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High Sodium Intake Linked to Greater Risk for Eczema
In a study of adults, an increase of 1 g in estimated 24-hour urinary sodium excretion was associated with 11% higher odds of an atopic dermatitis (AD) diagnosis, 16% higher odds of having active AD, and 11% higher odds of increased severity of AD.
Those are key findings from a cross-sectional analysis of data from the United Kingdom.
“Excessive dietary sodium, common in fast food, may be associated with AD,” corresponding author Katrina Abuabara, MD, MA, MSCE, and colleagues wrote in the study, which was published online in JAMA Dermatology. They referred to recent research using sodium MRI, which showed that “the majority of the body’s exchangeable sodium is stored in the skin and that skin sodium is associated with autoimmune and chronic inflammatory conditions, including AD.” And in another study published in 2019, lesional skin sodium was 30-fold greater in patients with AD than in healthy controls.
To investigate whether there is an association between higher levels of sodium consumption and AD prevalence, activity, and severity at the population level, Dr. Abuabara, of the program for clinical research in the Department of Dermatology at the University of California, San Francisco, and coauthors drew from the UK Biobank, a population-based cohort of more than 500,000 individuals aged 37-73 years at the time of recruitment by the National Health Service. The primary exposure was 24-hour urinary sodium excretion, which was calculated by using the INTERSALT equation, a sex-specific estimation that incorporates body mass index; age; and urine concentrations of potassium, sodium, and creatinine. The primary study outcome was AD or active AD based on diagnostic and prescription codes from linked electronic medical records. The researchers used multivariable logistic regression models adjusted for age, sex, race and ethnicity, Townsend deprivation index, and education to measure the association.
Of the 215,832 Biobank participants included in the analysis, 54% were female, their mean age was 57 years, 95% were White, their mean estimated 24-hour urine sodium excretion was 3.01 g/day, and 10,839 (5%) had a diagnosis of AD. The researchers observed that on multivariable logistic regression, a 1-g increase in estimated 24-hour urine sodium excretion was associated with increased odds of AD (adjusted odds ratio [AOR], 1.11; 95% CI, 1.07-1.14), increased odds of active AD (AOR, 1.16; 95% CI, 1.05-1.28), and increased odds of increasing severity of AD (AOR, 1.11; 95% CI, 1.07-1.15).
Validating Results With US Data
To validate the findings, the researchers evaluated a cohort of 13,014 participants from the US-based National Health and Nutrition Examination Survey (NHANES), using pooled data from the 1999-2000, 2001-2002, and 2003-2004 samples. Of the 13,014 participants, 796 reported current AD, and 1493 reported AD in the past year. The mean dietary sodium intake of overall NHANES participants estimated with 24-hour dietary recall questionnaires was 3.45 g, with a mean of 3.47 g for those with current AD and a mean of 3.44 g for those without AD.
The researchers observed that a 1-g/day higher dietary sodium intake was associated with a higher risk for current AD (AOR, 1.22; 95%CI, 1.01-1.47) and a somewhat higher risk for AD in the past year (AOR, 1.14; 95% CI, 0.97-1.35).
“Future work should examine whether variation of sodium intake over time might trigger AD flares and whether it helps to explain heterogeneity in response to new immunomodulatory treatments for AD,” the authors wrote. “Reduced sodium intake was recommended as a treatment for AD more than a century ago, but there have yet to be studies examining the association of dietary sodium reduction with skin sodium concentration or AD severity,” they added. Noting that sodium reduction “has been shown to be a cost-effective intervention for hypertension and other cardiovascular disease outcomes,” they said that their data “support experimental studies of this approach in AD.”
They acknowledged certain limitations of the study, including the fact that a single spot urine sample was used in the UK Biobank cohort, “which only captures dietary intake of the last 24 hours and is not the best measure of usual or long-term intake of sodium.” They also noted that the findings may not be generalizable to other populations and that AD was based on self-report in the NHANES validation cohort.
Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the results, said the study by Dr. Abuabara and colleagues “gives us another reason to avoid salt, showing that 1 g/day of higher salt intake increases the risk of AD in an adult population and more severe AD.”
He added that, “Now, can you say that reducing salt intake will have a therapeutic effect or clinically relevant impact? No. [That is] certainly worth exploring but at a minimum, gives some more credibility to keeping it bland.”
The study was supported by a grant from the Medical Student in Aging Research Program, the National Institute on Aging, and the National Eczema Association. Dr. Abuabara reported receiving research funding for her institution from Pfizer and Cosmetique Internacional/La Roche-Posay and consulting fees from Target RWE, Sanofi, Nektar, and Amgen. No other disclosures were reported. Dr. Friedman had no relevant disclosures.
A version of this article appeared on Medscape.com.
In a study of adults, an increase of 1 g in estimated 24-hour urinary sodium excretion was associated with 11% higher odds of an atopic dermatitis (AD) diagnosis, 16% higher odds of having active AD, and 11% higher odds of increased severity of AD.
Those are key findings from a cross-sectional analysis of data from the United Kingdom.
“Excessive dietary sodium, common in fast food, may be associated with AD,” corresponding author Katrina Abuabara, MD, MA, MSCE, and colleagues wrote in the study, which was published online in JAMA Dermatology. They referred to recent research using sodium MRI, which showed that “the majority of the body’s exchangeable sodium is stored in the skin and that skin sodium is associated with autoimmune and chronic inflammatory conditions, including AD.” And in another study published in 2019, lesional skin sodium was 30-fold greater in patients with AD than in healthy controls.
