navigation of the health care system and the existential threat that end-stage organ failure presents to them. Skilled palliative care and services can be the difference between failing and extended life with a higher quality of life for these very sick patients
Resuscitation of a patient, whether through restoration of organ function or interdicting the progression of disease, begins with resuscitation of hope. Nothing achieves this more quickly than amelioration of burdensome symptoms for the patient and family.
The barriers for transplant surgeons and teams referring and incorporating palliative care services in their practices are multiple and profound. The unique dilemma facing the transplant team is to balance the treatment of the failing organ, the treatment of the patient (and family and friends), and the best use of the graft, a precious gift of society.
Palliative surgery has been defined as any invasive procedure in which the main intention is to mitigate physical symptoms in patients with noncurable disease without causing premature death. The very success of transplantation over the past 3 decades has obscured our memory of transplantation as a type of palliative surgery. It is a well-known axiom of reconstructive surgery that the reconstructed site should be compared to what was there, not to “normal.” Even in the current era of improved immunosuppression and posttransplant support services, one could hardly describe even a successful transplant patient’s experience as “normal.” These patients’ lives may be extended and/or enhanced but they need palliative care before, during, and after transplantation. The growing availability of trained palliative care clinicians and teams, the increased familiarity of palliative and end-of-life care to surgical residents and fellows, and quality metrics measuring palliative care outcomes will provide reassurance and guidance to address reservations about the convergence of the two seemingly opposite realities.
A modest proposal
We propose that palliative care be presented to the entire spectrum of transplantation care: on the ward, in the ICU, and after transplantation. More specific “triggers” for palliative care for referral of transplant patients should be identified. Wentlandt et al.4 have described a promising model for an ambulatory clinic, which provides early, integrated palliative care to patients awaiting and receiving organ transplantation. In addition, we propose an application for grant funding for a conference and eventual formation of a work group of transplant surgeons and team members, palliative care clinicians, and patient/families who have experienced one of the aspects of the transplant spectrum. We await the subspecialty certification in hospice and palliative medicine of a transplant surgeon. Outside of transplantation, every other surgical specialty in the United States has diplomates certified in hospice and palliative medicine. We await the benefits that will accrue from research about the merging of these fields.
1. Molmenti EP, Dunn GP: Transplantation and palliative care: The convergence of two seemingly opposite realities. Surg Clin North Am. 2005;85:373-82.
2. Cook D, Rocker G. Dying with dignity in the intensive care unit. N Engl J Med. 2014;370:2506-14.
3. Lamba S, Murphy P, McVicker S, Smith JH, and Mosenthal AC. Changing end-of-life care practice for liver transplant patients: structured palliative care intervention in the surgical intensive care unit. J Pain Symptom Manage. 2012; 44(4):508-19.
4. Wentlandt, K., Dall’Osto, A., Freeman, N., Le, L. W., Kaya, E., Ross, H., Singer, L. G., Abbey, S., Clarke, H. and Zimmermann, C. (2016), The Transplant Palliative Care Clinic: An early palliative care model for patients in a transplant program. Clin Transplant. 2016 Nov 4; doi: 10.1111/ctr.12838.
Dr. Azoulay is a transplantation specialist of Assistance Publique – Hôpitaux de Paris, and the University of Paris. Dr. Dunn is medical director of the Palliative Care Consultation Service at the University of Pittsburgh Medical Center Hamot, and vice-chair of the ACS Committee on Surgical Palliative Care.
Over 10 years ago, a challenge was made in a surgical publication for increased collaboration between the fields of transplantation and palliative care.1
Since that time not much progress has been made bringing these fields together in a consistent way that would mutually benefit patients and the specialties. However, other progress has been made, particularly in the field of palliative care, which could brighten the prospects and broaden the opportunities to accomplish collaboration between palliative care and transplantation.
Growth of palliative services
During the past decade there has been a robust proliferation of hospital-based palliative care programs in the United States. In all, 67% of U.S. hospitals with 50 or more beds report palliative care teams, up from 63% in 2011 and 53% in 2008.
Only a decade ago, critical care and palliative care were generally considered mutually exclusive. Evidence is trickling in to suggest that this is no longer the case. Although palliative care was not an integral part of critical care at that time, patients, families, and even practitioners began to demand these services. Cook and Rocker have eloquently advocated the rightful place of palliative care in the ICU.2
Studies in recent years have shown that the integration of palliative care into critical care decreases in length of ICU and hospital stay, decreases costs, enhances patient/family satisfaction, and promotes a more rapid consensus about goals of care, without increasing mortality. The ICU experience to date could be considered a reassuring precedent for transplantation palliative care.
Integration of palliative care with transplantation
Early palliative care intervention has been shown to improve symptom burden and depression scores in end-stage liver disease patients awaiting transplant. In addition, early palliative care consultation in conjunction with cancer treatment has been associated with increased survival in non–small-cell lung cancer patients. It has been demonstrated that early integration of palliative care in the surgical ICU alongside disease-directed curative care can be accomplished without change in mortality, while improving end-of-life practice in liver transplant patients.3
What palliative care can do for transplant patients
What does palliative care mean for the person (and family) awaiting transplantation? For the cirrhotic patient with cachexia, ascites, and encephalopathy, it means access to the services of a team trained in the management of these symptoms. Palliative care teams can also provide psychosocial and spiritual support for patients and families who are intimidated by the complex navigation of the health care system and the existential threat that end-stage organ failure presents to them. Skilled palliative care and services can be the difference between failing and extended life with a higher quality of life for these very sick patients
Resuscitation of a patient, whether through restoration of organ function or interdicting the progression of disease, begins with resuscitation of hope. Nothing achieves this more quickly than amelioration of burdensome symptoms for the patient and family.
The barriers for transplant surgeons and teams referring and incorporating palliative care services in their practices are multiple and profound. The unique dilemma facing the transplant team is to balance the treatment of the failing organ, the treatment of the patient (and family and friends), and the best use of the graft, a precious gift of society.
Palliative surgery has been defined as any invasive procedure in which the main intention is to mitigate physical symptoms in patients with noncurable disease without causing premature death. The very success of transplantation over the past 3 decades has obscured our memory of transplantation as a type of palliative surgery. It is a well-known axiom of reconstructive surgery that the reconstructed site should be compared to what was there, not to “normal.” Even in the current era of improved immunosuppression and posttransplant support services, one could hardly describe even a successful transplant patient’s experience as “normal.” These patients’ lives may be extended and/or enhanced but they need palliative care before, during, and after transplantation. The growing availability of trained palliative care clinicians and teams, the increased familiarity of palliative and end-of-life care to surgical residents and fellows, and quality metrics measuring palliative care outcomes will provide reassurance and guidance to address reservations about the convergence of the two seemingly opposite realities.
A modest proposal
We propose that palliative care be presented to the entire spectrum of transplantation care: on the ward, in the ICU, and after transplantation. More specific “triggers” for palliative care for referral of transplant patients should be identified. Wentlandt et al.4 have described a promising model for an ambulatory clinic, which provides early, integrated palliative care to patients awaiting and receiving organ transplantation. In addition, we propose an application for grant funding for a conference and eventual formation of a work group of transplant surgeons and team members, palliative care clinicians, and patient/families who have experienced one of the aspects of the transplant spectrum. We await the subspecialty certification in hospice and palliative medicine of a transplant surgeon. Outside of transplantation, every other surgical specialty in the United States has diplomates certified in hospice and palliative medicine. We await the benefits that will accrue from research about the merging of these fields.
1. Molmenti EP, Dunn GP: Transplantation and palliative care: The convergence of two seemingly opposite realities. Surg Clin North Am. 2005;85:373-82.
2. Cook D, Rocker G. Dying with dignity in the intensive care unit. N Engl J Med. 2014;370:2506-14.
3. Lamba S, Murphy P, McVicker S, Smith JH, and Mosenthal AC. Changing end-of-life care practice for liver transplant patients: structured palliative care intervention in the surgical intensive care unit. J Pain Symptom Manage. 2012; 44(4):508-19.
4. Wentlandt, K., Dall’Osto, A., Freeman, N., Le, L. W., Kaya, E., Ross, H., Singer, L. G., Abbey, S., Clarke, H. and Zimmermann, C. (2016), The Transplant Palliative Care Clinic: An early palliative care model for patients in a transplant program. Clin Transplant. 2016 Nov 4; doi: 10.1111/ctr.12838.
Dr. Azoulay is a transplantation specialist of Assistance Publique – Hôpitaux de Paris, and the University of Paris. Dr. Dunn is medical director of the Palliative Care Consultation Service at the University of Pittsburgh Medical Center Hamot, and vice-chair of the ACS Committee on Surgical Palliative Care.
Best Practices: Protecting Dry Vulnerable Skin with CeraVe® Healing Ointment
A supplement to Dermatology News. This advertising supplement is sponsored by Valeant Pharmaceuticals.
- Reinforcing the Skin Barrier
- NEA Seal of Acceptance
- A Preventative Approach to Dry, Cracked Skin
- CeraVe Ointment in the Clinical Setting
Faculty/Faculty Disclosure
Sheila Fallon Friedlander, MD
Professor of Clinical Dermatology & Pediatrics
Director, Pediatric Dermatology Fellowship Training Program
University of California at San Diego School of Medicine
Rady Children’s Hospital,
San Diego, California
Dr. Friedlander was compensated for her participation in the development of this article.
CeraVe is a registered trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.
A supplement to Dermatology News. This advertising supplement is sponsored by Valeant Pharmaceuticals.
- Reinforcing the Skin Barrier
- NEA Seal of Acceptance
- A Preventative Approach to Dry, Cracked Skin
- CeraVe Ointment in the Clinical Setting
Faculty/Faculty Disclosure
Sheila Fallon Friedlander, MD
Professor of Clinical Dermatology & Pediatrics
Director, Pediatric Dermatology Fellowship Training Program
University of California at San Diego School of Medicine
Rady Children’s Hospital,
San Diego, California
Dr. Friedlander was compensated for her participation in the development of this article.
CeraVe is a registered trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.
A supplement to Dermatology News. This advertising supplement is sponsored by Valeant Pharmaceuticals.
- Reinforcing the Skin Barrier
- NEA Seal of Acceptance
- A Preventative Approach to Dry, Cracked Skin
- CeraVe Ointment in the Clinical Setting
Faculty/Faculty Disclosure
Sheila Fallon Friedlander, MD
Professor of Clinical Dermatology & Pediatrics
Director, Pediatric Dermatology Fellowship Training Program
University of California at San Diego School of Medicine
Rady Children’s Hospital,
San Diego, California
Dr. Friedlander was compensated for her participation in the development of this article.
CeraVe is a registered trademark of Valeant Pharmaceuticals International, Inc. or its affiliates.
Asymptomatic Papules on the Neck
THE DIAGNOSIS: White Fibrous Papulosis
Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al1 in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.2,4 Our patient elected not to proceed with treatment.
Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.
Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.6 This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.7 Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.8 Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.9
Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.10 This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.11 Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).
Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.12 The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.13 Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).
Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.14 Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).
- Shimizu H, Nishikawa T, Kimura S. White fibrous papulosis of the neck: review of our 16 cases. Nihon Hifuka Gakkai Zasshi. 1985;95:1077-1084.
- Teo W, Pang S. White fibrous papulosis of the chest and back. J Am Acad Dermatol. 2012;66:AB33.
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635.
- Lueangarun S, Panchaprateep R. White fibrous papulosis of the neck treated with fractionated 1550-nm erbium glass laser: a case report. J Lasers Med Sci. 2016;7:256-258.
- Rios-Gomez M, Ramos-Garibay JA, Perez-Santana ME, et al. White fibrous papulosis of the neck: a case report. Cureus. 2022;14:E25661.
- Váradi A, Szabó Z, Pomozi V, et al. ABCC6 as a target in pseudoxanthoma elasticum. Curr Drug Targets. 2011;12:671-682.
- Gliem M, Birtel J, Müller PL, et al. Acute retinopathy in pseudoxanthoma elasticum. JAMA Ophthalmol. 2019;137:1165-1173.
- Germain DP. Pseudoxanthoma elasticum. Orphanet J Rare Dis. 2017;12:85. doi:10.1186/s13023-017-0639-8
- Chisti MA, Binamer Y, Alfadley A, et al. D-penicillamine-induced pseudo-pseudoxanthoma elasticum and extensive elastosis perforans serpiginosa with excellent response to acitretin. Ann Saudi Med. 2019;39:56-60.
- Criscito MC, Mu EW, Meehan SA, et al. Dermoscopic features of a solitary fibrofolliculoma on the left cheek. J Am Acad Dermatol. 2017;76(2 suppl 1):S8-S9.
- Sattler EC, Steinlein OK. Birt-Hogg-Dubé syndrome. In: Adam MP, Everman DB, Mirzaa GM, et al, eds. GeneReviews® [Internet]. Updated January 30, 2020. Accessed February 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK1522
- Patnayak R, Jena A, Settipalli S, et al. Elastofibroma: an uncommon tumor revisited. J Cutan Aesthet Surg. 2016;9:34-37. doi:10.4103/0974- 2077.178543
- Chandrasekar CR, Grimer RJ, Carter SR, et al. Elastofibroma dorsi: an uncommon benign pseudotumour. Sarcoma. 2008;2008:756565. doi:10.1155/2008/756565
- Kwittken J. Papular elastosis. Cutis. 2000;66:81-83.
THE DIAGNOSIS: White Fibrous Papulosis
Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al1 in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.2,4 Our patient elected not to proceed with treatment.
Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.
Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.6 This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.7 Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.8 Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.9
Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.10 This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.11 Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).
Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.12 The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.13 Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).
Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.14 Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).
THE DIAGNOSIS: White Fibrous Papulosis
Given the histopathology findings, location on a sun-exposed site, lack of any additional systemic signs or symptoms, and no family history of similar lesions to suggest an underlying genetic condition, a diagnosis of white fibrous papulosis (WFP) was made. White fibrous papulosis is a relatively rare cutaneous disorder that was first reported by Shimizu et al1 in 1985. It is characterized by numerous grouped, 2- to 3-mm, white to flesh-colored papules that in most cases are confined to the neck in middle-aged to elderly individuals; however, cases involving the upper trunk and axillae also have been reported.1-3 The etiology of this condition is unclear but is thought to be related to aging and chronic exposure to UV light. Although treatment is not required, various modalities including tretinoin, excision, and laser therapy have been trialed with varying success.2,4 Our patient elected not to proceed with treatment.
Histologically, WFP may manifest similarly to connective tissue nevi; the overall architecture is nonspecific with focally thickened collagen and often elastic fibers that may be normal to reduced and/or fragmented, as well as an overall decrease in superficial dermal elastic tissue.3,5 Therefore, the differential diagnosis may include connective tissue nevi and require clinical correlation to make a correct diagnosis.
Pseudoxanthoma elasticum (PXE) is an autosomalrecessive disorder most commonly related to mutations in the ATP binding cassette subfamily C member 6 (ABCC6) gene that tends to manifest clinically on the neck and flexural extremities.6 This disease affects elastic fibers, which may become calcified over time. Pseudoxanthoma elasticum is associated with ocular complications relating to the Bruch membrane of the retina and angioid streaks; choroidal neovascularization involving the damaged Bruch membrane and episodes of acute retinopathy may result in vision loss in later stages of the disease.7 Involvement of the elastic laminae of arteries can be associated with cardiovascular and cerebrovascular complications such as stroke, coronary artery disease, claudication, and aneurysms. Involvement of the gastrointestinal or genitourinary tracts also may occur and most commonly manifests with bleeding. Pathologic alterations in the elastic fibers of the lungs also have been reported in patients with PXE.8 Histologically, PXE exhibits increased abnormally clumped and fragmented elastic fibers in the superficial dermis, often with calcification (Figure 1). Pseudo-PXE related to D-penicillamine use often lacks calcification and has a bramble bush appearance.9
Fibrofolliculomas may manifest alone or in association with an underlying condition such as Birt-Hogg-Dubé syndrome, in which lesions are most frequently seen scattered on the scalp, face, ears, neck, or upper trunk.10 This condition is related to a folliculin (FLCN) gene germline mutation. Birt-Hogg-Dubé syndrome also may be associated with acrochordons, trichodiscomas, renal cancer, and lung cysts with or without spontaneous pneumothorax. Less frequently noted findings include oral papules, epidermal cysts, angiofibromas, lipomas/angiolipomas, parotid gland tumors, and thyroid neoplasms. Connective tissue nevi/collagenomas can appear clinically similar to fibrofolliculomas; true connective tissue nevi are reported less commonly in Birt-Hogg-Dubé syndrome.11 Histologically, a fibrofolliculoma manifests with epidermal strands originating from a hair follicle associated with prominent surrounding connective tissue (Figure 2).