To investigate whether there is an association between higher levels of sodium consumption and AD prevalence, activity, and severity at the population level, Dr. Abuabara, of the program for clinical research in the Department of Dermatology at the University of California, San Francisco, and coauthors drew from the UK Biobank, a population-based cohort of more than 500,000 individuals aged 37-73 years at the time of recruitment by the National Health Service. The primary exposure was 24-hour urinary sodium excretion, which was calculated by using the INTERSALT equation, a sex-specific estimation that incorporates body mass index; age; and urine concentrations of potassium, sodium, and creatinine. The primary study outcome was AD or active AD based on diagnostic and prescription codes from linked electronic medical records. The researchers used multivariable logistic regression models adjusted for age, sex, race and ethnicity, Townsend deprivation index, and education to measure the association.
Of the 215,832 Biobank participants included in the analysis, 54% were female, their mean age was 57 years, 95% were White, their mean estimated 24-hour urine sodium excretion was 3.01 g/day, and 10,839 (5%) had a diagnosis of AD. The researchers observed that on multivariable logistic regression, a 1-g increase in estimated 24-hour urine sodium excretion was associated with increased odds of AD (adjusted odds ratio [AOR], 1.11; 95% CI, 1.07-1.14), increased odds of active AD (AOR, 1.16; 95% CI, 1.05-1.28), and increased odds of increasing severity of AD (AOR, 1.11; 95% CI, 1.07-1.15).
Validating Results With US Data
To validate the findings, the researchers evaluated a cohort of 13,014 participants from the US-based National Health and Nutrition Examination Survey (NHANES), using pooled data from the 1999-2000, 2001-2002, and 2003-2004 samples. Of the 13,014 participants, 796 reported current AD, and 1493 reported AD in the past year. The mean dietary sodium intake of overall NHANES participants estimated with 24-hour dietary recall questionnaires was 3.45 g, with a mean of 3.47 g for those with current AD and a mean of 3.44 g for those without AD.
The researchers observed that a 1-g/day higher dietary sodium intake was associated with a higher risk for current AD (AOR, 1.22; 95%CI, 1.01-1.47) and a somewhat higher risk for AD in the past year (AOR, 1.14; 95% CI, 0.97-1.35).
“Future work should examine whether variation of sodium intake over time might trigger AD flares and whether it helps to explain heterogeneity in response to new immunomodulatory treatments for AD,” the authors wrote. “Reduced sodium intake was recommended as a treatment for AD more than a century ago, but there have yet to be studies examining the association of dietary sodium reduction with skin sodium concentration or AD severity,” they added. Noting that sodium reduction “has been shown to be a cost-effective intervention for hypertension and other cardiovascular disease outcomes,” they said that their data “support experimental studies of this approach in AD.”
They acknowledged certain limitations of the study, including the fact that a single spot urine sample was used in the UK Biobank cohort, “which only captures dietary intake of the last 24 hours and is not the best measure of usual or long-term intake of sodium.” They also noted that the findings may not be generalizable to other populations and that AD was based on self-report in the NHANES validation cohort.
Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the results, said the study by Dr. Abuabara and colleagues “gives us another reason to avoid salt, showing that 1 g/day of higher salt intake increases the risk of AD in an adult population and more severe AD.”
He added that, “Now, can you say that reducing salt intake will have a therapeutic effect or clinically relevant impact? No. [That is] certainly worth exploring but at a minimum, gives some more credibility to keeping it bland.”
The study was supported by a grant from the Medical Student in Aging Research Program, the National Institute on Aging, and the National Eczema Association. Dr. Abuabara reported receiving research funding for her institution from Pfizer and Cosmetique Internacional/La Roche-Posay and consulting fees from Target RWE, Sanofi, Nektar, and Amgen. No other disclosures were reported. Dr. Friedman had no relevant disclosures.
A version of this article appeared on Medscape.com.
In a study of adults, an increase of 1 g in estimated 24-hour urinary sodium excretion was associated with 11% higher odds of an atopic dermatitis (AD) diagnosis, 16% higher odds of having active AD, and 11% higher odds of increased severity of AD.
Those are key findings from a cross-sectional analysis of data from the United Kingdom.
“Excessive dietary sodium, common in fast food, may be associated with AD,” corresponding author Katrina Abuabara, MD, MA, MSCE, and colleagues wrote in the study, which was published online in JAMA Dermatology. They referred to recent research using sodium MRI, which showed that “the majority of the body’s exchangeable sodium is stored in the skin and that skin sodium is associated with autoimmune and chronic inflammatory conditions, including AD.” And in another study published in 2019, lesional skin sodium was 30-fold greater in patients with AD than in healthy controls.
To investigate whether there is an association between higher levels of sodium consumption and AD prevalence, activity, and severity at the population level, Dr. Abuabara, of the program for clinical research in the Department of Dermatology at the University of California, San Francisco, and coauthors drew from the UK Biobank, a population-based cohort of more than 500,000 individuals aged 37-73 years at the time of recruitment by the National Health Service. The primary exposure was 24-hour urinary sodium excretion, which was calculated by using the INTERSALT equation, a sex-specific estimation that incorporates body mass index; age; and urine concentrations of potassium, sodium, and creatinine. The primary study outcome was AD or active AD based on diagnostic and prescription codes from linked electronic medical records. The researchers used multivariable logistic regression models adjusted for age, sex, race and ethnicity, Townsend deprivation index, and education to measure the association.
Of the 215,832 Biobank participants included in the analysis, 54% were female, their mean age was 57 years, 95% were White, their mean estimated 24-hour urine sodium excretion was 3.01 g/day, and 10,839 (5%) had a diagnosis of AD. The researchers observed that on multivariable logistic regression, a 1-g increase in estimated 24-hour urine sodium excretion was associated with increased odds of AD (adjusted odds ratio [AOR], 1.11; 95% CI, 1.07-1.14), increased odds of active AD (AOR, 1.16; 95% CI, 1.05-1.28), and increased odds of increasing severity of AD (AOR, 1.11; 95% CI, 1.07-1.15).
Validating Results With US Data
To validate the findings, the researchers evaluated a cohort of 13,014 participants from the US-based National Health and Nutrition Examination Survey (NHANES), using pooled data from the 1999-2000, 2001-2002, and 2003-2004 samples. Of the 13,014 participants, 796 reported current AD, and 1493 reported AD in the past year. The mean dietary sodium intake of overall NHANES participants estimated with 24-hour dietary recall questionnaires was 3.45 g, with a mean of 3.47 g for those with current AD and a mean of 3.44 g for those without AD.
The researchers observed that a 1-g/day higher dietary sodium intake was associated with a higher risk for current AD (AOR, 1.22; 95%CI, 1.01-1.47) and a somewhat higher risk for AD in the past year (AOR, 1.14; 95% CI, 0.97-1.35).
“Future work should examine whether variation of sodium intake over time might trigger AD flares and whether it helps to explain heterogeneity in response to new immunomodulatory treatments for AD,” the authors wrote. “Reduced sodium intake was recommended as a treatment for AD more than a century ago, but there have yet to be studies examining the association of dietary sodium reduction with skin sodium concentration or AD severity,” they added. Noting that sodium reduction “has been shown to be a cost-effective intervention for hypertension and other cardiovascular disease outcomes,” they said that their data “support experimental studies of this approach in AD.”
They acknowledged certain limitations of the study, including the fact that a single spot urine sample was used in the UK Biobank cohort, “which only captures dietary intake of the last 24 hours and is not the best measure of usual or long-term intake of sodium.” They also noted that the findings may not be generalizable to other populations and that AD was based on self-report in the NHANES validation cohort.
Adam Friedman, MD, professor and chair of dermatology at George Washington University, Washington, who was asked to comment on the results, said the study by Dr. Abuabara and colleagues “gives us another reason to avoid salt, showing that 1 g/day of higher salt intake increases the risk of AD in an adult population and more severe AD.”
He added that, “Now, can you say that reducing salt intake will have a therapeutic effect or clinically relevant impact? No. [That is] certainly worth exploring but at a minimum, gives some more credibility to keeping it bland.”
The study was supported by a grant from the Medical Student in Aging Research Program, the National Institute on Aging, and the National Eczema Association. Dr. Abuabara reported receiving research funding for her institution from Pfizer and Cosmetique Internacional/La Roche-Posay and consulting fees from Target RWE, Sanofi, Nektar, and Amgen. No other disclosures were reported. Dr. Friedman had no relevant disclosures.
A version of this article appeared on Medscape.com.
Losing Weight, Decreasing Alcohol, and Improving Sex Life?
Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail.
When I met him in December 2023, he had hit rock bottom and was willing to try anything.
At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone.
Richard shared some feedback after his first 2 weeks:
The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.
And after 6 weeks:
Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.
And finally, after 8 weeks:
Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you.
Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine.
Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors.
Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone.
At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity.
*Patient’s name has been changed.
Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail.
When I met him in December 2023, he had hit rock bottom and was willing to try anything.
At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone.
Richard shared some feedback after his first 2 weeks:
The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.
And after 6 weeks:
Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.
And finally, after 8 weeks:
Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you.
Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine.
Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors.
Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone.
At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity.
*Patient’s name has been changed.
Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Richard* was a master-of-the-universe type. He went to Wharton, ran a large hedge fund, and lived in Greenwich, Connecticut. His three children attended Ivy League schools. He played golf on the weekends and ate three healthy meals per day. There was just one issue: He had gained 90 pounds since the 1990s from consuming six to seven alcoholic beverages per day. He already had one DUI under his belt, and his marriage was on shaky ground. He had tried to address his alcohol abuse disorder on multiple occasions: He went to a yearlong class on alcoholism, saw a psychologist for cognitive-behavioral therapy, and joined Alcoholics Anonymous, all to no avail.
When I met him in December 2023, he had hit rock bottom and was willing to try anything.
At our first visit, I prescribed him weekly tirzepatide (Zepbound) off label, along with a small dose of naltrexone.
Richard shared some feedback after his first 2 weeks:
The naltrexone works great and is strong ... small dose for me effective ... I haven’t wanted to drink and when I do I can’t finish a glass over 2 hours … went from 25 drinks a week to about 4 … don’t notice other side effects … sleeping better too.
And after 6 weeks:
Some more feedback … on week 6-7 and all going well ... drinking very little alcohol and still on half tab of naltrexone ... that works well and have no side effects ... the Zepbound works well too. I do get hungry a few days after the shot but still don’t crave sugar or bad snacks … weight down 21 pounds since started … 292 to 271.
And finally, after 8 weeks:
Looking at my last text to you I see the progress … been incredible ... now down 35 pounds and at 257 … continue to feel excellent with plenty of energy … want to exercise more ... and no temptation to eat or drink unhealthy stuff ... I’m very happy this has surpassed my expectations on how fast it’s worked and I don’t feel any side effects. Marriage has never been better … all thanks to you.
Tirzepatide contains two hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), that are naturally produced by our bodies after meals. Scientists recently learned that the GLP-1 system contributes to the feedback loop of addictive behaviors. Increasing synthetic GLP-1, through medications like tirzepatide, appears to minimize addictive behaviors by limiting their ability to upregulate the brain’s production of dopamine.
Dopamine is a neurotransmitter produced in the brain’s reward center, which regulates how people experience pleasure and control impulses. Dopamine reinforces the pleasure experienced by certain behaviors like drinking, smoking, and eating sweets. These new medications reduce the amount of dopamine released after these activities and thereby lower the motivation to repeat these behaviors.
Contrary to some reports in the news, the vast majority of my male patients using these medications for alcohol abuse disorder experience concurrent increases in testosterone, for two reasons: (1) testosterone increases as body mass index decreases and (2) chronic alcohol use can damage the cells in the testicles that produce testosterone and also decrease the brain’s ability to stimulate the testicles to produce testosterone.