Elastofibroma dorsi is a benign tumor of connective tissue that most commonly manifests clinically as a solitary subcutaneous mass on the back near the inferior angle of the scapula; it typically develops below the rhomboid major and latissimus dorsi muscles.12 The pathogenesis is uncertain, but some patients have reported a family history of the condition or a history of repetitive shoulder movement/trauma prior to onset; the mass may be asymptomatic or associated with pain and/or swelling. Those affected tend to be older than 50 years.13 Histologically, thickened and rounded to beaded elastic fibers are seen admixed with collagen (Figure 3).
Actinic (solar) elastosis frequently is encountered in many skin biopsies and is caused by chronic photodamage. More hypertrophic variants, such as papular or nodular solar elastosis, may clinically manifest similarly to WFP.14 Histologically, actinic elastosis manifests as a considerable increase in elastic tissue in the papillary and superficial reticular dermis (Figure 4).
- Shimizu H, Nishikawa T, Kimura S. White fibrous papulosis of the neck: review of our 16 cases. Nihon Hifuka Gakkai Zasshi. 1985;95:1077-1084.
- Teo W, Pang S. White fibrous papulosis of the chest and back. J Am Acad Dermatol. 2012;66:AB33.
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635.
- Lueangarun S, Panchaprateep R. White fibrous papulosis of the neck treated with fractionated 1550-nm erbium glass laser: a case report. J Lasers Med Sci. 2016;7:256-258.
- Rios-Gomez M, Ramos-Garibay JA, Perez-Santana ME, et al. White fibrous papulosis of the neck: a case report. Cureus. 2022;14:E25661.
- Váradi A, Szabó Z, Pomozi V, et al. ABCC6 as a target in pseudoxanthoma elasticum. Curr Drug Targets. 2011;12:671-682.
- Gliem M, Birtel J, Müller PL, et al. Acute retinopathy in pseudoxanthoma elasticum. JAMA Ophthalmol. 2019;137:1165-1173.
- Germain DP. Pseudoxanthoma elasticum. Orphanet J Rare Dis. 2017;12:85. doi:10.1186/s13023-017-0639-8
- Chisti MA, Binamer Y, Alfadley A, et al. D-penicillamine-induced pseudo-pseudoxanthoma elasticum and extensive elastosis perforans serpiginosa with excellent response to acitretin. Ann Saudi Med. 2019;39:56-60.
- Criscito MC, Mu EW, Meehan SA, et al. Dermoscopic features of a solitary fibrofolliculoma on the left cheek. J Am Acad Dermatol. 2017;76(2 suppl 1):S8-S9.
- Sattler EC, Steinlein OK. Birt-Hogg-Dubé syndrome. In: Adam MP, Everman DB, Mirzaa GM, et al, eds. GeneReviews® [Internet]. Updated January 30, 2020. Accessed February 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK1522
- Patnayak R, Jena A, Settipalli S, et al. Elastofibroma: an uncommon tumor revisited. J Cutan Aesthet Surg. 2016;9:34-37. doi:10.4103/0974- 2077.178543
- Chandrasekar CR, Grimer RJ, Carter SR, et al. Elastofibroma dorsi: an uncommon benign pseudotumour. Sarcoma. 2008;2008:756565. doi:10.1155/2008/756565
- Kwittken J. Papular elastosis. Cutis. 2000;66:81-83.
- Shimizu H, Nishikawa T, Kimura S. White fibrous papulosis of the neck: review of our 16 cases. Nihon Hifuka Gakkai Zasshi. 1985;95:1077-1084.
- Teo W, Pang S. White fibrous papulosis of the chest and back. J Am Acad Dermatol. 2012;66:AB33.
- Dokic Y, Tschen J. White fibrous papulosis of the axillae and neck. Cureus. 2020;12:E7635.
- Lueangarun S, Panchaprateep R. White fibrous papulosis of the neck treated with fractionated 1550-nm erbium glass laser: a case report. J Lasers Med Sci. 2016;7:256-258.
- Rios-Gomez M, Ramos-Garibay JA, Perez-Santana ME, et al. White fibrous papulosis of the neck: a case report. Cureus. 2022;14:E25661.
- Váradi A, Szabó Z, Pomozi V, et al. ABCC6 as a target in pseudoxanthoma elasticum. Curr Drug Targets. 2011;12:671-682.
- Gliem M, Birtel J, Müller PL, et al. Acute retinopathy in pseudoxanthoma elasticum. JAMA Ophthalmol. 2019;137:1165-1173.
- Germain DP. Pseudoxanthoma elasticum. Orphanet J Rare Dis. 2017;12:85. doi:10.1186/s13023-017-0639-8
- Chisti MA, Binamer Y, Alfadley A, et al. D-penicillamine-induced pseudo-pseudoxanthoma elasticum and extensive elastosis perforans serpiginosa with excellent response to acitretin. Ann Saudi Med. 2019;39:56-60.
- Criscito MC, Mu EW, Meehan SA, et al. Dermoscopic features of a solitary fibrofolliculoma on the left cheek. J Am Acad Dermatol. 2017;76(2 suppl 1):S8-S9.
- Sattler EC, Steinlein OK. Birt-Hogg-Dubé syndrome. In: Adam MP, Everman DB, Mirzaa GM, et al, eds. GeneReviews® [Internet]. Updated January 30, 2020. Accessed February 23, 2023. https://www.ncbi.nlm.nih.gov/books/NBK1522
- Patnayak R, Jena A, Settipalli S, et al. Elastofibroma: an uncommon tumor revisited. J Cutan Aesthet Surg. 2016;9:34-37. doi:10.4103/0974- 2077.178543
- Chandrasekar CR, Grimer RJ, Carter SR, et al. Elastofibroma dorsi: an uncommon benign pseudotumour. Sarcoma. 2008;2008:756565. doi:10.1155/2008/756565
- Kwittken J. Papular elastosis. Cutis. 2000;66:81-83.
A 70-year-old woman with a history of osteoporosis and breast cancer presented for evaluation of asymptomatic, 2- to 3-mm, white to flesh-colored papules concentrated on the inferior occipital scalp and posterior neck (inset) for at least several months. She had no additional systemic signs or symptoms, and there was no family history of similar skin findings. A punch biopsy was performed.
Eating Disorder Risk Factors and the Impact of Obesity in Patients With Psoriasis
Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.
Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.1 Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.1
Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.2 Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.3 Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.5 Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.
Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.6 According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,7 binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).7 Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).8 The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.9
The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.
Materials and Methods
This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).
Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.
Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), and obese (≥30 kg/m2).13
Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.8 In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.
The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).10
The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).11
The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.12
Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ2 test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.
Results
Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m2. According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).
Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.
Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).
Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).
Comment
Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes14) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.
The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.15 Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al17 emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.17 Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.18 The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.5 Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.
Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.19 In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.20 It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.18 In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.5 All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al21 conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.21 Mrowietz et al22 also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.23 Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.
Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.26 Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.28
There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al29 demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al30 demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.30 In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.
Conclusion
Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.
References
1. Kalkan G. Comorbidities in psoriasis: the recognition of psoriasis as a systemic disease and current management. Turkderm-Turk Arch Dermatol Venereol. 2017;51:71-77.
2. Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and obesity: a systematic review and meta-analysis of observational studies. Nutr Diabetes. 2012;2:E54.
3. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
4. Mirghani H, Altemani AT, Altemani ST, et al. The cross talk between psoriasis, obesity, and dyslipidemia: a meta-analysis. Cureus. 2023;15:e49253.
5. Roehring M, Mashep MR, White MA, et al. The metabolic syndrome and behavioral correlates in obese patients with binge disorders. Obesity. 2009;17:481-486.
6. da Luz FQ, Hay P, Touyz S, et al. Obesity with comorbid eating disorders: associated health risks and treatment approaches. Nutrients. 2018;10:829.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association; 2013.
8. Ergüney Okumus¸ FE, Sertel Berk HÖ. The psychometric properties of the Eating Attitudes Test short form (EAT-26) in a college sample. Stud Psychol. 2020;40:57-78.
9. Stoleru G, Leopold A, Auerbach A, et al. Female gender, dissatisfaction with weight, and number of IBD related surgeries as independent risk factors for eating disorders among patients with inflammatory bowel diseases. BMC Gastroenterol. 2022;22:438.
10. Öztürkcan S, Ermertcan AT, Eser E, et al. Cross validation of the Turkish version of dermatology life quality index. Int J Dermatol. 2006;45:1300-1307.
11. Demir GT, Ciciog˘lu HI˙. Attitude scale for healthy nutrition (ASHN): validity and reliability study. Gaziantep Univ J Sport Sci. 2019;4:256-274.
12. Yılmaz O, Boz H, Arslan A. The validity and reliability of depression stress and anxiety scale (DASS 21) Turkish short form. Res Financial Econ Soc Stud. 2017;2:78-91.
13. Nuttall FQ. Body mass index: obesity, BMI, and health: a critical review. Nutr Today. 2015;50:117-128.
14. Strumia R, Manzata E, Gualandi M. Is there a role for dermatologists in eating disorders? Expert Rev Dermatol. 2017; 2:109-112.
15. Henseler T, Christophers E. Disease concomitance in psoriasis. J Am Acad Dermatol. 1995;32:982-986.
16. Naldi L, Addis A, Chimenti S, et al. Impact of body mass index and obesity on clinical response to systemic treatment for psoriasis. evidence from the Psocare project. Dermatology. 2008;217:365-373.
17. Barros G, Duran P, Vera I, et al. Exploring the links between obesity and psoriasis: a comprehensive review. Int J Mol Sci. 2022;23:7499.
18. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060.
19. Jing D, Xiao H, Shen M, et al. Association of psoriasis with anxiety and depression: a case–control study in Chinese patients. Front Med (Lausanne). 2021;8:771645.
20. Sahi FM, Masood A, Danawar NA, et al. Association between psoriasis and depression: a traditional review. Cureus. 2020;12:E9708.
21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.
22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.
23. Pavlova NT, Kioskli K, Smith C, et al. Psychosocial aspects of obesity in adults with psoriasis: a systematic review. Skin Health Dis. 2021;1:E33.
24. Innamorati M, Quinto RM, Imperatori C, et al. Health-related quality of life and its association with alexithymia and difficulties in emotion regulation in patients with psoriasis. Compr Psychiatry. 2016;70:200-208.
25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.
26. Albuquerque D, Nóbrega C, Manco L, et al. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123:159‐173.
27. Balantekin KN, Grammer AC, Fitzsimmons-Craft EE, et al. Overweight and obesity are associated with increased eating disorder correlates and general psychopathology in university women with eating disorders. Eat Behav. 2021;41:101482.
28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.
29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.
30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.
Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.
Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.1 Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.1
Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.2 Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.3 Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.5 Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.
Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.6 According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,7 binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).7 Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).8 The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.9
The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.
Materials and Methods
This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).
Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.
Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), and obese (≥30 kg/m2).13
Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.8 In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.
The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).10
The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).11
The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.12
Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ2 test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.
Results
Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m2. According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).
Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.
Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).
Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).
Comment
Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes14) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.
The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.15 Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al17 emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.17 Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.18 The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.5 Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.
Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.19 In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.20 It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.18 In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.5 All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al21 conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.21 Mrowietz et al22 also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.23 Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.
Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.26 Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.28
There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al29 demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al30 demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.30 In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.
Conclusion
Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.
References
1. Kalkan G. Comorbidities in psoriasis: the recognition of psoriasis as a systemic disease and current management. Turkderm-Turk Arch Dermatol Venereol. 2017;51:71-77.
2. Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and obesity: a systematic review and meta-analysis of observational studies. Nutr Diabetes. 2012;2:E54.
3. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
4. Mirghani H, Altemani AT, Altemani ST, et al. The cross talk between psoriasis, obesity, and dyslipidemia: a meta-analysis. Cureus. 2023;15:e49253.
5. Roehring M, Mashep MR, White MA, et al. The metabolic syndrome and behavioral correlates in obese patients with binge disorders. Obesity. 2009;17:481-486.
6. da Luz FQ, Hay P, Touyz S, et al. Obesity with comorbid eating disorders: associated health risks and treatment approaches. Nutrients. 2018;10:829.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association; 2013.
8. Ergüney Okumus¸ FE, Sertel Berk HÖ. The psychometric properties of the Eating Attitudes Test short form (EAT-26) in a college sample. Stud Psychol. 2020;40:57-78.
9. Stoleru G, Leopold A, Auerbach A, et al. Female gender, dissatisfaction with weight, and number of IBD related surgeries as independent risk factors for eating disorders among patients with inflammatory bowel diseases. BMC Gastroenterol. 2022;22:438.
10. Öztürkcan S, Ermertcan AT, Eser E, et al. Cross validation of the Turkish version of dermatology life quality index. Int J Dermatol. 2006;45:1300-1307.
11. Demir GT, Ciciog˘lu HI˙. Attitude scale for healthy nutrition (ASHN): validity and reliability study. Gaziantep Univ J Sport Sci. 2019;4:256-274.
12. Yılmaz O, Boz H, Arslan A. The validity and reliability of depression stress and anxiety scale (DASS 21) Turkish short form. Res Financial Econ Soc Stud. 2017;2:78-91.
13. Nuttall FQ. Body mass index: obesity, BMI, and health: a critical review. Nutr Today. 2015;50:117-128.
14. Strumia R, Manzata E, Gualandi M. Is there a role for dermatologists in eating disorders? Expert Rev Dermatol. 2017; 2:109-112.
15. Henseler T, Christophers E. Disease concomitance in psoriasis. J Am Acad Dermatol. 1995;32:982-986.
16. Naldi L, Addis A, Chimenti S, et al. Impact of body mass index and obesity on clinical response to systemic treatment for psoriasis. evidence from the Psocare project. Dermatology. 2008;217:365-373.
17. Barros G, Duran P, Vera I, et al. Exploring the links between obesity and psoriasis: a comprehensive review. Int J Mol Sci. 2022;23:7499.
18. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060.
19. Jing D, Xiao H, Shen M, et al. Association of psoriasis with anxiety and depression: a case–control study in Chinese patients. Front Med (Lausanne). 2021;8:771645.
20. Sahi FM, Masood A, Danawar NA, et al. Association between psoriasis and depression: a traditional review. Cureus. 2020;12:E9708.
21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.
22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.
23. Pavlova NT, Kioskli K, Smith C, et al. Psychosocial aspects of obesity in adults with psoriasis: a systematic review. Skin Health Dis. 2021;1:E33.
24. Innamorati M, Quinto RM, Imperatori C, et al. Health-related quality of life and its association with alexithymia and difficulties in emotion regulation in patients with psoriasis. Compr Psychiatry. 2016;70:200-208.
25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.
26. Albuquerque D, Nóbrega C, Manco L, et al. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123:159‐173.
27. Balantekin KN, Grammer AC, Fitzsimmons-Craft EE, et al. Overweight and obesity are associated with increased eating disorder correlates and general psychopathology in university women with eating disorders. Eat Behav. 2021;41:101482.
28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.
29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.
30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.
Current evidence indicates that obesity may initiate psoriasis or worsen existing disease. Various factors contribute to the development of obesity, including eating disorders (EDs). The aim of this study was to screen for and identify factors associated with EDs in patients with psoriasis and their impact on the development of obesity in this population. Demographic information including body mass index (BMI), Eating Attitude Test (EAT-26), Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale 21 (DASS-21) scores were statistically analyzed for 82 participants with psoriasis at a tertiary dermatology clinic. It is important to manage obesity and other comorbidities of psoriasis in addition to treating its cutaneous manifestations, which may require a biopsychosocial approach.