At his most recent checkup last month, Richard’s testosterone had risen from borderline to robust levels, his libido and sleep had improved, and he reported never having felt so healthy or confident. Fingers crossed that the US Food and Drug Administration won’t wait too long before approving this class of medications for more than just diabetes, heart disease, and obesity.
*Patient’s name has been changed.
Dr. Messer is clinical assistant professor, Icahn School of Medicine at Mount Sinai, New York, and associate professor, Zucker School of Medicine at Hofstra University, Hempstead, New York. She has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Study Finds Mace Risk Remains High in Patients with Psoriasis, Dyslipidemia
Over a period of 5 years, the, even after adjusting for covariates, results from a large retrospective study showed.
“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.
Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.
To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.
Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).
“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.
She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.
Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”
The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.
A version of this article appeared on Medscape.com .
Over a period of 5 years, the, even after adjusting for covariates, results from a large retrospective study showed.
“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.
Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.
To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.
Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).
“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.
She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.
Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”
The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.
A version of this article appeared on Medscape.com .
Over a period of 5 years, the, even after adjusting for covariates, results from a large retrospective study showed.
“It is well-established that psoriasis is an independent risk factor for the development of MACE, with cardiometabolic risk factors being more prevalent and incident among patients with psoriasis,” the study’s first author Ana Ormaza Vera, MD, a dermatology research fellow at Eastern Virginia Medical School, Norfolk, said in an interview after the annual meeting of the Society for Investigational Dermatology, where the study was presented during a late-breaking abstract session.
Current guidelines from the joint American Academy of Dermatology/National Psoriasis Foundation and the American Academy of Cardiology/American Heart Association Task Force recommend statins, a lipid-lowering and anti-inflammatory therapy, “for patients with psoriasis who have additional risk-enhancing factors, similar to recommendations made for the general population without psoriasis,” she noted. But how the incidence of MACE differs between patients with and without psoriasis while on statin therapy “has not been explored in real-world settings,” she added.
To address this question, the researchers used real-world data from the TriNetX health research network to identify individuals aged 18-90 years with a diagnosis of both psoriasis and lipid disorders who were undergoing treatment with statins. Those with a prior history of MACE were excluded from the analysis. Patients with lipid disorders on statin therapy, but without psoriatic disease, were matched 1:1 by age, sex, race, ethnicity, common risk factors for MACE, and medications shown to reduce MACE risk. The researchers then assessed the cohorts 5 years following their first statin prescription and used the TriNetX analytics tool to calculate the odds ratio (OR) with 95% CI to evaluate the likelihood of MACE in the presence of statin therapy.
Dr. Ormaza Vera and colleagues identified 20,660 patients with psoriasis and 2,768,429 patients without psoriasis who met the criteria for analysis. After propensity score matching, each cohort included 20,660 patients with a mean age of 60 years. During the 5-year observation period, 2725 patients in the psoriasis cohort experienced MACE compared with 2203 patients in the non-psoriasis cohort (OR, 1.40; 95% CI, 1.317-1.488).
“This was an unexpected outcome that challenges the current understanding and highlights the need for further research into tailored treatments for cardiovascular risk in psoriasis patients,” Dr. Ormaza Vera told this news organization.
She acknowledged certain limitations of the study, including its retrospective design, the inherent limitations of an observational study, and the use of electronic medical record data.
Lawrence J. Green, MD, clinical professor of dermatology, George Washington University, Washington, who was asked to comment on the study results, said that the findings imply that there is more than statin use alone to protect someone with psoriasis from having an increased risk for MACE. “This is not really surprising because statin use alone is only part of a prevention strategy in someone with psoriasis who usually has multiple comorbidities,” Dr. Green said. “On the other hand, the study only went out for 5 years and cardiovascular disease is a long accumulating process, so it could also be too early to demonstrate MACE prevention.”
The study was funded by a grant from the American Skin Association. Dr. Ormaza Vera and her coauthors reported having no relevant disclosures. Dr. Green disclosed that he is a speaker, consultant, or investigator for many pharmaceutical companies.
A version of this article appeared on Medscape.com .
FROM SID 2024
Dupilumab Evaluated as Treatment for Pediatric Alopecia Areata
showed.
“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”
When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”
“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
Case Series of 20 Pediatric Patients
As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.
At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.
In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”
She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.
Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.
Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.
A version of this article appeared on Medscape.com.
showed.
“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”
When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”
“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
Case Series of 20 Pediatric Patients
As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.
At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.
In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”
She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.
Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.
Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.
A version of this article appeared on Medscape.com.
showed.
“We might be opening a new avenue for a safe, long-term treatment for our children with AA,” the study’s lead investigator, Emma Guttman-Yassky, MD, PhD, professor and chair of dermatology at the Icahn School of Medicine at Mount Sinai, New York City, said in an interview during the annual meeting of the Society for Investigative Dermatology (SID), where the results were presented during a poster session. “I think AA is likely joining the atopic march, which may allow us to adapt some treatments from the atopy world to AA.”
When the original phase 2 and phase 3 trials of dupilumab for patients with moderate to severe AD were being conducted, Dr. Guttman-Yassky, one of the investigators, recalled observing that some patients who also had patch alopecia experienced hair regrowth. “I was scratching my head because, at the time, AA was considered to be only a Th1-driven disease,” she said. “I asked myself, ‘How can this happen?’ I looked in the literature and found many publications linking atopy in general to alopecia areata. The largest of the dermatologic publications showed that eczema and atopy in general are the highest comorbidities in alopecia areata.”