Psoriasis is a chronic multisystemic inflammatory skin disease with a worldwide prevalence of 2% to 3%.1 Psoriasis can be accompanied by other conditions such as psoriatic arthritis, obesity, metabolic syndrome, diabetes mellitus, hypertension, dyslipidemia, atherosclerotic disease, inflammatory bowel disease, and anxiety/depression. It is important to manage comorbidities of psoriasis in addition to treating the cutaneous manifestations of the disease.1
Obesity is a major public health concern worldwide. Numerous observational and epidemiologic studies have reported a high prevalence of obesity among patients with psoriasis.2 Current evidence indicates that obesity may initiate or worsen psoriasis; furthermore, it is important to note that obesity may negatively impact the effectiveness of psoriasis-specific treatments or increase the incidence of adverse effects. Therefore, managing obesity is crucial in the treatment of psoriasis.3 Numerous studies have investigated the association between psoriasis and obesity, and they commonly conclude that both conditions share the same genetic metabolic pathways.2-4 However, it is important to consider environmental factors such as dietary habits, smoking, alcohol consumption, and a sedentary lifestyle—all of which are associated with psoriasis and also can contribute to the development of obesity.5 Because of the effects of obesity in psoriasis patients, factors that impact the development of obesity have become a popular research topic.
Eating disorders (EDs) are a crucial risk factor for both developing and maintaining obesity. In particular, two EDs that are associated with obesity include binge eating disorder and bulimia nervosa.6 According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,7 binge eating disorder can be diagnosed when a patient has at least 1 episode of binge eating per week over a 3-month period. Bulimia nervosa can be diagnosed when a patient is excessively concerned with their body weight and shape and engages in behaviors to prevent weight gain (eg, forced vomiting, excessive use of laxatives).7 Psychiatrists who specialize in EDs make diagnoses based on these criteria. In daily practice, there are several quick and simple questionnaires available to screen for EDs that can be used by nonpsychiatrist physicians, including the commonly used 26-item Eating Attitudes Test (EAT-26).8 The EAT-26 has been used to screen for EDs in patients with inflammatory disorders.9
The aim of this study was to screen for EDs in patients with psoriasis to identify potential risk factors for development of obesity.
Materials and Methods
This study included patients with psoriasis who were screened for EDs at a tertiary dermatology clinic in Turkey between January 2021 and December 2023. This study was approved by the local ethics committee and was in accordance with the Declaration of Helsinki (decision number E-93471371-514.99-225000079).
Study Design and Patient Inclusion Criteria—This quantitative cross-sectional study utilized EAT-26, Dermatology Life Quality Index (DLQI), Attitude Scale for Healthy Nutrition (ASHN), and Depression Anxiety Stress Scale-21 (DASS-21) scores. All the questionnaire scales used in the study were adapted and validated in Turkey.8,10-12 The inclusion criteria consisted of being older than 18 years of age, being literate, having psoriasis for at least 1 year that was not treated topically or systemically, and having no psychiatric diseases outside an ED. The questionnaires were presented in written format following the clinical examination. Literacy was an inclusion criterion in this study due to the absence of auxiliary health personnel.
Study Variables—The study variables included age, sex, marital status (single/divorced or married), education status (primary/secondary school or high school/university), employment status (employed or unemployed/retired), body mass index (BMI), smoking status, alcohol-consumption status, Psoriasis Area Severity Index score, presence of nail psoriasis and psoriatic arthritis, duration of psoriasis, family history of psoriasis, EAT-26 score, ASHN score, DLQI score, and DASS-21 score. Body mass index was calculated by taking a participant’s weight in kilograms and dividing it by their height in meters squared. The BMI values were classified into 3 categories: normal (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), and obese (≥30 kg/m2).13
Questionnaires—The EAT-26 questionnaire includes 26 questions that are used to detect EDs. Responses to each question include Likert-type answer options (ie, “always,” “usually,” “often,” “sometimes,” “rarely,” and “never.”) Patients with scores of 20 points or higher (range, 0–78) are classified as high risk for EDs.8 In our study, EAT-26 scores were grouped into 2 categories: patients scoring less than 20 points and those scoring 20 points or higher.
The DLQI questionnaire includes 10 questions to measure dermatologic symptoms and qualiy of life. Responses to each question include Likert-type answer options (ie, “not at all,” “a little,” “a lot,” or “very much.”) On the DLQI scale, the higher the score, the lower the quality of life (score range, 0–30).10
The ASHN questionnaire includes 21 questions that measure attitudes toward healthy nutrition with 5 possible answer options (“strongly disagree,” “disagree,” “undecided,” “agree,” and “strongly agree”). On this scale, higher scores indicate the participant is more knowledgeable about healthy nutrition (score range, 0–78).11
The DASS-21 questionnaire includes 21 questions that measure the severity of a range of symptoms common to depression, anxiety, and stress. Responses include Likert-type answer options (eg, “never,” “sometimes,” “often,” and “almost always.”) On this scale, a higher score (range of 0–21 for each) indicates higher levels of depression, anxiety, and stress.12
Statistical Analysis—Descriptive statistics were analyzed using SPSS software version 22.0 (IBM). The Shapiro-Wilk test was applied to determine whether the data were normally distributed. For categorical variables, frequency differences among groups were compared using the Pearson χ2 test. A t test was used to compare the means of 2 independent groups with a normal distribution. One-way analysis of variance and Tukey Honest Significant Difference post hoc analysis were used to test whether there was a statistically significant difference among the normally distributed means of independent groups. Pearson correlation analysis was used to determine whether there was a linear relationship between 2 numeric measurements and, if so, to determine the direction and severity of this relationship. P<.05 indicated statistical significance in this study.
Results
Study Participant Demographics—This study included 82 participants with a mean age of 44.3 years; 52.4% (43/82) were female, and 85.4% (70/82) were married. The questionnaire took an average of 4.2 minutes for participants to complete. A total of 57.3% (47/82) of patients had completed primary/secondary education and 59.8% (49/82) were employed. The mean BMI was 28.1 kg/m2. According to the BMI classification, 26.8% (22/82) participants had a normal weight, 36.6% (30/82) were overweight, and 43.9% (36/82) were obese. A total of 48.8% (40/82) of participants smoked, and 4.9% (4/82) consumed alcohol. The mean Psoriasis Area and Severity Index score was 5.4. A total of 54.9% (45/82) of participants had nail psoriasis, and 24.4% (20/82) had psoriatic arthritis. The mean duration of psoriasis was 153 months. A total of 29.3% (24/82) of participants had a positive family history of psoriasis. The mean EAT-26 score was 11.1. A total of 12.2% (10/82) of participants had an EAT-26 score of 20 points or higher and were considered at high risk for an ED. The mean ASHN score was 72.9; the mean DLQI score was 5.5; and on the DASS-21 scale, mean scores for depression, anxiety, and stress were 6.3, 8.7, and 10.0, respectively (Table).
Comparative Evaluation of the BMI Groups—The only statistically significant differences among the 3 BMI groups were related to marital status, EAT-26 score, and anxiety and stress scores (P=.02, <.01, <.01, and <.01, respectively)(eTable 1). The number of single/divorced participants in the overweight group was significantly (P=.02) greater than in the normal weight group. The mean EAT-26 score for the normal weight group was significantly (P<.01) lower than for the overweight and obese groups; there was no significant difference in mean EAT-26 scores between the overweight and obese groups. The mean anxiety score was significantly (P<.01) lower in the normal weight group compared with the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean depression score. The mean stress and anxiety scores were significantly (P<.01) lower in the normal weight group than in the overweight and obese groups. There was no significant difference between the overweight and obese groups according to the mean anxiety score.
Comparative Evaluation of the EAT-26 Scores—There were statistically significant differences among the EAT-26 scores related to sex; BMI; and depression, anxiety, and stress scores (P=.04, .02, <.01, <.01, and <.01, respectively). The number of females in the group with a score of 20 points or higher was significantly (P=.04) less than that in the group scoring less than 20 points. The mean BMI in the group with a score of 20 points or higher was significantly (P=.02) greater than in group scoring less than 20 points. The mean depression, anxiety, and stress scores of the group scoring 20 points or higher were significantly (P<.01 for all) greater than in the group scoring less than 20 points (eTable 2).
Correlation Analysis of the Study Variables—The EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress (P<.01 for all)(eTable 3).
Comment
Eating disorders are psychiatric conditions that require a multidisciplinary approach. Nonpsychiatric medical departments may be involved due to the severe consequences (eg, various skin changes14) of these disorders. Psoriasis is not known to be directly affected by the presence of an ED; however, it is possible that EDs could indirectly affect patients with psoriasis by influencing obesity. Therefore, this study aimed to examine the relationship between ED risk factors and obesity in this population.
The relationship between psoriasis and obesity has been a popular research topic in dermatology since the 1990s.15 Epidemiologic and observational studies have reported that patients with psoriasis are more likely to be overweight or have obesity, which is an independent risk factor for psoriasis.3,16 However, the causal relationship between psoriasis and obesity remains unclear. In a comprehensive review, Barros et al17 emphasized the causal relationship between obesity and psoriasis under several headings. Firstly, a higher BMI increases the risk for psoriasis by promoting cytokine release and immune system dysregulation. Secondly, a Western diet (eg, processed foods and fast food) triggers obesity and psoriasis by increasing adipose tissue. Thirdly, the alteration of the skin and gut microbiota triggers chronic inflammation as a result of bacterial translocation in patients with obesity. Fourthly, a high-fat diet and palmitic acid disrupt the intestinal integrity of the gut and increase the risk for psoriasis and obesity by triggering chronic inflammation of bacterial fragments that pass into the blood. Finally, the decrease in the amount of adiponectin and the increase in the amount of leptin in patients with obesity may cause psoriasis by increasing proinflammatory cytokines, which are similar to those involved in the pathogenesis of psoriasis.17 Additionally, psoriatic inflammation can cause insulin resistance and metabolic dysfunction, leading to obesity.18 The relationship between psoriasis and obesity cannot be solely explained by metabolic pathways. Smoking, alcohol consumption, and a sedentary lifestyle all are associated with psoriasis and also can contribute to obesity.5 Our study revealed no significant difference in smoking or alcohol consumption between the normal weight and overweight/obesity groups. Based on our data, we determined that smoking and alcohol consumption did not affect obesity in our patients with psoriasis.
Observational and epidemiologic studies have shown that patients with psoriasis experience increased rates of depression, anxiety, and stress.19 In studies of pathogenesis, a connection between depression and psoriatic inflammation has been established.20 It is known that inflammatory cytokines similar to those in psoriasis are involved in the development of obesity.18 In addition, depression and anxiety can lead to binge eating, unhealthy food choices, and a more sedentary lifestyle.5 All of these variables may contribute to the associations between depression and anxiety with psoriasis and obesity. Zafiriou et al21 conducted a study to investigate the relationship between psoriasis, obesity, and depression through inflammatory pathways with a focus on the importance of IL-17. Data showing that IL-17–producing Th17-cell subgroups play a considerable role in the development of obesity and depression prompted the authors to suggest that psoriasis, obesity, and anxiety/depression may be interconnected manifestations of immune dysregulation, potentially linked to IL-17 and its associated cells.21 Mrowietz et al22 also suggested that metabolic inflammation may contribute to obesity and depression in patients with psoriasis and highlighted the importance of several cytokines, including tumor necrosis factor α, IL-6, IL-8, IL-17, and IL-23. Our study revealed no significant differences in depression scores between BMI groups. Another meta-analysis reported conflicting findings on the incidence of depression in obese patients with psoriasis.23 Some of the studies had a small number of participants. Compared to depression, anxiety has received less attention in studies of patients with obesity with psoriasis. However, these studies have shown a positive correlation between anxiety scores and BMI in patients with psoriasis.24,25 In our study, similar to the findings of previous studies, overweight patients and those with obesitywho have psoriasis had significantly (P<.01) greater anxiety and stress scores than did normal weight patients with psoriasis.
Obesity should be assessed in patients with psoriasis via a biopsychosocial approach that takes into account genetic, behavioral, and environmental factors.26 Eating disorders are considered to be one of the factors contributing to obesity. Numerous studies in the literature have demonstrated a greater incidence of EDs in patients with obesity vs those without obesity.5,6,27 Obesity and EDs have a bidirectional relationship: individuals with obesity are at risk for EDs due to body dissatisfaction, dieting habits, and depressive states. Conversely, poor eating behaviors in individuals with a normal weight can lead to obesity.28
There are few studies in the literature exploring the relationship between psoriasis and EDs. Crosta et al29 demonstrated that patients with psoriasis had impaired results on ED screening tests and that these scores deteriorated further as BMI increased. Moreover, Altunay et al30 demonstrated that patients with psoriasis and metabolic syndrome had higher scores on the ED screening test. In this study, patients with higher scores also exhibited high levels of anxiety.30 In our study, similar to the findings of previous studies, patients with psoriasis who were overweight or had obesity had significantly (P<.01) greater EAT-26 scores than those in the normal weight group. Patients with high EAT-26 scores also exhibited elevated levels of depression, anxiety, and stress. Additionally, EAT-26 scores were positively correlated with BMI, anxiety, depression, and stress scores. Our study as well as other studies in the literature indicate that additional research is needed to determine the associations between EDs and obesity in psoriasis.
Conclusion
Managing obesity is crucial for patients with psoriasis. This study showed that EAT-26 scores were higher in patients with psoriasis who were overweight or had obesity than in those who were normal weight. Participants with high EAT-26 scores (≥20 points) were more likely to be female and have higher anxiety and stress scores. In addition, EAT-26 scores were positively correlated with BMI as well as depression, anxiety, and stress scores. Eating disorders may contribute to the development of obesity in patients with psoriasis. Although our study was limited by a small sample size, the results suggest that there is a need for large-scale multicenter studies to investigate the relationship between psoriasis and EDs.
References
1. Kalkan G. Comorbidities in psoriasis: the recognition of psoriasis as a systemic disease and current management. Turkderm-Turk Arch Dermatol Venereol. 2017;51:71-77.
2. Armstrong AW, Harskamp CT, Armstrong EJ. The association between psoriasis and obesity: a systematic review and meta-analysis of observational studies. Nutr Diabetes. 2012;2:E54.
3. Jensen P, Skov L. Psoriasis and obesity. Dermatology. 2016;232:633-639.
4. Mirghani H, Altemani AT, Altemani ST, et al. The cross talk between psoriasis, obesity, and dyslipidemia: a meta-analysis. Cureus. 2023;15:e49253.
5. Roehring M, Mashep MR, White MA, et al. The metabolic syndrome and behavioral correlates in obese patients with binge disorders. Obesity. 2009;17:481-486.
6. da Luz FQ, Hay P, Touyz S, et al. Obesity with comorbid eating disorders: associated health risks and treatment approaches. Nutrients. 2018;10:829.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association; 2013.
8. Ergüney Okumus¸ FE, Sertel Berk HÖ. The psychometric properties of the Eating Attitudes Test short form (EAT-26) in a college sample. Stud Psychol. 2020;40:57-78.
9. Stoleru G, Leopold A, Auerbach A, et al. Female gender, dissatisfaction with weight, and number of IBD related surgeries as independent risk factors for eating disorders among patients with inflammatory bowel diseases. BMC Gastroenterol. 2022;22:438.
10. Öztürkcan S, Ermertcan AT, Eser E, et al. Cross validation of the Turkish version of dermatology life quality index. Int J Dermatol. 2006;45:1300-1307.
11. Demir GT, Ciciog˘lu HI˙. Attitude scale for healthy nutrition (ASHN): validity and reliability study. Gaziantep Univ J Sport Sci. 2019;4:256-274.
12. Yılmaz O, Boz H, Arslan A. The validity and reliability of depression stress and anxiety scale (DASS 21) Turkish short form. Res Financial Econ Soc Stud. 2017;2:78-91.
13. Nuttall FQ. Body mass index: obesity, BMI, and health: a critical review. Nutr Today. 2015;50:117-128.
14. Strumia R, Manzata E, Gualandi M. Is there a role for dermatologists in eating disorders? Expert Rev Dermatol. 2017; 2:109-112.
15. Henseler T, Christophers E. Disease concomitance in psoriasis. J Am Acad Dermatol. 1995;32:982-986.
16. Naldi L, Addis A, Chimenti S, et al. Impact of body mass index and obesity on clinical response to systemic treatment for psoriasis. evidence from the Psocare project. Dermatology. 2008;217:365-373.