“This and other findings such as IL [interleukin]-13 genetic linkage with AA and high IgE in patients with AA link AA with Th2 immune skewing, particularly in the setting of atopy,” she continued. In addition, she said, in a large biomarker study involving the scalp and blood of patients with AA, “we found increases in Th2 biomarkers that were associated with alopecia severity.”
Case Series of 20 Pediatric Patients
As part of a case series of children with both AD and AA, Dr. Guttman-Yassky and colleagues evaluated hair regrowth using the Severity of Alopecia Tool (SALT) in 20 pediatric patients (mean age, 10.8 years) who were being treated at Mount Sinai. They collected patient demographics, atopic history, immunoglobulin E (IgE) levels, and SALT scores at follow-up visits every 12-16 weeks for more than 72 weeks and performed Spearman correlations between clinical scores, demographics, and IgE levels.
At baseline, the mean SALT score was 54.4, the mean IgE level was 1567.7 IU/mL, and 75% of patients also had a family history of atopy. The mean follow-up was 67.6 weeks. The researchers observed a significant reduction in SALT scores at week 48 compared with baseline (a mean score of 20.4; P < .01) and continued improvement up to at least 72 weeks (P < .01 vs baseline). They also noted that patients who achieved a treatment response at week 24 had baseline IgE levels > 200 IU/mL.
In other findings, baseline IgE positively correlated with improvement in SALT scores at week 36 (P < .05), while baseline SALT scores positively correlated with disease duration (P < .01) and negatively correlated with improvement in SALT scores at weeks 24, 36, and 48 (P < .005). “The robustness of the response surprised me,” Dr. Guttman-Yassky said in the interview. “Dupilumab for AA takes time to work, but once it kicks in, it kicks in. It takes anywhere from 6 to 12 months to see hair regrowth.”
She acknowledged certain limitations of the analysis, including its small sample size and the fact that it was not a standardized trial. “But, based on our data and the adult data, we are very encouraged about the potential of using dupilumab for children with AA,” she said.
Mount Sinai recently announced that the National Institutes of Health awarded a $6.6 million, 5-year grant to Dr. Guttman-Yassky to further investigate dupilumab as a treatment for children with AA. She will lead a multicenter controlled trial of 76 children with alopecia affecting at least 30% of the scalp, who will be randomized 2:1 (dupilumab:placebo) for 48 weeks, followed by 48 weeks of open-label dupilumab for all participants, with 16 weeks of follow-up, for a total of 112 weeks. Participating sites include Mount Sinai, Yale University, Northwestern University, and the University of California, Irvine.
Dr. Guttman-Yassky disclosed that she is a consultant to many pharmaceutical companies, including dupilumab manufacturers Sanofi and Regeneron.
A version of this article appeared on Medscape.com.
FROM SID 2024
Analysis Finds Minority of Chronic Wounds Treated by Dermatologists
. However, fewer than 8% of chronic wounds were managed by dermatologists during this time.
Those are among key findings from an analysis of National Ambulatory Medical Care Survey (NAMCS) data between 2011 and 2019 presented as a late-breaking abstract at the annual meeting of the Society for Investigative Dermatology. “Cutaneous wounds were estimated to account for 28.1 to 96.1 billion dollars in US health care costs in 2014,” one of the study authors, Rithi Chandy, MD, MS, a research fellow at the Center for Dermatology Research at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in an interview following the meeting. “By examining national trends in patient visits and treatment, we may be able to better inform health care utilization for cutaneous wounds.”
Dr. Chandy and colleagues analyzed de-identified patient data from the 2011 to 2019 NAMCS for acute and chronic wound diagnoses, medications prescribed, and physician specialty categories. During the time studied, 5.76 billion patient visits were made, including 45.1 million visits for cutaneous wounds. Of these, the most common diagnoses were open wounds of the thumb without nail damage (7.96%), the lower leg (5.75%), nonpressure chronic ulcers of other parts of the foot (5.08%), and open wounds of the ear (5%).
Among all visits for cutaneous wounds, about one third were chronic cutaneous wounds, with the following descriptions: “Nonpressure chronic ulcer of other part of foot” (17.8%); “nonpressure chronic ulcer of skin, not elsewhere classified” (9.38%); and “ulcer of lower limbs, excluding decubitus, unspecified” (8.72%). “The frequency of patient visits per year during the study period remained stable for both acute and chronic wounds,” Dr. Chandy said. The number of visits for which antimicrobials were used was stable over time for both acute and chronic cutaneous wounds, with the exception of increased use of antivirals for chronic cutaneous wounds, he added.
Specifically, prescriptions were issued in 156 million visits over the time studied, most commonly cephalexin (4.22%), topical silver sulfadiazine (1.59%), topical mupirocin (1.12%), and miscellaneous antibiotics (1.18%).
“Our data shows that topical mupirocin is the most commonly used topical antimicrobial for cutaneous wounds,” Dr. Chandy said. “However, there are reports of emerging bacterial resistance to mupirocin. Our data can inform ongoing efforts to promote antimicrobial stewardship and drug development to provide alternative options that are less likely to induce antimicrobial resistance.”
In findings limited to specialty-specific NAMCS data available from 2011 and from 2013 to 2016, dermatologists managed 3.85% of overall cutaneous wounds, 2.35% of acute wounds, and 7.39% of chronic wounds. By contrast, Dr. Chandy said, 21.1% of chronic wounds were managed by general/family practice physicians, 20.7% by internists, 6.84% by general surgeons, and 5.65% by orthopedic surgeons.
“As dermatologists are experts in the structure and function of the skin and are trained to manage cutaneous disorders including wound healing, we [believe that] dermatologists are equipped with the skill set” for managing wounds, especially for chronic ulcers, he said. The decline in dermatologists who specialize in wound care, he added, “underscores the need for structured dermatology fellowship programs to prepare next-generation dermatologists to address this shortage and ensure dermatology leadership in cutaneous wound healing.”