17. Barros G, Duran P, Vera I, et al. Exploring the links between obesity and psoriasis: a comprehensive review. Int J Mol Sci. 2022;23:7499.
18. Hao Y, Zhu YJ, Zou S, et al. Metabolic syndrome and psoriasis: mechanisms and future directions. Front Immunol. 2021;12:711060.
19. Jing D, Xiao H, Shen M, et al. Association of psoriasis with anxiety and depression: a case–control study in Chinese patients. Front Med (Lausanne). 2021;8:771645.
20. Sahi FM, Masood A, Danawar NA, et al. Association between psoriasis and depression: a traditional review. Cureus. 2020;12:E9708.
21. Zafiriou E, Daponte AI, Siokas V, et al. Depression and obesity in patients with psoriasis and psoriatic arthritis: is IL-17–mediated immune dysregulation the connecting link? Front Immunol. 2021;12:699848.
22. Mrowietz U, Sümbül M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37:1731-1738.
23. Pavlova NT, Kioskli K, Smith C, et al. Psychosocial aspects of obesity in adults with psoriasis: a systematic review. Skin Health Dis. 2021;1:E33.
24. Innamorati M, Quinto RM, Imperatori C, et al. Health-related quality of life and its association with alexithymia and difficulties in emotion regulation in patients with psoriasis. Compr Psychiatry. 2016;70:200-208.
25. Tabolli S, Naldi L, Pagliarello C, et al. Evaluation of the impact of writing exercises interventions on quality of life in patients with psoriasis undergoing systemic treatments. Br J Dermatol. 2012;167:1254‐1264.
26. Albuquerque D, Nóbrega C, Manco L, et al. The contribution of genetics and environment to obesity. Br Med Bull. 2017;123:159‐173.
27. Balantekin KN, Grammer AC, Fitzsimmons-Craft EE, et al. Overweight and obesity are associated with increased eating disorder correlates and general psychopathology in university women with eating disorders. Eat Behav. 2021;41:101482.
28. Jebeile H, Lister NB, Baur LA, et al. Eating disorder risk in adolescents with obesity. Obes Rev. 2021;22:E13173.
29. Crosta ML, Caldarola G, Fraietta S, et al. Psychopathology and eating disorders in patients with psoriasis. G Ital Dermatol Venereol. 2014;149:355-361.
30. Altunay I, Demirci GT, Ates B, et al. Do eating disorders accompany metabolic syndrome in psoriasis patients? results of a preliminary study. Clin Cosmet Investig Dermatol. 2011;4:139-143.
<p class='insidehead'>Practice <strong>Points</strong></p> <ul class='insidebody'> <li>Eating disorders are considered a contributing factor in obesity.</li> <li>Obesity is prevalent in patients with psoriasis, and current evidence indicates that obesity may initiate psoriasis or worsen existing disease.</li> <li>Obesity should be considered as contributory to the development of psoriasis via a biopsychosocial approach that accounts for genetic, behavioral, and environmental factors.</li> </ul>
Disparities in Skin Cancer Outcomes in the Latine/Hispanic Population
The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.3
It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.4 Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.2 The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.
Terminology
Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.10 Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their distinct countries.11
In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.13
More recently, the term Latine has been introduced as an alternative to the gender binary inherent in the Spanish language.12 For the purposes of this article, the terms Latine and Hispanic will be used interchangeably (unless otherwise specified) depending on how they are cited in the existing literature. Furthermore, the term non-Hispanic White (NHW) will be used to refer to individuals who have been socially ascribed or who self-identify as White in terms of race or ethnicity.
Melanoma
Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.14 While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).15,16
Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–pigmented macule.18 The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.18
Although the lifetime risk for melanoma among Hispanic individuals in the United States is lower than that for NHW individuals, Hispanic patients who are diagnosed with melanoma are more likely to present with increased tumor thickness and later-stage diagnosis compared to NHW individuals.8,16,20 In a recent study by Qian et al,8 advanced stage melanoma—defined as regional or distant stage disease—was present in 12.6% of NHW individuals. In contrast, the percentage of Hispanics with advanced disease was higher at 21%.8 Even after controlling for insurance and poverty status, Hispanic individuals were at greater risk than NHW individuals for late-stage diagnosis.16,20
Morbidity and mortality also have been shown to be higher in Hispanic patients with cutaneous melanoma.9,17 Reasons for this are multifactorial, with studies specific to melanoma citing challenges associated with early detection in individuals with deeply pigmented skin, a lack of awareness and knowledge about skin cancer among Latine/Hispanic patients, and treatment disparities.21-23 Moreover, very few studies have reported comprehensive data on patients from Africa and Latin America. Studies examining the role of genetic ancestry, epigenetic variants, and skin pigmentation and the risk for melanoma among the Latine/Hispanic population therefore are much needed.24
Keratinocyte Carcinomas
Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.25 As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.25,26
Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.29 The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.30 Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.30
Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.31 In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.32,33
The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.34 Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.35-37
Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.25
More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.39 Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.9,32
Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).9,32,36
Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.40 Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.41 Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.42
Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,44 ultimately impacting incidence.45
Dermatofibrosarcoma Protuberans
Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.46
Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.47 This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.48 In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.47 As the tumor grows, it tends to become firm and nodular. The most common location for
Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.49 Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.50 A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.51
Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.52 Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.
Factors Influencing Skin Cancer Outcomes
In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.53,54 These systemic inequities, which are rooted in structural racism,55 have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.
Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),58 inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.58 Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).59
Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.60
With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.61-65 For instance, Vargas et al64 found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.58
Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.53 For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.53 Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.65 Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.53
It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.66 In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.67 These beliefs have undermined the trust that these populations have in clinicians and the health care system.54,67
Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.68,69 In other examples, language barriers contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.68,70
Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.26 Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.71 Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).71-73
Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population.
Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.74 Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.
Final Thoughts
The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.
- Noe-Bustamnate L, Lopez MH, Krogstad JM. US Hispanic population surpassed 60 million in 2019, but growth has slowed. July 7, 2020. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2020/07/07/u-s-hispanic-population-surpassed-60-million-in-2019-but-growth-has-slowed/
- Frank C, Lopez MH. Hispanic Americans’ trust in and engagement with science. Pew Research Center. June 14, 2022. Accessed September 3, 2024. https://www.pewresearch.org/wp-content/uploads/sites/20/2022/06/PS_2022.06.14_hispanic-americans-science_REPORT.pdf
- US Census Bureau. Projections of the size and composition of the US population: 2014 to 2060. US Government Printing Office; 2015. Accessed September 5, 2024. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
- Zong J. A mosaic, not a monolith: a profile of the U.S. Latino population, 2000-2020. October 26, 2022. Accessed September 3, 2024. https://latino.ucla.edu/research/latino-population-2000-2020/
- Latinos in California, Texas, New York, Florida and New Jersey. Pew Research Center. March 19, 2004. Accessed September 3, 2024. https://www.pewresearch.org/hispanic/2004/03/19/latinos-in-california-texas-new-york-florida-and-new-jersey/
- Pinheiro PS, Sherman RL, Trapido EJ, et al. Cancer incidence in first generation US Hispanics: Cubans, Mexicans, Puerto Ricans, and new Latinos. Cancer Epidemiol Biomarkers Prev. 2009;18:2162-2169.
- Pinheiro PS, Callahan KE, Kobetz EN. Disaggregated Hispanic groups and cancer: importance, methodology, and current knowledge. In: Ramirez AG, Trapido EJ, eds. Advancing the Science of Cancer in Latinos. Springer; 2020:17-34.
- Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
- Hogue L, Harvey VM. Basal cell carcinoma, squamous cell carcinoma, and cutaneous melanoma in skin of color patients. Dermatol Clin. 2019;37:519-526.
- Cruzval-O’Reilly E, Lugo-Somolinos A. Melanoma in Hispanics: we may have it all wrong. Cutis. 2020;106:28-30.
- Borrell LN, Elhawary JR, Fuentes-Afflick E, et al. Race and genetic ancestry in medicine—a time for reckoning with racism. N Engl J Med. 2021;384:474-480.
- Lopez MH, Krogstad JM, Passel JS. Who is Hispanic? September 5, 2023. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2023/09/05/who-is-hispanic/
- Carrasquillo OY, Lambert J, Merritt BG. Comment on “Disparities in nonmelanoma skin cancer in Hispanic/Latino patients based on Mohs micrographic surgery defect size: a multicenter retrospective study.”J Am Acad Dermatol. 2022;87:E129-E130.
- American Cancer Society. Key statistics for melanoma skin cancer. Updated January 17, 2024. Accessed September 3, 2024. https://www.cancer.org/cancer/types/melanoma-skin-cancer/about/key-statistics.html
- National Cancer Institute. Melanoma of the skin: recent trends in SEER age-adjusted incidence rates, 2000-2021. Updated June 27, 2024. Accessed September 3, 2024. https://seer.cancer.gov/statistics-network/explorer/application.htmlsite=53&data_type=1&graph_type=2&compareBy=sex&chk_sex_3=3&chk_sex_2=2&rate_type=2&race=6&age_range=1&stage=101&advopt_precision=1&advopt_show_ci=on&hdn_view=0&advopt_display=2
- Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659.
- Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801.
- Bristow IR, de Berker DA, Acland KM, et al. Clinical guidelines for the recognition of melanoma of the foot and nail unit. J Foot Ankle Res. 2010;3:25.
- Fernandez JM, Mata EM, Behbahani S, et al. Survival of Hispanic patients with cutaneous melanoma: a retrospective cohort analysis of 6016 cases from the National Cancer Database. J Am Acad Dermatol. 2023;88:1135-1138.
- Hu S, Sherman R, Arheart K, et al. Predictors of neighborhood risk for late-stage melanoma: addressing disparities through spatial analysis and area-based measures. J Investigative Dermatol. 2014;134:937-945.
- Buster KJ, You Z, Fouad M, et al. Skin cancer risk perceptions: a comparison across ethnicity, age, education, gender, and income. J Am Acad Dermatol. 2012;66:771-779.
- Halpern MT, Ward EM, Pavluck AL, et al. Association of insurance status and ethnicity with cancer stage at diagnosis for 12 cancer sites: a retrospective analysis. Lancet Oncology. 2008;9:222-231.
- Weiss J, Kirsner RS, Hu S. Trends in primary skin cancer prevention among US Hispanics: a systematic review. J Drugs Dermatol. 2012;11:580-586.
- Carvalho LAD, Aguiar FC, Smalley KSM, et al. Acral melanoma: new insights into the immune and genomic landscape. Neoplasia. 2023;46:100947.
- Kolitz E, Lopes F, Arffa M, et al. UV Exposure and the risk of keratinocyte carcinoma in skin of color: a systematic review. JAMA Dermatol. 2022;158:542-546.
- Lukowiak TM, Aizman L, Perz A, et al. Association of age, sex, race, and geographic region with variation of the ratio of basal cell to cutaneous squamous cell carcinomas in the United States. JAMA Dermatol. 2020;156:1192-1198.
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- Bigler C, Feldman J, Hall E, et al. Pigmented basal cell carcinoma in Hispanics. J Am Acad Dermatol. 1996;34(5 pt 1):751-752.
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- Soliman YS, Mieczkowska K, Zhu TR, et al. Characterizing basal cell carcinoma in Hispanic individuals undergoing Mohs micrographic surgery: a 7-year retrospective review at an academic institution in the Bronx. Brit J Dermatol. 2022;187:597-599.
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- Hao X, Billings SD, Wu F, et al. Dermatofibrosarcoma protuberans: update on the diagnosis and treatment. J Clin Med. 2020;9:1752.
- Mosallaei D, Lee EB, Lobl M, et al. Rare cutaneous malignancies in skin of color. Dermatol Surg. 2022;48:606-612.
- Criscito MC, Martires KJ, Stein JA. Prognostic factors, treatment, and survival in dermatofibrosarcoma protuberans. JAMA Dermatol. 2016;152:1365-1371.
- Orenstein LAV, Nelson MM, Wolner Z, et al. Differences in outpatient dermatology encounter work relative value units and net payments by patient race, sex, and age. JAMA Dermatol. 2021;157:406-412.
- Lowe GC, Onajin O, Baum CL, et al. A comparison of Mohs micrographic surgery and wide local excision for treatment of dermatofibrosarcoma protuberans with long-term follow-up: the Mayo Clinic experience. Dermatol Surg. 2017;43:98-106.
- Moore KJ, Chang MS, Weiss J, et al. Racial and ethnic differences in the surgical treatment of dermatofibrosarcoma protuberans: a retrospective cohort analysis. J Am Acad Dermatol. 2022;87:245-247.
- Trofymenko O, Bordeaux JS, Zeitouni NC. Survival in patients with primary dermatofibrosarcoma protuberans: National Cancer Database analysis. J Am Acad Dermatol. 2018;78:1125-1134.
- Bazargan M, Cobb S, Assari S. Discrimination and medical mistrust in a racially and ethnically diverse sample of California adults. Ann Fam Med. 2021;19:4-15.
- Smedley BD, Stith AY, Nelson AR, eds. Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care. Washington, DC; 2003.
- Bailey ZD, Krieger N, Agenor M, et al. Structural racism and health inequities in the USA: evidence and interventions. Lancet. 2017;389:1453-1463.
- Tackett KJ, Jenkins F, Morrell DS, et al. Structural racism and its influence on the severity of atopic dermatitis in African American children. Pediatric Dermatol. 2020;37:142-146.
- Greif C, Srivastava D, Nijhawan RI. A retrospective cohort study of dermatofibrosarcoma protuberans at a large metropolitan academic center. JAAD Int. 2022;6:104-106.
- Office of the Assistant Secretary for Planning and Evaluation. Health insurance coverage and access to care among Latinos: recent rrends and key challenges (HP-2021-22). October 8, 2021. Accessed September 3, 2024. https://aspe.hhs.gov/reports/health-insurance-coverage-access-care-among-latinos
- Keisler-Starkey K, Bunch LN. Health insurance coverage in the United States: 2020 (Current Population Reports No. P60-274). US Census Bureau; 2021. https://www.census.gov/content/dam/Census/library/publications/2021/demo/p60-274.pdf
- Kaiser Family Foundation. Key facts on health coverage of immigrants. Updated June 26, 2024. Accessed September 3, 2024. https://www.kff.org/racial-equity-and-health-policy/fact-sheet/key-facts-on-health-coverage-of-immigrants/
- Pew Research Center. Unauthorized immigrants: length of residency, patterns of parenthood. Published December 1, 2011. Accessed October 28, 2024. https://www.pewresearch.org/race-and-ethnicity/2011/12/01/unauthorized-immigrants-length-of-residency-patterns-of-parenthood/
- Schneider J, Schmitt M. Understanding the relationship between racial discrimination and mental health among African American adults: a review. SAGE Open. 2015;5:1-10.
- Philbin MM, Flake M, Hatzenbuehler ML, et al. State-level immigration and immigrant-focused policies as drivers of Latino health disparities in the United States. Soc Sci Med. 2018;199:29-38.
- Vargas ED, Sanchez GR, Juarez M. The impact of punitive immigrant laws on the health of Latina/o Populations. Polit Policy. 2017;45:312-337.
- Sutton AL, He J, Edmonds MC, et al. Medical mistrust in Black breast cancer patients: acknowledging the roles of the trustor and the trustee. J Cancer Educ. 2019;34:600-607.
- Jacobs J. An overview of Latin American healthcare systems. Pacific Prime Latin America. July 31, 2023. Accessed September 3, 2024. https://www.pacificprime.lat/blog/an-overview-of-latin-american-healthcare-systems/
- CDC. Unfair and unjust practices and conditions harm Hispanic and Latino people and drive health disparities. May 15, 2024. Accessed September 3, 2024. https://www.cdc.gov/tobacco-health-equity/collection/hispanic-latino-unfair-and-unjust.html
- Hall IJ, Rim SH, Dasari S. Preventive care use among Hispanic adults with limited comfort speaking English: an analysis of the Medical Expenditure Panel Survey data. Prev Med. 2022;159:107042.