Dr. Chandy acknowledged certain limitations of the study, including the potential for misclassification of diagnoses or medications prescribed and the fact that the NAMCS database is unable to provide insight into individual patient experiences such as continual cutaneous wound management for the same patient over time.
In the opinion of Shari R. Lipner, MD, PhD, associate professor of clinical dermatology and director of the Nail Division at Weill Cornell Medicine, New York, who was asked to comment on the study, the most interesting finding was that dermatologists cared for a small minority of patients with cutaneous wounds. “It would be interesting to know whether this is due to dermatologist shortages or knowledge gaps on the part of primary care physicians or patients that dermatologists are trained to care for wounds,” Dr. Lipner told this news organization. Other unanswered questions, she noted, “are patient demographics, geographic locations, and comorbidities.”
One of the study authors, Steven R. Feldman, MD, PhD, professor of dermatology at Wake Forest University, disclosed that he has received research, speaking and/or consulting support from numerous pharmaceutical companies. No other authors reported having relevant disclosures. Dr. Lipner reported having no disclosures.
A version of this article appeared on Medscape.com .
. However, fewer than 8% of chronic wounds were managed by dermatologists during this time.
Those are among key findings from an analysis of National Ambulatory Medical Care Survey (NAMCS) data between 2011 and 2019 presented as a late-breaking abstract at the annual meeting of the Society for Investigative Dermatology. “Cutaneous wounds were estimated to account for 28.1 to 96.1 billion dollars in US health care costs in 2014,” one of the study authors, Rithi Chandy, MD, MS, a research fellow at the Center for Dermatology Research at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in an interview following the meeting. “By examining national trends in patient visits and treatment, we may be able to better inform health care utilization for cutaneous wounds.”
Dr. Chandy and colleagues analyzed de-identified patient data from the 2011 to 2019 NAMCS for acute and chronic wound diagnoses, medications prescribed, and physician specialty categories. During the time studied, 5.76 billion patient visits were made, including 45.1 million visits for cutaneous wounds. Of these, the most common diagnoses were open wounds of the thumb without nail damage (7.96%), the lower leg (5.75%), nonpressure chronic ulcers of other parts of the foot (5.08%), and open wounds of the ear (5%).
Among all visits for cutaneous wounds, about one third were chronic cutaneous wounds, with the following descriptions: “Nonpressure chronic ulcer of other part of foot” (17.8%); “nonpressure chronic ulcer of skin, not elsewhere classified” (9.38%); and “ulcer of lower limbs, excluding decubitus, unspecified” (8.72%). “The frequency of patient visits per year during the study period remained stable for both acute and chronic wounds,” Dr. Chandy said. The number of visits for which antimicrobials were used was stable over time for both acute and chronic cutaneous wounds, with the exception of increased use of antivirals for chronic cutaneous wounds, he added.
Specifically, prescriptions were issued in 156 million visits over the time studied, most commonly cephalexin (4.22%), topical silver sulfadiazine (1.59%), topical mupirocin (1.12%), and miscellaneous antibiotics (1.18%).
“Our data shows that topical mupirocin is the most commonly used topical antimicrobial for cutaneous wounds,” Dr. Chandy said. “However, there are reports of emerging bacterial resistance to mupirocin. Our data can inform ongoing efforts to promote antimicrobial stewardship and drug development to provide alternative options that are less likely to induce antimicrobial resistance.”
In findings limited to specialty-specific NAMCS data available from 2011 and from 2013 to 2016, dermatologists managed 3.85% of overall cutaneous wounds, 2.35% of acute wounds, and 7.39% of chronic wounds. By contrast, Dr. Chandy said, 21.1% of chronic wounds were managed by general/family practice physicians, 20.7% by internists, 6.84% by general surgeons, and 5.65% by orthopedic surgeons.
“As dermatologists are experts in the structure and function of the skin and are trained to manage cutaneous disorders including wound healing, we [believe that] dermatologists are equipped with the skill set” for managing wounds, especially for chronic ulcers, he said. The decline in dermatologists who specialize in wound care, he added, “underscores the need for structured dermatology fellowship programs to prepare next-generation dermatologists to address this shortage and ensure dermatology leadership in cutaneous wound healing.”
Dr. Chandy acknowledged certain limitations of the study, including the potential for misclassification of diagnoses or medications prescribed and the fact that the NAMCS database is unable to provide insight into individual patient experiences such as continual cutaneous wound management for the same patient over time.
In the opinion of Shari R. Lipner, MD, PhD, associate professor of clinical dermatology and director of the Nail Division at Weill Cornell Medicine, New York, who was asked to comment on the study, the most interesting finding was that dermatologists cared for a small minority of patients with cutaneous wounds. “It would be interesting to know whether this is due to dermatologist shortages or knowledge gaps on the part of primary care physicians or patients that dermatologists are trained to care for wounds,” Dr. Lipner told this news organization. Other unanswered questions, she noted, “are patient demographics, geographic locations, and comorbidities.”
One of the study authors, Steven R. Feldman, MD, PhD, professor of dermatology at Wake Forest University, disclosed that he has received research, speaking and/or consulting support from numerous pharmaceutical companies. No other authors reported having relevant disclosures. Dr. Lipner reported having no disclosures.
A version of this article appeared on Medscape.com .
. However, fewer than 8% of chronic wounds were managed by dermatologists during this time.
Those are among key findings from an analysis of National Ambulatory Medical Care Survey (NAMCS) data between 2011 and 2019 presented as a late-breaking abstract at the annual meeting of the Society for Investigative Dermatology. “Cutaneous wounds were estimated to account for 28.1 to 96.1 billion dollars in US health care costs in 2014,” one of the study authors, Rithi Chandy, MD, MS, a research fellow at the Center for Dermatology Research at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in an interview following the meeting. “By examining national trends in patient visits and treatment, we may be able to better inform health care utilization for cutaneous wounds.”
Dr. Chandy and colleagues analyzed de-identified patient data from the 2011 to 2019 NAMCS for acute and chronic wound diagnoses, medications prescribed, and physician specialty categories. During the time studied, 5.76 billion patient visits were made, including 45.1 million visits for cutaneous wounds. Of these, the most common diagnoses were open wounds of the thumb without nail damage (7.96%), the lower leg (5.75%), nonpressure chronic ulcers of other parts of the foot (5.08%), and open wounds of the ear (5%).
Among all visits for cutaneous wounds, about one third were chronic cutaneous wounds, with the following descriptions: “Nonpressure chronic ulcer of other part of foot” (17.8%); “nonpressure chronic ulcer of skin, not elsewhere classified” (9.38%); and “ulcer of lower limbs, excluding decubitus, unspecified” (8.72%). “The frequency of patient visits per year during the study period remained stable for both acute and chronic wounds,” Dr. Chandy said. The number of visits for which antimicrobials were used was stable over time for both acute and chronic cutaneous wounds, with the exception of increased use of antivirals for chronic cutaneous wounds, he added.
Specifically, prescriptions were issued in 156 million visits over the time studied, most commonly cephalexin (4.22%), topical silver sulfadiazine (1.59%), topical mupirocin (1.12%), and miscellaneous antibiotics (1.18%).
“Our data shows that topical mupirocin is the most commonly used topical antimicrobial for cutaneous wounds,” Dr. Chandy said. “However, there are reports of emerging bacterial resistance to mupirocin. Our data can inform ongoing efforts to promote antimicrobial stewardship and drug development to provide alternative options that are less likely to induce antimicrobial resistance.”
In findings limited to specialty-specific NAMCS data available from 2011 and from 2013 to 2016, dermatologists managed 3.85% of overall cutaneous wounds, 2.35% of acute wounds, and 7.39% of chronic wounds. By contrast, Dr. Chandy said, 21.1% of chronic wounds were managed by general/family practice physicians, 20.7% by internists, 6.84% by general surgeons, and 5.65% by orthopedic surgeons.
“As dermatologists are experts in the structure and function of the skin and are trained to manage cutaneous disorders including wound healing, we [believe that] dermatologists are equipped with the skill set” for managing wounds, especially for chronic ulcers, he said. The decline in dermatologists who specialize in wound care, he added, “underscores the need for structured dermatology fellowship programs to prepare next-generation dermatologists to address this shortage and ensure dermatology leadership in cutaneous wound healing.”
Dr. Chandy acknowledged certain limitations of the study, including the potential for misclassification of diagnoses or medications prescribed and the fact that the NAMCS database is unable to provide insight into individual patient experiences such as continual cutaneous wound management for the same patient over time.
In the opinion of Shari R. Lipner, MD, PhD, associate professor of clinical dermatology and director of the Nail Division at Weill Cornell Medicine, New York, who was asked to comment on the study, the most interesting finding was that dermatologists cared for a small minority of patients with cutaneous wounds. “It would be interesting to know whether this is due to dermatologist shortages or knowledge gaps on the part of primary care physicians or patients that dermatologists are trained to care for wounds,” Dr. Lipner told this news organization. Other unanswered questions, she noted, “are patient demographics, geographic locations, and comorbidities.”
One of the study authors, Steven R. Feldman, MD, PhD, professor of dermatology at Wake Forest University, disclosed that he has received research, speaking and/or consulting support from numerous pharmaceutical companies. No other authors reported having relevant disclosures. Dr. Lipner reported having no disclosures.
A version of this article appeared on Medscape.com .
FROM SID 2024
Prenatal Antibiotics May Increase Seborrheic Dermatitis Risk in Babies
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
, but this association was not as strong for childhood-onset SD.
The findings come from a large analysis of data from the United Kingdom that was presented during a late-breaking abstract session at the annual meeting of the Society for Investigative Dermatology.
SD is a common skin disease “that shares similarities with atopic dermatitis or atopic eczema as both are prevalent inflammatory skin diseases that can present with a chronic relapsing, remitting course,” the study’s corresponding author Zelma C. Chiesa Fuxench, MD, MSCE, assistant professor of dermatology at the University of Pennsylvania, Philadelphia, said in an interview. “Like atopic dermatitis, the pathophysiology of seborrheic dermatitis is thought to be complex and involves an interplay between genetics, immune dysregulation, and alterations in lipid composition and the skin microbiome, among others.”
In a previous study, she and colleagues showed that exposure to antibiotics both in utero and during the first 90 days of life increases the risk for atopic dermatitis (AD) in children, with risk being highest with exposure to penicillin even among children whose mothers did not have a history of AD.
For the current study, the researchers drew from a large electronic medical records database in the United Kingdom to perform a prospective cohort analysis of mother-child pairs that used proportional hazards models to examine the association between maternal in utero antibiotic exposure and SD in the child. The population included 1,023,140 children with linked maternal data who were followed for a mean of 10.2 years, which amounts to more than 10-million-person years of data. At baseline, the mean age of mothers was 28 years, 3% had SD, 14% had AD, and 51% of the children were male.
In unadjusted analyses, mothers with SD were more likely to receive an antibiotic during pregnancy than were those who did not have SD (odds ratio [OR], 1.42; 95% CI, 1.39-1.46). In addition, maternal in utero exposure to any antibiotic was associated with an increased risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) but less for childhood-onset SD (OR, 1.26; 95% CI, 1.20-1.32). “This effect changed little after adjustment and was still observed if mothers with SD and their babies were excluded,” the authors wrote in their poster abstract.