- Brach C, Chevarley FM. Demographics and health care access and utilization of limited-English-proficient and English-proficient Hispanics. Agency for Healthcare Research and Quality. February 2008. http://meps.ahrq.gov/mepsweb/data_files/publications//rf28/rf28.pdf
- Berdahl TA, Kirby JB. Patient-provider communication disparities by limited English proficiency (LEP): trends from the US Medical Expenditure Panel Survey, 2006-2015. J General Intern Med. 2019;34:1434-1440.
- Robinson JK, Joshi KM, Ortiz S, et al. Melanoma knowledge, perception, and awareness in ethnic minorities in Chicago: recommendations regarding education. Psychooncology. 2011;20:313-320.
- Robinson JK, Nodal M, Chavez L, et al. Enhancing the relevance of skin self-examination for Latinos. JAMA Dermatol. 2017;153:717-718.
- Buchanan Lunsford N, Berktold J, Holman DM, et al. Skin cancer knowledge, awareness, beliefs and preventive behaviors among black and hispanic men and women. Prev Med Rep. 2018;12:203-209.
- Madrigal JM, Correa-Mendez M, Arias JD, et al. Hispanic, Latino/a, Latinx, Latine: disentangling the identities of Hispanic/Latino Americans. National Cancer Institute Division of Cancer Epidemiology & Genetics. October 20, 2022. Accessed September 3, 2024. https://dceg.cancer.gov/about/diversity-inclusion/inclusivity-minute/2022/disentangling-identities-hispanic-latino-americans
The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.3
It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.4 Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.2 The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.
Terminology
Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.10 Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their distinct countries.11
In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.13
More recently, the term Latine has been introduced as an alternative to the gender binary inherent in the Spanish language.12 For the purposes of this article, the terms Latine and Hispanic will be used interchangeably (unless otherwise specified) depending on how they are cited in the existing literature. Furthermore, the term non-Hispanic White (NHW) will be used to refer to individuals who have been socially ascribed or who self-identify as White in terms of race or ethnicity.
Melanoma
Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.14 While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).15,16
Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–pigmented macule.18 The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.18
Although the lifetime risk for melanoma among Hispanic individuals in the United States is lower than that for NHW individuals, Hispanic patients who are diagnosed with melanoma are more likely to present with increased tumor thickness and later-stage diagnosis compared to NHW individuals.8,16,20 In a recent study by Qian et al,8 advanced stage melanoma—defined as regional or distant stage disease—was present in 12.6% of NHW individuals. In contrast, the percentage of Hispanics with advanced disease was higher at 21%.8 Even after controlling for insurance and poverty status, Hispanic individuals were at greater risk than NHW individuals for late-stage diagnosis.16,20
Morbidity and mortality also have been shown to be higher in Hispanic patients with cutaneous melanoma.9,17 Reasons for this are multifactorial, with studies specific to melanoma citing challenges associated with early detection in individuals with deeply pigmented skin, a lack of awareness and knowledge about skin cancer among Latine/Hispanic patients, and treatment disparities.21-23 Moreover, very few studies have reported comprehensive data on patients from Africa and Latin America. Studies examining the role of genetic ancestry, epigenetic variants, and skin pigmentation and the risk for melanoma among the Latine/Hispanic population therefore are much needed.24
Keratinocyte Carcinomas
Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.25 As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.25,26
Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.29 The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.30 Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.30
Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.31 In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.32,33
The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.34 Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.35-37
Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.25
More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.39 Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.9,32
Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).9,32,36
Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.40 Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.41 Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.42
Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,44 ultimately impacting incidence.45
Dermatofibrosarcoma Protuberans
Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.46
Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.47 This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.48 In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.47 As the tumor grows, it tends to become firm and nodular. The most common location for
Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.49 Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.50 A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.51
Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.52 Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.
Factors Influencing Skin Cancer Outcomes
In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.53,54 These systemic inequities, which are rooted in structural racism,55 have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.
Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),58 inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.58 Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).59
Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.60
With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.61-65 For instance, Vargas et al64 found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.58
Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.53 For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.53 Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.65 Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.53
It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.66 In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.67 These beliefs have undermined the trust that these populations have in clinicians and the health care system.54,67
Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.68,69 In other examples, language barriers contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.68,70
Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.26 Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.71 Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).71-73
Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population.
Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.74 Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.
Final Thoughts
The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.
The Latine/Hispanic population in the United States comprises one of the largest and youngest skin of color communities.1,2 In 2020, this group accounted for 19% of all Americans—a percentage expected to increase to more than 25% by 2060.3
It must be emphasized that the Latine/Hispanic community in the United States is incredibly diverse.4 Approximately one-third of individuals in this group are foreign-born, and this community is made up of people from all racialized groups, religions, languages, and cultural identities.2 The heterogeneity of the Latine/Hispanic population translates into a wide representation of skin tones, reflecting a rich range of ancestries, ethnicities, and cultures. The percentage of individuals from each origin group may differ according to where they live in the United States; for instance, individuals who identify as Mexican comprise more than 80% of the Latine/Hispanic population in both Texas and California but only 17% in Florida, where more than half of Latine/Hispanic people identify as Cuban or Puerto Rican.4,5 As a result, when it comes to skin cancer epidemiology, variations in incidence and mortality may exist within each of these subgroups who identify as part of the Latine/Hispanic community, as reported for other cancers.6,7 Further research is needed to investigate these potential differences.Unfortunately, considerable health disparities persist among this rapidly growing population, including increased morbidity and mortality from melanoma and keratinocyte carcinomas (KCs) despite overall low lifetime incidence.8,9 In this review, the epidemiology, clinical manifestation, and ethnic disparities for skin cancer among the US Latine/Hispanic population are summarized; other factors impacting overall health and health care, including sociocultural factors, also are briefly discussed.
Terminology
Before a meaningful dialogue can be had about skin cancer in the Latine/Hispanic population, it is important to contextualize the terms used to identify this patient population, including Latino/Latine and Hispanic. In the early 1970s, the United States adopted the term Hispanic as a way of conglomerating Spanish-speaking individuals from Spain, the Caribbean, and Central and South America. The goal was to implement a common identifier that enabled the US government to study the economic and social development of these groups.10 Nevertheless, considerable differences (eg, variations in skin pigmentation, sun sensitivity) exist among Hispanic communities, with some having stronger European, African, or Amerindian influences due to colonization of their distinct countries.11
In contrast, Latino is a geographic term and refers to people with roots in Latin America and the Caribbean (Table 1).12,13 For example, a person from Brazil may be considered Latino but not Hispanic as Brazilians speak Portuguese; alternatively, Spaniards (who are considered Hispanic) are not Latino because Spain is not a Latin American country. A person from Mexico would be considered both Latino and Hispanic.13
More recently, the term Latine has been introduced as an alternative to the gender binary inherent in the Spanish language.12 For the purposes of this article, the terms Latine and Hispanic will be used interchangeably (unless otherwise specified) depending on how they are cited in the existing literature. Furthermore, the term non-Hispanic White (NHW) will be used to refer to individuals who have been socially ascribed or who self-identify as White in terms of race or ethnicity.
Melanoma
Melanoma, the deadliest form of skin cancer, is more likely to metastasize compared to other forms of skin cancer, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). For Latine/Hispanic individuals living in the United States, the lifetime risk for melanoma is 1 in 200 compared to 1 in 33 for NHW individuals.14 While the lifetime risk for melanoma is low for the Latine/Hispanic population, Hispanic individuals are diagnosed with melanoma at an earlier age (mean, 56 years), and the rate of new cases is marginally higher for women (4.9 per 100,000) compared to men (4.8 per 100,000).15,16
Typical sites of melanoma manifestation in Latine/Hispanic individuals include the torso (most common site in Hispanic men), lower extremities (most common site in Hispanic women), and acral sites (palms, soles, and nails).9,16,17 Anatomic location also can vary according to age for both men and women. For men, the incidence of melanoma on the trunk appears to decrease with age, while the incidence on the head and neck may increase. For women, the incidence of melanoma on the lower extremities and hip increases with age. Cutaneous melanoma may manifest as a lesion with asymmetry, irregular borders, variation in pigmentation, large diameter (>6 mm), and evolution over time. In patients with skin of color, melanoma easily can be missed, as it also typically mimics more benign skin conditions and may develop from an existing black- or dark brown–pigmented macule.18 The most common histologic subtype reported among Latine/Hispanic individuals in the United States is superficial spreading melanoma (20%–23%) followed by nodular melanoma and acral lentiginous melanoma.16,19 Until additional risk factors associated with melanoma susceptibility in Hispanic/Latine people are better elucidated, it may be appropriate to use an alternative acronym, such as CUBED (Table 2), in addition to the standard ABCDE system to help recognize potential melanoma on acral sites.18
Although the lifetime risk for melanoma among Hispanic individuals in the United States is lower than that for NHW individuals, Hispanic patients who are diagnosed with melanoma are more likely to present with increased tumor thickness and later-stage diagnosis compared to NHW individuals.8,16,20 In a recent study by Qian et al,8 advanced stage melanoma—defined as regional or distant stage disease—was present in 12.6% of NHW individuals. In contrast, the percentage of Hispanics with advanced disease was higher at 21%.8 Even after controlling for insurance and poverty status, Hispanic individuals were at greater risk than NHW individuals for late-stage diagnosis.16,20
Morbidity and mortality also have been shown to be higher in Hispanic patients with cutaneous melanoma.9,17 Reasons for this are multifactorial, with studies specific to melanoma citing challenges associated with early detection in individuals with deeply pigmented skin, a lack of awareness and knowledge about skin cancer among Latine/Hispanic patients, and treatment disparities.21-23 Moreover, very few studies have reported comprehensive data on patients from Africa and Latin America. Studies examining the role of genetic ancestry, epigenetic variants, and skin pigmentation and the risk for melanoma among the Latine/Hispanic population therefore are much needed.24
Keratinocyte Carcinomas
Keratinocyte carcinomas, also known as nonmelanoma skin cancers, include BCC and SCC. In comparison to the high-quality data available for melanoma from cancer registries, there are less reliable incidence data for KCs, especially among individuals with skin of color.25 As a result, KC epidemiology in the United States is drawn largely from case series (especially for individuals with skin of color) or claims data from small data sets often from geographically restricted regions within the United States.25,26
Basal Cell Carcinoma—Basal cell carcinoma is the most common malignant skin cancer in Latine/Hispanic individuals. Among those with lighter skin tones, the lifetime risk for BCC is about 30%.27,28 Men typically are affected at a higher rate than women, and the median age for diagnosis is 68 years.29 The development of BCC primarily is linked to lifetime accumulated UV radiation exposure. Even though BCC has a low mortality rate, it can lead to substantial morbidity due to factors such as tumor location, size, and rate of invasion, resulting in cosmetic and functional issues. Given its low metastatic potential, treatment of BCC typically is aimed at local control.30 Options for treatment include Mohs micrographic surgery (MMS), curettage and electrodessication, cryosurgery, photodynamic therapy, radiation therapy, and topical therapies. Systemic therapies are reserved for patients with locally advanced or metastatic disease.30
Latine/Hispanic patients characteristically present with BCCs on sun-exposed areas of the skin such as the head and neck region. In most patients, BCC manifests as a translucent pearly nodule with superficial telangiectasias and/or a nonhealing ulcer with a central depression and rolled nontender borders. However, in patients with skin of color, 66% of BCCs manifest with pigmentation; in fact, pigmented BCC (a subtype of BCC) has been shown to have a higher prevalence among Hispanic individuals, with an incidence twice as frequent as in NHW individuals.31 In addition, there are reports of increased tendency among Latine/Hispanic individuals to develop multiple BCCs.32,33
The relationship between UV exposure and KCs could explain the relatively higher incidence in populations with skin of color living in warmer climates, including Hispanic individuals.34 Even so, the development of BCCs appears to correlate directly with the degree of pigmentation in the skin, as it is most common in individuals with lighter skin tones within the Hispanic population.25,34,35 Other risk factors associated with BCC development include albinism, arsenic ingestion, chronic infections, immunosuppression, history of radiation treatment, and history of scars or ulcers due to physical/thermal trauma.35-37
Squamous Cell Carcinoma—Squamous cell carcinoma is the second most common skin cancer among Latine/Hispanic patients. In contrast with NHW patients, evidence supporting the role of UV exposure as a primary risk factor for SCC in patients with skin of color remains limited.25,38 Reports linking UV exposure and KCs in Hispanic and Black individuals predominantly include case series or population-based studies that do not consider levels of UV exposure.25
More recently, genetic ancestry analyses of a large multiethnic cohort found an increased risk for cutaneous SCC among Latine/Hispanic individuals with European ancestry compared to those with Native American or African ancestry; however, these genetic ancestry associations were attenuated (although not eliminated) after considering skin pigmentation (using loci associated with skin pigmentation), history of sun exposure (using actinic keratoses as a covariate for chronic sun exposure), and sun-protected vs sun-exposed anatomic sites, supporting the role of other environmental or sociocultural factors in the development of SCC.39 Similar to BCCs, immunosuppression, chronic scarring, skin irritation, and inflammatory disease also are documented risk factors.9,32
Among NHW individuals with lighter skin tones, SCC characteristically manifests on sun-exposed areas of the skin such as the head and neck region. Typically, a lesion may appear as a scaly erythematous papule or plaque that may be verrucous in nature or a nonhealing bleeding ulcer. In patients with more deeply pigmented skin, SCC tends to develop in the perianal region and on the penis and lower legs; pigmented lesions also may be present (as commonly reported in BCCs).9,32,36
Unfortunately, the lower incidence of KCs and lack of surveillance in populations with skin of color result in a low index of clinical suspicion, leading to delayed diagnoses and increased morbidity.40 Keratinocyte carcinomas are more costly to treat and require more health care resources for Latine/Hispanic and Black patients compared to their NHW counterparts; for example, KCs are associated with more ambulatory visits, more prescription medications, and greater cost on a per-person, per-year basis in Latine/Hispanic and Black patients compared with NHW patients.41 Moreover, a recent multicenter retrospective study found Hispanic patients had 17% larger MMS defects following treatment for KCs compared to NHW patients after adjustment for age, sex, and insurance type.42
Hispanic patients tend to present initially with SCCs in areas associated with advanced disease, such as the anogenital region, penis, and the lower extremities. Latine and Black men have the highest incidence of penile SCC, which is rare with high morbidity and mortality.32,43,44 The higher incidence of penile SCC among Hispanic individuals living in southern states could correspond to circumcision or HPV infection rates,44 ultimately impacting incidence.45
Dermatofibrosarcoma Protuberans
Dermatofibrosarcoma protuberans (DFSP) is a rare locally aggressive cutaneous sarcoma. According to population studies, overall incidence of DFSP is around 4.1 to 4.2 per million in the United States. Population-based studies on DFSP are limited, but available data suggest that Black patients as well as women have the highest incidence.46
Dermatofibrosarcoma protuberans is characterized by its capacity to invade surrounding tissues in a tentaclelike pattern.47 This characteristic often leads to inadequate initial resection of the lesion as well as a high recurrence rate despite its low metastatic potential.48 In early stages, DFSP typically manifests as an asymptomatic plaque with a slow growth rate. The color of the lesion ranges from reddish brown to flesh colored. The pigmented form of DFSP, known as Bednar tumor, is the most common among Black patients.47 As the tumor grows, it tends to become firm and nodular. The most common location for
Although current guidelines designate MMS as the first-line treatment for DFSP, the procedure may be inaccessible for certain populations.49 Patients with skin of color are more likely to undergo wide local excision (WLE) than MMS; however, WLE is less effective, with a recurrence rate of 30% compared with 3% in those treated with MMS.50 A retrospective cohort study of more than 2000 patients revealed that Hispanic and Black patients were less likely to undergo MMS. In addition, the authors noted that WLE recipients more commonly were deceased at the end of the study.51
Despite undergoing treatment for a primary DFSP, Hispanic patients also appear to be at increased risk for a second surgery.52 Additional studies are needed to elucidate the reasons behind higher recurrence rates in Latine/Hispanic patients compared to NHW individuals.
Factors Influencing Skin Cancer Outcomes
In recent years, racial and ethnic disparities in health care use, medical treatment, and quality of care among minoritized populations (including Latine/Hispanic groups) have been documented in the medical literature.53,54 These systemic inequities, which are rooted in structural racism,55 have contributed to poorer health outcomes, worse health status, and lower-quality care for minoritized patients living in the United States, including those impacted by dermatologic conditions.8,43,55-57 Becoming familiar with the sociocultural factors influencing skin cancer outcomes in the Latine/Hispanic community (including the lack of or inadequate health insurance, medical mistrust, language, and other cultural elements) and the paucity of research in this domain could help eliminate existing health inequities in this population.
Health Insurance Coverage—Although the uninsured rates in the Latine population have decreased since the passage of the Affordable Care Act (from 30% in 2013 to a low of 19% in 2017),58 inadequate health insurance coverage remains one of the largest barriers to health care access and a contributor to health disparities among the Latine community. Nearly 1 in 5 Latine individuals in the United States are uninsured compared to 8% of NHW individuals.58 Even though Latine individuals are more likely than non-Latine individuals to be part of the workforce, Latine employees are less likely to receive employer-sponsored coverage (27% vs 53% for NHW individuals).59
Not surprisingly, noncitizens are far less likely to be insured; this includes lawfully present immigrants (ie, permanent residents or green card holders, refugees, asylees, and others who are authorized to live in the United States temporarily or permanently) and undocumented immigrants (including individuals who entered the country without authorization and individuals who entered the country lawfully and stayed after their visa or status expired). The higher uninsured rate among noncitizens reflects not only limited access to employer-sponsored coverage but includes immigrant eligibility restrictions for federal programs such as Medicaid, the Children’s Health Insurance Program, and the Affordable Care Act Marketplace coverage.60
With approximately 9 million Americans living in mixed-status families (and nearly 10% of babies born each year with at least one undocumented parent), restrictive federal or state health care policies may extend beyond their stated target and impact both Latine citizens and noncitizens.61-65 For instance, Vargas et al64 found that both Latine citizens and noncitizens who lived in states with a high number of immigration-related laws had decreased odds of reporting optimal health as compared to Latine respondents in states with fewer immigration-related laws.Other barriers to enrollment include fears and confusion about program qualification, even if eligible.58
Medical Mistrust and Unfamiliarity—Mistrust of medical professionals has been shown to reduce patient adherence to treatment as prescribed by their medical provider and can negatively influence health outcomes.53 For racial/ethnic minoritized groups (including Latine/Hispanic patients), medical mistrust may be rooted in patients’ experience of discrimination in the health care setting. In a recent cross-sectional study, results from a survey of California adults (including 704 non-Hispanic Black, 711 Hispanic, and 913 NHW adults) found links between levels of medical mistrust and perceived discrimination based on race/ethnicity and language as well as perceived discrimination due to income level and type or lack of insurance.53 Interestingly, discrimination attributed to income level and insurance status remained after controlling for race/ethnicity and language. As expected, patients reliant on public insurance programs such as Medicare have been reported to have greater medical mistrust and suspicion compared with private insurance holders.65 Together, these findings support the notion that individuals who have low socioeconomic status and lack insurance coverage—disproportionately historically marginalized populations—are more likely to perceive discrimination in health care settings, have greater medical mistrust, and experience poorer health outcomes.53
It also is important for health care providers to consider that the US health care system is unfamiliar to many Latine/Hispanic individuals. Costs of medical services tend to be substantially higher in the United States, which can contribute to mistrust in the system.66 In addition, unethical medical experimentations have negatively affected both Latine and especially non-Hispanic Black populations, with long-lasting perceptions of deception and exploitation.67 These beliefs have undermined the trust that these populations have in clinicians and the health care system.54,67
Language and Other Cultural Elements—The inability to effectively communicate with health care providers could contribute to disparities in access to and use of health care services among Latine/Hispanic individuals. In a Medical Expenditure Panel Survey analysis, half of Hispanic patients with limited comfort speaking English did not have a usual source of care, and almost 90% of those with a usual source of care had a provider who spoke Spanish or used interpreters—indicating that few Hispanic individuals with limited comfort speaking English selected a usual source of care without language assistance.68,69 In other examples, language barriers contributed to disparities in cancer screening, and individuals with limited English proficiency were more likely to have difficulty understanding their physician due to language barriers.68,70
Improving cultural misconceptions regarding skin conditions, especially skin cancer, is another important consideration in the Latine/Hispanic community. Many Latine/Hispanic individuals wrongly believe they cannot develop skin cancer due to their darker skin tones and lack of family history.26 Moreover, multiple studies assessing melanoma knowledge and perception among participants with skin of color (including one with an equal number of Latine/Hispanic, Black/African American, and Asian individuals for a total of 120 participants) revealed that many were unaware of the risk for melanoma on acral sites.71 Participants expressed a need for more culturally relevant content from both clinicians and public materials (eg, images of acral melanoma in a person with skin of color).71-73
Paucity of Research—There is limited research regarding skin cancer risks and methods of prevention for patients with skin of color, including the Latine/Hispanic population. Efforts to engage and include patients from these communities, as well as clinicians or investigators from similar backgrounds, in clinical studies are desperately needed. It also is important that clinical studies collect data beyond population descriptors to account for both clinical and genetic variations observed in the Latine/Hispanic population.
Latine/Hispanic individuals are quite diverse with many variable factors that may influence skin cancer outcomes. Often, cancer surveillance data are available in aggregate only, which could mask this heterogeneity.74 Rigorous studies that collect more granular data, including objective measures of skin pigmentation beyond self-reported Fitzpatrick skin type, culture/beliefs, lifestyle/behavior, geographic location, socioeconomic status, genetics, or epigenetics could help fully elucidate skin cancer risks and mitigate health disparities among individuals who identify as part of this population.
Final Thoughts
The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by dermatologic health disparities. We hope this review helps to increase recognition of the clinical manifestations of skin cancer in Latine/Hispanic patients. Other factors that may impact skin cancer outcomes in this population include (but are not limited to) lack of or inadequate health insurance, medical mistrust, linguistic barriers and/or individual/cultural perspectives, along with limited research. Recognizing and addressing these (albeit complex) barriers that contribute to the inequitable access to health care in this population remains a critical step toward improving skin cancer outcomes.
- Noe-Bustamnate L, Lopez MH, Krogstad JM. US Hispanic population surpassed 60 million in 2019, but growth has slowed. July 7, 2020. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2020/07/07/u-s-hispanic-population-surpassed-60-million-in-2019-but-growth-has-slowed/
- Frank C, Lopez MH. Hispanic Americans’ trust in and engagement with science. Pew Research Center. June 14, 2022. Accessed September 3, 2024. https://www.pewresearch.org/wp-content/uploads/sites/20/2022/06/PS_2022.06.14_hispanic-americans-science_REPORT.pdf
- US Census Bureau. Projections of the size and composition of the US population: 2014 to 2060. US Government Printing Office; 2015. Accessed September 5, 2024. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
- Zong J. A mosaic, not a monolith: a profile of the U.S. Latino population, 2000-2020. October 26, 2022. Accessed September 3, 2024. https://latino.ucla.edu/research/latino-population-2000-2020/
- Latinos in California, Texas, New York, Florida and New Jersey. Pew Research Center. March 19, 2004. Accessed September 3, 2024. https://www.pewresearch.org/hispanic/2004/03/19/latinos-in-california-texas-new-york-florida-and-new-jersey/
- Pinheiro PS, Sherman RL, Trapido EJ, et al. Cancer incidence in first generation US Hispanics: Cubans, Mexicans, Puerto Ricans, and new Latinos. Cancer Epidemiol Biomarkers Prev. 2009;18:2162-2169.
- Pinheiro PS, Callahan KE, Kobetz EN. Disaggregated Hispanic groups and cancer: importance, methodology, and current knowledge. In: Ramirez AG, Trapido EJ, eds. Advancing the Science of Cancer in Latinos. Springer; 2020:17-34.
- Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
- Hogue L, Harvey VM. Basal cell carcinoma, squamous cell carcinoma, and cutaneous melanoma in skin of color patients. Dermatol Clin. 2019;37:519-526.
- Cruzval-O’Reilly E, Lugo-Somolinos A. Melanoma in Hispanics: we may have it all wrong. Cutis. 2020;106:28-30.
- Borrell LN, Elhawary JR, Fuentes-Afflick E, et al. Race and genetic ancestry in medicine—a time for reckoning with racism. N Engl J Med. 2021;384:474-480.
- Lopez MH, Krogstad JM, Passel JS. Who is Hispanic? September 5, 2023. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2023/09/05/who-is-hispanic/
- Carrasquillo OY, Lambert J, Merritt BG. Comment on “Disparities in nonmelanoma skin cancer in Hispanic/Latino patients based on Mohs micrographic surgery defect size: a multicenter retrospective study.”J Am Acad Dermatol. 2022;87:E129-E130.
- American Cancer Society. Key statistics for melanoma skin cancer. Updated January 17, 2024. Accessed September 3, 2024. https://www.cancer.org/cancer/types/melanoma-skin-cancer/about/key-statistics.html
- National Cancer Institute. Melanoma of the skin: recent trends in SEER age-adjusted incidence rates, 2000-2021. Updated June 27, 2024. Accessed September 3, 2024. https://seer.cancer.gov/statistics-network/explorer/application.htmlsite=53&data_type=1&graph_type=2&compareBy=sex&chk_sex_3=3&chk_sex_2=2&rate_type=2&race=6&age_range=1&stage=101&advopt_precision=1&advopt_show_ci=on&hdn_view=0&advopt_display=2
- Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659.
- Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801.
- Bristow IR, de Berker DA, Acland KM, et al. Clinical guidelines for the recognition of melanoma of the foot and nail unit. J Foot Ankle Res. 2010;3:25.
- Fernandez JM, Mata EM, Behbahani S, et al. Survival of Hispanic patients with cutaneous melanoma: a retrospective cohort analysis of 6016 cases from the National Cancer Database. J Am Acad Dermatol. 2023;88:1135-1138.
- Hu S, Sherman R, Arheart K, et al. Predictors of neighborhood risk for late-stage melanoma: addressing disparities through spatial analysis and area-based measures. J Investigative Dermatol. 2014;134:937-945.
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- Carvalho LAD, Aguiar FC, Smalley KSM, et al. Acral melanoma: new insights into the immune and genomic landscape. Neoplasia. 2023;46:100947.
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- Noe-Bustamnate L, Lopez MH, Krogstad JM. US Hispanic population surpassed 60 million in 2019, but growth has slowed. July 7, 2020. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2020/07/07/u-s-hispanic-population-surpassed-60-million-in-2019-but-growth-has-slowed/
- Frank C, Lopez MH. Hispanic Americans’ trust in and engagement with science. Pew Research Center. June 14, 2022. Accessed September 3, 2024. https://www.pewresearch.org/wp-content/uploads/sites/20/2022/06/PS_2022.06.14_hispanic-americans-science_REPORT.pdf
- US Census Bureau. Projections of the size and composition of the US population: 2014 to 2060. US Government Printing Office; 2015. Accessed September 5, 2024. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
- Zong J. A mosaic, not a monolith: a profile of the U.S. Latino population, 2000-2020. October 26, 2022. Accessed September 3, 2024. https://latino.ucla.edu/research/latino-population-2000-2020/
- Latinos in California, Texas, New York, Florida and New Jersey. Pew Research Center. March 19, 2004. Accessed September 3, 2024. https://www.pewresearch.org/hispanic/2004/03/19/latinos-in-california-texas-new-york-florida-and-new-jersey/
- Pinheiro PS, Sherman RL, Trapido EJ, et al. Cancer incidence in first generation US Hispanics: Cubans, Mexicans, Puerto Ricans, and new Latinos. Cancer Epidemiol Biomarkers Prev. 2009;18:2162-2169.
- Pinheiro PS, Callahan KE, Kobetz EN. Disaggregated Hispanic groups and cancer: importance, methodology, and current knowledge. In: Ramirez AG, Trapido EJ, eds. Advancing the Science of Cancer in Latinos. Springer; 2020:17-34.
- Qian Y, Johannet P, Sawyers A, et al. The ongoing racial disparities in melanoma: an analysis of the Surveillance, Epidemiology, and End Results database (1975-2016). J Am Acad Dermatol. 2021;84:1585-1593.
- Hogue L, Harvey VM. Basal cell carcinoma, squamous cell carcinoma, and cutaneous melanoma in skin of color patients. Dermatol Clin. 2019;37:519-526.
- Cruzval-O’Reilly E, Lugo-Somolinos A. Melanoma in Hispanics: we may have it all wrong. Cutis. 2020;106:28-30.
- Borrell LN, Elhawary JR, Fuentes-Afflick E, et al. Race and genetic ancestry in medicine—a time for reckoning with racism. N Engl J Med. 2021;384:474-480.
- Lopez MH, Krogstad JM, Passel JS. Who is Hispanic? September 5, 2023. Accessed September 3, 2024. https://www.pewresearch.org/short-reads/2023/09/05/who-is-hispanic/
- Carrasquillo OY, Lambert J, Merritt BG. Comment on “Disparities in nonmelanoma skin cancer in Hispanic/Latino patients based on Mohs micrographic surgery defect size: a multicenter retrospective study.”J Am Acad Dermatol. 2022;87:E129-E130.
- American Cancer Society. Key statistics for melanoma skin cancer. Updated January 17, 2024. Accessed September 3, 2024. https://www.cancer.org/cancer/types/melanoma-skin-cancer/about/key-statistics.html
- National Cancer Institute. Melanoma of the skin: recent trends in SEER age-adjusted incidence rates, 2000-2021. Updated June 27, 2024. Accessed September 3, 2024. https://seer.cancer.gov/statistics-network/explorer/application.htmlsite=53&data_type=1&graph_type=2&compareBy=sex&chk_sex_3=3&chk_sex_2=2&rate_type=2&race=6&age_range=1&stage=101&advopt_precision=1&advopt_show_ci=on&hdn_view=0&advopt_display=2
- Garnett E, Townsend J, Steele B, et al. Characteristics, rates, and trends of melanoma incidence among Hispanics in the USA. Cancer Causes Control. 2016;27:647-659.
- Higgins S, Nazemi A, Feinstein S, et al. Clinical presentations of melanoma in African Americans, Hispanics, and Asians. Dermatol Surg. 2019;45:791-801.
- Bristow IR, de Berker DA, Acland KM, et al. Clinical guidelines for the recognition of melanoma of the foot and nail unit. J Foot Ankle Res. 2010;3:25.
- Fernandez JM, Mata EM, Behbahani S, et al. Survival of Hispanic patients with cutaneous melanoma: a retrospective cohort analysis of 6016 cases from the National Cancer Database. J Am Acad Dermatol. 2023;88:1135-1138.
- Hu S, Sherman R, Arheart K, et al. Predictors of neighborhood risk for late-stage melanoma: addressing disparities through spatial analysis and area-based measures. J Investigative Dermatol. 2014;134:937-945.
- Buster KJ, You Z, Fouad M, et al. Skin cancer risk perceptions: a comparison across ethnicity, age, education, gender, and income. J Am Acad Dermatol. 2012;66:771-779.
- Halpern MT, Ward EM, Pavluck AL, et al. Association of insurance status and ethnicity with cancer stage at diagnosis for 12 cancer sites: a retrospective analysis. Lancet Oncology. 2008;9:222-231.
- Weiss J, Kirsner RS, Hu S. Trends in primary skin cancer prevention among US Hispanics: a systematic review. J Drugs Dermatol. 2012;11:580-586.
- Carvalho LAD, Aguiar FC, Smalley KSM, et al. Acral melanoma: new insights into the immune and genomic landscape. Neoplasia. 2023;46:100947.
- Kolitz E, Lopes F, Arffa M, et al. UV Exposure and the risk of keratinocyte carcinoma in skin of color: a systematic review. JAMA Dermatol. 2022;158:542-546.
- Lukowiak TM, Aizman L, Perz A, et al. Association of age, sex, race, and geographic region with variation of the ratio of basal cell to cutaneous squamous cell carcinomas in the United States. JAMA Dermatol. 2020;156:1192-1198.
- Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Derm Venereol. 2020;100:adv00140.
- McDaniel B, Badri T, Steele RB. Basal cell carcinoma. StatPearls [Internet]. Updated March 13, 2024. Accessed September 3, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/
- Dessinioti C, Antoniou C, Katsambas A, et al. Basal cell carcinoma: what’s new under the sun. Photochem Photobiol. 2010;86:481-491.
- Kim DP, Kus KJB, Ruiz E. Basal cell carcinoma review. Hematol Oncol Clin North Am. 2019;33:13-24.
- Bigler C, Feldman J, Hall E, et al. Pigmented basal cell carcinoma in Hispanics. J Am Acad Dermatol. 1996;34(5 pt 1):751-752.
- Higgins S, Nazemi A, Chow M, et al. Review of nonmelanoma skin cancer in African Americans, Hispanics, and Asians. Dermatol Surg. 2018;44:903-910.
- Byrd-Miles K, Toombs EL, Peck GL. Skin cancer in individuals of African, Asian, Latin-American, and American-Indian descent: differences in incidence, clinical presentation, and survival compared to Caucasians. J Drugs Dermatol. 2007;6:10-16.
- Rivas M, Rojas E, Calaf GM, et al. Association between non-melanoma and melanoma skin cancer rates, vitamin D and latitude. Oncol Lett. 2017;13:3787-3792.
- Bradford PT. Skin cancer in skin of color. Dermatol Nurs. 2009;21:170-177, 206.
- Davis DS, Robinson C, Callender VD. Skin cancer in women of color: epidemiology, pathogenesis and clinical manifestations. Int J Womens Dermatol. 2021;7:127-134.
- Maafs E, De la Barreda F, Delgado R, et al. Basal cell carcinoma of trunk and extremities. Int J Dermatol. 1997;36:622-628.
- Munjal A, Ferguson N. Skin cancer in skin of color. Dermatol Clin. 2023;41:481-489.
- Jorgenson E, Choquet H, Yin J, et al. Genetic ancestry, skin pigmentation, and the risk of cutaneous squamous cell carcinoma in Hispanic/Latino and non-Hispanic white populations. Commun Biol. 2020;3:765.
- Soliman YS, Mieczkowska K, Zhu TR, et al. Characterizing basal cell carcinoma in Hispanic individuals undergoing Mohs micrographic surgery: a 7-year retrospective review at an academic institution in the Bronx. Brit J Dermatol. 2022;187:597-599.
- Sierro TJ, Blumenthal LY, Hekmatjah J, et al. Differences in health care resource utilization and costs for keratinocyte carcinoma among racioethnic groups: a population-based study. J Am Acad Dermatol. 2022;86:373-378.
- Blumenthal LY, Arzeno J, Syder N, et al. Disparities in nonmelanoma skin cancer in Hispanic/Latino patients based on Mohs micrographic surgery defect size: a multicenter retrospective study. J Am Acad Dermatol. 2022;86:353-358.
- Slopnick EA, Kim SP, Kiechle JE, et al. Racial disparities differ for African Americans and Hispanics in the diagnosis and treatment of penile cancer. Urology. 2016;96:22-28.
- Goodman MT, Hernandez BY, Shvetsov YB. Demographic and pathologic differences in the incidence of invasive penile cancer in the United States, 1995-2003. Cancer Epidemiol Biomarkers Prev. 2007;16:1833-1839.
- Thompson EL, Rosen BL, Maness SB. Social determinants of health and human papillomavirus vaccination among young adults, National Health Interview Survey 2016. J Community Health. 2019;44:149-158.
- Hao X, Billings SD, Wu F, et al. Dermatofibrosarcoma protuberans: update on the diagnosis and treatment. J Clin Med. 2020;9:1752.
- Mosallaei D, Lee EB, Lobl M, et al. Rare cutaneous malignancies in skin of color. Dermatol Surg. 2022;48:606-612.
- Criscito MC, Martires KJ, Stein JA. Prognostic factors, treatment, and survival in dermatofibrosarcoma protuberans. JAMA Dermatol. 2016;152:1365-1371.
- Orenstein LAV, Nelson MM, Wolner Z, et al. Differences in outpatient dermatology encounter work relative value units and net payments by patient race, sex, and age. JAMA Dermatol. 2021;157:406-412.
- Lowe GC, Onajin O, Baum CL, et al. A comparison of Mohs micrographic surgery and wide local excision for treatment of dermatofibrosarcoma protuberans with long-term follow-up: the Mayo Clinic experience. Dermatol Surg. 2017;43:98-106.
- Moore KJ, Chang MS, Weiss J, et al. Racial and ethnic differences in the surgical treatment of dermatofibrosarcoma protuberans: a retrospective cohort analysis. J Am Acad Dermatol. 2022;87:245-247.
- Trofymenko O, Bordeaux JS, Zeitouni NC. Survival in patients with primary dermatofibrosarcoma protuberans: National Cancer Database analysis. J Am Acad Dermatol. 2018;78:1125-1134.
- Bazargan M, Cobb S, Assari S. Discrimination and medical mistrust in a racially and ethnically diverse sample of California adults. Ann Fam Med. 2021;19:4-15.
- Smedley BD, Stith AY, Nelson AR, eds. Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care. Washington, DC; 2003.
- Bailey ZD, Krieger N, Agenor M, et al. Structural racism and health inequities in the USA: evidence and interventions. Lancet. 2017;389:1453-1463.
- Tackett KJ, Jenkins F, Morrell DS, et al. Structural racism and its influence on the severity of atopic dermatitis in African American children. Pediatric Dermatol. 2020;37:142-146.
- Greif C, Srivastava D, Nijhawan RI. A retrospective cohort study of dermatofibrosarcoma protuberans at a large metropolitan academic center. JAAD Int. 2022;6:104-106.
- Office of the Assistant Secretary for Planning and Evaluation. Health insurance coverage and access to care among Latinos: recent rrends and key challenges (HP-2021-22). October 8, 2021. Accessed September 3, 2024. https://aspe.hhs.gov/reports/health-insurance-coverage-access-care-among-latinos
- Keisler-Starkey K, Bunch LN. Health insurance coverage in the United States: 2020 (Current Population Reports No. P60-274). US Census Bureau; 2021. https://www.census.gov/content/dam/Census/library/publications/2021/demo/p60-274.pdf
- Kaiser Family Foundation. Key facts on health coverage of immigrants. Updated June 26, 2024. Accessed September 3, 2024. https://www.kff.org/racial-equity-and-health-policy/fact-sheet/key-facts-on-health-coverage-of-immigrants/
- Pew Research Center. Unauthorized immigrants: length of residency, patterns of parenthood. Published December 1, 2011. Accessed October 28, 2024. https://www.pewresearch.org/race-and-ethnicity/2011/12/01/unauthorized-immigrants-length-of-residency-patterns-of-parenthood/
- Schneider J, Schmitt M. Understanding the relationship between racial discrimination and mental health among African American adults: a review. SAGE Open. 2015;5:1-10.
- Philbin MM, Flake M, Hatzenbuehler ML, et al. State-level immigration and immigrant-focused policies as drivers of Latino health disparities in the United States. Soc Sci Med. 2018;199:29-38.
- Vargas ED, Sanchez GR, Juarez M. The impact of punitive immigrant laws on the health of Latina/o Populations. Polit Policy. 2017;45:312-337.
- Sutton AL, He J, Edmonds MC, et al. Medical mistrust in Black breast cancer patients: acknowledging the roles of the trustor and the trustee. J Cancer Educ. 2019;34:600-607.
- Jacobs J. An overview of Latin American healthcare systems. Pacific Prime Latin America. July 31, 2023. Accessed September 3, 2024. https://www.pacificprime.lat/blog/an-overview-of-latin-american-healthcare-systems/
- CDC. Unfair and unjust practices and conditions harm Hispanic and Latino people and drive health disparities. May 15, 2024. Accessed September 3, 2024. https://www.cdc.gov/tobacco-health-equity/collection/hispanic-latino-unfair-and-unjust.html
- Hall IJ, Rim SH, Dasari S. Preventive care use among Hispanic adults with limited comfort speaking English: an analysis of the Medical Expenditure Panel Survey data. Prev Med. 2022;159:107042.
- Brach C, Chevarley FM. Demographics and health care access and utilization of limited-English-proficient and English-proficient Hispanics. Agency for Healthcare Research and Quality. February 2008. http://meps.ahrq.gov/mepsweb/data_files/publications//rf28/rf28.pdf
- Berdahl TA, Kirby JB. Patient-provider communication disparities by limited English proficiency (LEP): trends from the US Medical Expenditure Panel Survey, 2006-2015. J General Intern Med. 2019;34:1434-1440.
- Robinson JK, Joshi KM, Ortiz S, et al. Melanoma knowledge, perception, and awareness in ethnic minorities in Chicago: recommendations regarding education. Psychooncology. 2011;20:313-320.
- Robinson JK, Nodal M, Chavez L, et al. Enhancing the relevance of skin self-examination for Latinos. JAMA Dermatol. 2017;153:717-718.
- Buchanan Lunsford N, Berktold J, Holman DM, et al. Skin cancer knowledge, awareness, beliefs and preventive behaviors among black and hispanic men and women. Prev Med Rep. 2018;12:203-209.
- Madrigal JM, Correa-Mendez M, Arias JD, et al. Hispanic, Latino/a, Latinx, Latine: disentangling the identities of Hispanic/Latino Americans. National Cancer Institute Division of Cancer Epidemiology & Genetics. October 20, 2022. Accessed September 3, 2024. https://dceg.cancer.gov/about/diversity-inclusion/inclusivity-minute/2022/disentangling-identities-hispanic-latino-americans
Practice Points
- The Latine/Hispanic community—the largest ethnic minoritized group in the United States—is disproportionately affected by disparities in skin cancer outcomes.
- Factors influencing skin cancer outcomes in Latine/Hispanic patients in the United States are complex and multidimensional, including lack of familiarity among dermatologists with skin cancer manifestation in this population compared to non-Hispanic White individuals as well as limited data elucidating risk factors for skin cancer in patients with skin of color and sociocultural factors.
Pinto Bean Pressure Wraps: A Novel Approach to Treating Digital Warts
Practice Gap
Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.4 Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.
Technique
Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.
What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).
Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.
Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.
Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.
Practice Implications
The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.1 This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.5
The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.
- Cardoso J, Calonje E. Cutaneous manifestations of human papillomaviruses: a review. Acta Dermatovenerol Alp Pannonica Adriat. 2011;20:145-154.
- Lipke M. An armamentarium of wart treatments. Clin Med Res. 2006;4:273-293. doi:10.3121/cmr.4.4.273
- Muse M, Stiff K, Glines K, et al. A review of intralesional wart therapy. Dermatol Online J. 2020;26:2. doi:10.5070/D3263048027
- Berna R, Margolis D, Barbieri J. Annual health care utilization and costs for treatment of cutaneous and anogenital warts among a commercially insured population in the US, 2017-2019. JAMA Dermatol. 2022;158:695-697. doi:10.1001/jamadermatol.2022.0964
- Fredriksson C, Ilias M, Anderson C. New mechanical device for effective removal of skin tags in routine health care. Dermatol Online J. 2009;15:9. doi:10.5070/D37tj2800k
Practice Gap
Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.4 Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.
Technique
Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.
What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).
Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.
Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.
Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.
Practice Implications
The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.1 This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.5
The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.
Practice Gap
Verruca vulgaris is a common dermatologic challenge due to its high prevalence and tendency to recur following routinely employed destructive modalities (eg, cryotherapy, electrosurgery), which can incur a considerable amount of pain and some risk for scarring.1,2 Other treatment methods for warts such as topical salicylic acid preparations, topical immunotherapy, or intralesional allergen injections often require multiple treatment sessions.3,4 Furthermore, the financial burden of traditional wart treatment can be substantial.4 Better techniques are needed to improve the clinician’s approach to treating warts. We describe a home-based technique to treat common digital warts using pinto bean pressure wraps to induce ischemic changes in wart tissue with similar response rates to commonly used modalities.
Technique
Our technique utilizes a small, hard, convex object that is applied directly over the digital wart. A simple self-adhesive wrap is used to cover the object and maintain constant pressure on the wart overnight. We typically use a dried pinto bean (a variety of the common bean Phaseolus vulgaris) acquired from a local grocery store due to its ideal size, hard surface, and convex shape (Figure 1). The bean is taped in place directly overlying the wart and covered with a self-adhesive wrap overnight. The wrap is removed in the morning, and often no further treatment is needed. The ischemic wart tissue is allowed to slough spontaneously over 1 to 2 weeks. No wound care or dressing is necessary (Figure 2). Larger warts may require application of the pressure wraps for 2 to 3 additional nights. While most warts resolve with this technique, we have observed a recurrence rate similar to that for cryotherapy. Patients are advised that any recurrent warts can be re-treated monthly, if needed, until resolution.
What to Use and How to Prepare—Any small, hard, convex object can be used for the pressure wrap; we also have used appropriately sized and shaped plastic shirt buttons with similar results. Home kits can be assembled in advance and provided to patients at their initial visit along with appropriate instructions (Figure 1A).
Effects on the Skin and Distal Digit—Application of pressure wraps does not harm normal skin; however, care should be taken when the self-adherent wrap is applied so as not to induce ischemia of the distal digit. The wrap should be applied using gentle pressure with patients experiencing minimal discomfort from the overnight application.
Indications—This pressure wrap technique can be employed on most digital warts, including periungual warts, which can be difficult to treat by other means. However, in our experience this technique is not effective for nondigital warts, likely due to the inability to maintain adequate pressure with the overlying dressing. Patients at risk for compromised digital perfusion, such as those with Raynaud phenomenon or systemic sclerosis, should not be treated with pressure wraps due to possible digital ischemia.
Precautions—Patients should be advised that the pinto bean should only be used if dry and should not be ingested. The bean can be a choking hazard for small children, therefore appropriate precautions should be used. Allergic contact dermatitis to the materials used in this technique is possible, but we have never observed this. The pinto bean can be reused for future application as long as it remains dry and provides a hard convex surface.
Practice Implications
The probable mechanism of the ischemic changes to the wart tissue likely is the occlusion of tortuous blood vessels in the dermal papillae, which are intrinsic to wart tissue and absent in normal skin.1 This pressure-induced ischemic injury allows for selective destruction of the wart tissue with sparing of the normal skin. Our technique is fairly novel, although at least one report in the literature has described the use of a mechanical device to induce ischemic changes in skin tags.5
The use of pinto bean pressure wraps to induce ischemic change in digital warts provides a low-risk and nearly pain-free alternative to more expensive and invasive treatment methods. Moreover, this technique allows for a low-cost home-based therapy that can be repeated easily for other digital sites or if recurrence is noted.
- Cardoso J, Calonje E. Cutaneous manifestations of human papillomaviruses: a review. Acta Dermatovenerol Alp Pannonica Adriat. 2011;20:145-154.
- Lipke M. An armamentarium of wart treatments. Clin Med Res. 2006;4:273-293. doi:10.3121/cmr.4.4.273
- Muse M, Stiff K, Glines K, et al. A review of intralesional wart therapy. Dermatol Online J. 2020;26:2. doi:10.5070/D3263048027
- Berna R, Margolis D, Barbieri J. Annual health care utilization and costs for treatment of cutaneous and anogenital warts among a commercially insured population in the US, 2017-2019. JAMA Dermatol. 2022;158:695-697. doi:10.1001/jamadermatol.2022.0964
- Fredriksson C, Ilias M, Anderson C. New mechanical device for effective removal of skin tags in routine health care. Dermatol Online J. 2009;15:9. doi:10.5070/D37tj2800k
- Cardoso J, Calonje E. Cutaneous manifestations of human papillomaviruses: a review. Acta Dermatovenerol Alp Pannonica Adriat. 2011;20:145-154.
- Lipke M. An armamentarium of wart treatments. Clin Med Res. 2006;4:273-293. doi:10.3121/cmr.4.4.273
- Muse M, Stiff K, Glines K, et al. A review of intralesional wart therapy. Dermatol Online J. 2020;26:2. doi:10.5070/D3263048027
- Berna R, Margolis D, Barbieri J. Annual health care utilization and costs for treatment of cutaneous and anogenital warts among a commercially insured population in the US, 2017-2019. JAMA Dermatol. 2022;158:695-697. doi:10.1001/jamadermatol.2022.0964
- Fredriksson C, Ilias M, Anderson C. New mechanical device for effective removal of skin tags in routine health care. Dermatol Online J. 2009;15:9. doi:10.5070/D37tj2800k
Alopecia Induced by Poly-L-Lactic Acid Injection
Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bedridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.
Case Report
A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.
The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.
Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.
Intralesional triamcinolone acetonide 5 mg/mL was administered at 1-cm intervals in the subdermal space (0.1 mL/puncture site). After 14 days, the patient developed an additional patch of alopecia in the same vascular territory as the right temporal artery, positioned just beneath the initial patch, with similar trichoscopy findings. The patches were treated with intralesional triamcinolone acetonide for 3 additional sessions, administered every 4 weeks. Long-term monitoring of the patient revealed regrowth with comparable hair count to the unaffected contralateral scalp, indicative of a nonscarring alopecia.
Comment
Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.4 Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.5 Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.6-9
Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.10 In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.11 The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.
The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.12 This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.
The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.13
Conclusion
Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.
We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.
- Issa NT, Kaiser M, Martinez-Velasco A, et al. Alopecia after cosmetic injection procedures: a review. Dermatol Surg. 2022;48:855-861.
- Alopecia with foreign body granulomas induced by Radiesse injection: a case report. J Cosmet Laser Ther. 2018;20:462-464.
- Munia C, Parada M, de Alvarenga Morais MH. Changes in facial morphology using poly-L-lactic acid application according to vector technique: a case series. J Clin Aesthet Dermatol. 2022;15:38-42.
- Attenello NH, Maas CS. Injectable fillers: review of material and properties. Facial Plast Surg. 2015;31:29-34.
- Mastrokalos DS, Paessler HH. Allergic reaction to biodegradable interference poly-L-lactic acid screws after anterior cruciate ligament reconstruction with bone-patellar tendon-bone graft. Arthroscopy. 2008;24:732-733.
- Wu CW, Wu HJ. Retinal artery occlusion following cosmetic injection of poly-L-lactic acid. Taiwan J Ophthalmol. 2021;11:317-320.
- Yuan JT, Chang TW, Yu SS, et al. Mental artery occlusion from poly-L-lactic acid injection at the lateral chin. Dermatol Surg. 2017;43:1402-1405.
- Ragam A, Agemy SA, Dave SB, et al. Ipsilateral ophthalmic and cerebral infarctions after cosmetic polylactic acid injection into the forehead. J Neuroophthalmol. 2017;37:77-80.
- Witmanowski H, Błochowiak K. Another face of dermal fillers. Postepy Dermatol Alergol. 2020;37:651-659.
- Yang Q, Qiu L, Yi C, et al. Reversible alopecia with localized scalp necrosis after accidental embolization of the parietal artery with hyaluronic acid. Aesthetic Plast Surg. 2017;41:695-699.
- Asz-Sigall D, Iñigo-Gomez K, Ortega-Springall MF, et al. Alopecia secondary to hyaluronic acid embolization: trichoscopic findings. Skin Appendage Disord. 2019;5:396-400.
- Oh S, Lee JH, Kim HM, et al. Poly-L-lactic acid fillers improved dermal collagen synthesis by modulating M2 macrophage polarization in aged animal skin. Cells. 2023;12:1320. doi:10.3390/cells12091320
- Natarelli N, Gahoonia N, Sivamani RK. Integrative and mechanistic approach to the hair growth cycle and hair loss. J Clin Med. 2023;12:893.2. Liu RF, Kuo TT, Chao YY, et al.
Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bedridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.
Case Report
A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.
The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.
Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.
Intralesional triamcinolone acetonide 5 mg/mL was administered at 1-cm intervals in the subdermal space (0.1 mL/puncture site). After 14 days, the patient developed an additional patch of alopecia in the same vascular territory as the right temporal artery, positioned just beneath the initial patch, with similar trichoscopy findings. The patches were treated with intralesional triamcinolone acetonide for 3 additional sessions, administered every 4 weeks. Long-term monitoring of the patient revealed regrowth with comparable hair count to the unaffected contralateral scalp, indicative of a nonscarring alopecia.
Comment
Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.4 Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.5 Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.6-9
Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.10 In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.11 The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.
The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.12 This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.
The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.13
Conclusion
Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.
We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.
Cosmetic procedures carry inherent risks of adverse events. Transient and permanent alopecia are rare complications of these procedures. Although they have not been fully elucidated, several pathologic mechanisms for hair loss following cosmetic procedures have been proposed, including extravascular compression (a phenomenon that has been well documented in bedridden patients) as well as intravascular occlusion leading to inflammation and necrosis, which has been associated with hyaluronic acid (HA) fillers.¹ Cases of alopecia also have been reported following mesotherapy and calcium hydroxyapatite, deoxycholic acid, and botulinum toxin injections.² We report a case of alopecia resulting from poly-L-lactic acid (PLLA) injection in a 35-year-old woman with the intent to raise awareness of this rare adverse event.
Case Report
A healthy 35-year-old woman received aesthetic PLLA injections on the face and frontal hairline performed by an outside dermatologist using the vector technique. During the procedure, the patient experienced intense itchiness at the right temporal artery vascular territory and reported a substantial headache the next day. She also presented with erythema and edema of the frontal and right parietal scalp with a well-delimited livedoid vascular area along the temporal artery territory on the right side of the head 1 day after the procedure (Figure 1). These signs were reported to the outside dermatologist who performed the procedure, but they were not assumed to be adverse events at that time.
The condition persisted for 4 days followed by the development of an irregular 3×2-cm patch of alopecia on the right parietal scalp. A 3-day course of self-administered oral prednisolone 0.2 mg/kg/d was prescribed.
Twenty-seven days after the procedure, the patient presented to our trichology clinic for evaluation of a single patch of nonscarring alopecia on the right parietal scalp. Trichoscopy showed multiple yellow and black dots, broken hairs, pigment deposits, and an erythematous background mainly composed of linear telangiectatic vessels (Figure 2). Histopathologic analysis revealed a lymphocytic inflammatory infiltrate surrounding the follicular units that was compatible with an alopecia areata–like pattern as well as PLLA deposits in the subcutaneous tissue forming foreign body granulomas (Figure 3). The diagnosis of PLLA-induced alopecia was made based on the detection of PLLA at the biopsy site within the patchy alopecia.
Intralesional triamcinolone acetonide 5 mg/mL was administered at 1-cm intervals in the subdermal space (0.1 mL/puncture site). After 14 days, the patient developed an additional patch of alopecia in the same vascular territory as the right temporal artery, positioned just beneath the initial patch, with similar trichoscopy findings. The patches were treated with intralesional triamcinolone acetonide for 3 additional sessions, administered every 4 weeks. Long-term monitoring of the patient revealed regrowth with comparable hair count to the unaffected contralateral scalp, indicative of a nonscarring alopecia.
Comment
Poly-L-lactic acid is a biostimulator synthesized from the α-hydroxy acid family in 1954 that has been safely used in suture materials, resorbable plates, and orthopedic screws.4 Alopecia has been reported as a systemic allergic reaction to biodegradable screws following an orthopedic procedure.5 Prior reports of embolization and retinal ischemia with PLLA have raised concerns regarding its occlusive potential.6-9
Approved by the US Food and Drug Administration in 2004 for soft tissue restoration in HIV-related lipoatrophy, PLLA was expanded to cosmetic applications in 2009. As previously reported with HA fillers, we hypothesize that extravascular compression resulting from the placement of the filler material (due to the volume injected in the scalp area) contributes to the development of alopecia plus PLLA embolism–induced ischemic alopecia in the affected areas.10 In our case, the diagnosis of PLLA-induced alopecia was confirmed based on the finding of the filler material in the subcutaneous tissue on histopathology, probably due to embolization. Moreover, trichoscopic findings were all similar to those described after HA embolization.11 The features found in our patient due to the PLLA local reaction were similar to those seen in other conditions such as alopecia areata, pressure alopecia, and chemotherapy-induced alopecia; therefore, histopathology confirmation is mandatory in cases of hair loss associated with PLLA.
The emergence of a secondary patch of alopecia prompts consideration of an intrinsic late inflammatory propensity of PLLA. Immune cells recognize PLLA as a foreign body, and subclinical inflammatory foreign body reactions can cause PLLA-induced collagen synthesis.12 This phenomenon underscores the need for further investigation into the immunologic implications of PLLA in alopecia pathogenesis.
The angiogenic properties of the anagen phase require an adequate blood supply for effective hair growth; therefore, the lack of blood and nutrient supply to the hair bulb triggers miniaturization, a possible explanation for the hair thinning found in the alopecic patch.13
Conclusion
Alopecia as an adverse effect of cosmetic procedures can be distressing for patients, even when reversible. A detailed understanding of scalp anatomy is critical for satisfactory outcomes with aesthetic procedures. Physicians must pay attention to the amount and area of material injected in order to avoid possible mechanisms of ischemia—embolization and/or extravascular compression—especially in highly vascularized areas.
We present a rare report of alopecia as an adverse event of PLLA injection. Dermatologists must be aware of this rare condition, and trichoscopy combined with histopathologic analysis are encouraged for early recognition and proper management.
- Issa NT, Kaiser M, Martinez-Velasco A, et al. Alopecia after cosmetic injection procedures: a review. Dermatol Surg. 2022;48:855-861.
- Alopecia with foreign body granulomas induced by Radiesse injection: a case report. J Cosmet Laser Ther. 2018;20:462-464.
- Munia C, Parada M, de Alvarenga Morais MH. Changes in facial morphology using poly-L-lactic acid application according to vector technique: a case series. J Clin Aesthet Dermatol. 2022;15:38-42.
- Attenello NH, Maas CS. Injectable fillers: review of material and properties. Facial Plast Surg. 2015;31:29-34.
- Mastrokalos DS, Paessler HH. Allergic reaction to biodegradable interference poly-L-lactic acid screws after anterior cruciate ligament reconstruction with bone-patellar tendon-bone graft. Arthroscopy. 2008;24:732-733.
- Wu CW, Wu HJ. Retinal artery occlusion following cosmetic injection of poly-L-lactic acid. Taiwan J Ophthalmol. 2021;11:317-320.
- Yuan JT, Chang TW, Yu SS, et al. Mental artery occlusion from poly-L-lactic acid injection at the lateral chin. Dermatol Surg. 2017;43:1402-1405.
- Ragam A, Agemy SA, Dave SB, et al. Ipsilateral ophthalmic and cerebral infarctions after cosmetic polylactic acid injection into the forehead. J Neuroophthalmol. 2017;37:77-80.
- Witmanowski H, Błochowiak K. Another face of dermal fillers. Postepy Dermatol Alergol. 2020;37:651-659.
- Yang Q, Qiu L, Yi C, et al. Reversible alopecia with localized scalp necrosis after accidental embolization of the parietal artery with hyaluronic acid. Aesthetic Plast Surg. 2017;41:695-699.
- Asz-Sigall D, Iñigo-Gomez K, Ortega-Springall MF, et al. Alopecia secondary to hyaluronic acid embolization: trichoscopic findings. Skin Appendage Disord. 2019;5:396-400.
- Oh S, Lee JH, Kim HM, et al. Poly-L-lactic acid fillers improved dermal collagen synthesis by modulating M2 macrophage polarization in aged animal skin. Cells. 2023;12:1320. doi:10.3390/cells12091320
- Natarelli N, Gahoonia N, Sivamani RK. Integrative and mechanistic approach to the hair growth cycle and hair loss. J Clin Med. 2023;12:893.2. Liu RF, Kuo TT, Chao YY, et al.
- Issa NT, Kaiser M, Martinez-Velasco A, et al. Alopecia after cosmetic injection procedures: a review. Dermatol Surg. 2022;48:855-861.
- Alopecia with foreign body granulomas induced by Radiesse injection: a case report. J Cosmet Laser Ther. 2018;20:462-464.
- Munia C, Parada M, de Alvarenga Morais MH. Changes in facial morphology using poly-L-lactic acid application according to vector technique: a case series. J Clin Aesthet Dermatol. 2022;15:38-42.
- Attenello NH, Maas CS. Injectable fillers: review of material and properties. Facial Plast Surg. 2015;31:29-34.
- Mastrokalos DS, Paessler HH. Allergic reaction to biodegradable interference poly-L-lactic acid screws after anterior cruciate ligament reconstruction with bone-patellar tendon-bone graft. Arthroscopy. 2008;24:732-733.
- Wu CW, Wu HJ. Retinal artery occlusion following cosmetic injection of poly-L-lactic acid. Taiwan J Ophthalmol. 2021;11:317-320.
- Yuan JT, Chang TW, Yu SS, et al. Mental artery occlusion from poly-L-lactic acid injection at the lateral chin. Dermatol Surg. 2017;43:1402-1405.
- Ragam A, Agemy SA, Dave SB, et al. Ipsilateral ophthalmic and cerebral infarctions after cosmetic polylactic acid injection into the forehead. J Neuroophthalmol. 2017;37:77-80.
- Witmanowski H, Błochowiak K. Another face of dermal fillers. Postepy Dermatol Alergol. 2020;37:651-659.
- Yang Q, Qiu L, Yi C, et al. Reversible alopecia with localized scalp necrosis after accidental embolization of the parietal artery with hyaluronic acid. Aesthetic Plast Surg. 2017;41:695-699.
- Asz-Sigall D, Iñigo-Gomez K, Ortega-Springall MF, et al. Alopecia secondary to hyaluronic acid embolization: trichoscopic findings. Skin Appendage Disord. 2019;5:396-400.
- Oh S, Lee JH, Kim HM, et al. Poly-L-lactic acid fillers improved dermal collagen synthesis by modulating M2 macrophage polarization in aged animal skin. Cells. 2023;12:1320. doi:10.3390/cells12091320
- Natarelli N, Gahoonia N, Sivamani RK. Integrative and mechanistic approach to the hair growth cycle and hair loss. J Clin Med. 2023;12:893.2. Liu RF, Kuo TT, Chao YY, et al.
Practice Points
- Alopecia is a potential adverse event of poly-L-lactic acid (PLLA) injection, and prior reports of embolization and retinal ischemia with PLLA use raise the concern of its occlusive potential.
- The combination of extravascular compression due to the presence of the filler material in the subcutaneous tissue as well as intravascular PLLA embolism may contribute to tissue ischemia–induced alopecia in the affected areas.
- Poly-L-lactic acid also may cause a local inflammatory reaction that is alopecia areata–like, which would explain its similar trichoscopy findings.
Hospital Dermatology: Review of Research in 2023-2024
Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).
Severe Cutaneous Adverse Drug Reactions
Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.
A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4
In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5
Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6
Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7
In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9
Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention
Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13
In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14
Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16
Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17
Autoimmune Blistering Diseases
Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19
By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).
Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23
Final Thoughts
Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.
- Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
- Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
- Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
- Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
- Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
- Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
- Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
- Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
- Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
- Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
- Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
- Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
- Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
- Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
- Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
- Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
- Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
- Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
- Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
- Chebani R, Lombart F, Chaby G, et al; French Study Group on Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
- Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
- Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
- Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).
Severe Cutaneous Adverse Drug Reactions
Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.
A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4
In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5
Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6
Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7
In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9
Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention
Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13
In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14
Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16
Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17
Autoimmune Blistering Diseases
Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19
By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).
Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23
Final Thoughts
Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.
Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).
Severe Cutaneous Adverse Drug Reactions
Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.
A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4
In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5
Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6
Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7
In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9
Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention
Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13
In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14
Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16
Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17
Autoimmune Blistering Diseases
Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19
By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).
Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23
Final Thoughts
Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.
- Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
- Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
- Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
- Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
- Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
- Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
- Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
- Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
- Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
- Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
- Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
- Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
- Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
- Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
- Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
- Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
- Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
- Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
- Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
- Chebani R, Lombart F, Chaby G, et al; French Study Group on Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
- Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
- Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
- Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
- Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
- Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
- Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
- Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
- Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
- Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
- Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
- Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
- Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
- Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
- Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
- Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
- Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
- Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
- Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
- Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
- Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
- Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
- Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
- Chebani R, Lombart F, Chaby G, et al; French Study Group on Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
- Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
- Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
- Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
Practice Points
- An international Delphi study reached consensus on 93 statements regarding workup, severity assessment, and management of DRESS syndrome.
- In nursing homes, universal decolonization with chlorhexidine and nasal iodophor greatly reduced the risk for hospital transfers due to infection compared to routine care.
- Rituximab as the first-line therapy for pemphigus vulgaris is associated with long-term sustained complete remission without corticosteroid therapy.
- Dupilumab and omalizumab are emerging safe and effective treatment options for bullous pemphigoid.