Any penicillin exposure during pregnancy increased the likelihood of a child having SD (OR, 1.54; 95% CI, 1.50-1.59), with the greater risk for infantile SD (OR, 1.70; 95% CI, 1.65-1.76) than for childhood-onset SD (OR, 1.25; 95% CI, 1.18-1.32). “The trimester of the in utero penicillin exposure did not seem to affect the association with SD,” the authors wrote. The risk was also increased with cephalosporin exposure but was less for sulfonamides and not for childhood-onset SD.
“We observed that antibiotic exposure in utero was primarily associated with an increased risk of infantile SD regardless of the mother’s history of SD, but this association was not as strong for childhood-onset SD,” Dr. Chiesa Fuxench said. “This would suggest that in utero exposure to antibiotics, particularly penicillin, may have its greatest effect on the colonization of skin microbiota in the newborn period leading to the development of infantile SD. Aside from seeking to improve our understanding of the pathophysiology of SD, our findings also suggest that infantile SD and childhood-onset SD may be separate entities with different risk factors, a hypothesis that needs to be further studied.”
She acknowledged certain limitations of the analysis, including the potential for unrecorded diagnoses of SD or misclassified cases in the database. For example, AD and psoriasis “may appear clinically like SD,” she said, although they performed sensitivity analysis excluding patients with these diagnoses and found similar results. In addition, there is the possibility that not all antibiotic exposures were captured in this database, and data on antibiotic exposure may be missing, she added.
Dr. Chiesa Fuxench disclosed that she received research grants from Lilly, LEO Pharma, Regeneron, Sanofi, Tioga, Vanda, and Incyte for work related to AD and from Menlo Therapeutics and Galderma for work related to prurigo nodularis. She has served as a consultant for the Asthma and Allergy Foundation of America, National Eczema Association, AbbVie, Incyte Corporation, and Pfizer and received honoraria for CME work in AD sponsored by education grants from Regeneron/Sanofi and Pfizer and from Beiersdorf for work related to skin cancer and sun protection.
A version of this article appeared on Medscape.com .
FROM SID 2024
Frontal Fibrosing Alopecia: Study Finds Oral Contraceptive Use Modulates Risk In Women with Genetic Variant
TOPLINE:
Investigators found that .
METHODOLOGY:
- OC use has been considered a possible factor behind the increased incidence of FFA because it was first documented in 1994, and a recent genome-wide association study of FFA identified a signal for an association with a variant in CYP1B1.
- The same researchers conducted a gene-environment interaction study with a case-control design involving 489 White female patients (mean age, 65.8 years) with FFA and 34,254 controls, matched for age and genetic ancestry.
- Data were collected from July 2015 to September 2017 and analyzed from October 2022 to December 2023.
- The study aimed to investigate the modulatory effect of OC use on the CYP1B1 variant’s impact on FFA risk, using logistic regression models for analysis.
TAKEAWAY:
- The use of OCs was associated with a 1.9 times greater risk for FFA in individuals with the specific CYP1B1 genetic variant, but there was no association among those with no history of OC use.
- The study suggests a significant gene-environment interaction, indicating that OC use may influence FFA risk in genetically predisposed individuals.
IN PRACTICE:
“This gene-environment interaction analysis suggests that the protective effect of the CYPIB1 missense variant on FFA risk might be mediated by exposure” to OCs, the authors wrote. The study, they added, “underscores the importance of considering genetic predispositions and environmental factors, such as oral contraceptive use, in understanding and managing frontal fibrosing alopecia.”
SOURCE:
Tuntas Rayinda, MD, MSc, PhD, of St. John’s Institute of Dermatology, King’s College London, led the study, which was published online May 29, 2024, in JAMA Dermatology.
LIMITATIONS:
The study’s reliance on self-reported OC use may have introduced recall and differences in ascertainment of OC use between patient and control groups and could have affected the study’s findings. The study also did not collect information on the type of OC used, which could have influenced the observed interaction.
DISCLOSURES:
The study was supported by the British Skin Foundation Young Investigator Award. One investigator reported being a subinvestigator on an alopecia areata study funded by Pfizer. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
TOPLINE:
Investigators found that .
METHODOLOGY:
- OC use has been considered a possible factor behind the increased incidence of FFA because it was first documented in 1994, and a recent genome-wide association study of FFA identified a signal for an association with a variant in CYP1B1.
- The same researchers conducted a gene-environment interaction study with a case-control design involving 489 White female patients (mean age, 65.8 years) with FFA and 34,254 controls, matched for age and genetic ancestry.
- Data were collected from July 2015 to September 2017 and analyzed from October 2022 to December 2023.
- The study aimed to investigate the modulatory effect of OC use on the CYP1B1 variant’s impact on FFA risk, using logistic regression models for analysis.
TAKEAWAY:
- The use of OCs was associated with a 1.9 times greater risk for FFA in individuals with the specific CYP1B1 genetic variant, but there was no association among those with no history of OC use.
- The study suggests a significant gene-environment interaction, indicating that OC use may influence FFA risk in genetically predisposed individuals.
IN PRACTICE:
“This gene-environment interaction analysis suggests that the protective effect of the CYPIB1 missense variant on FFA risk might be mediated by exposure” to OCs, the authors wrote. The study, they added, “underscores the importance of considering genetic predispositions and environmental factors, such as oral contraceptive use, in understanding and managing frontal fibrosing alopecia.”
SOURCE:
Tuntas Rayinda, MD, MSc, PhD, of St. John’s Institute of Dermatology, King’s College London, led the study, which was published online May 29, 2024, in JAMA Dermatology.
LIMITATIONS:
The study’s reliance on self-reported OC use may have introduced recall and differences in ascertainment of OC use between patient and control groups and could have affected the study’s findings. The study also did not collect information on the type of OC used, which could have influenced the observed interaction.
DISCLOSURES:
The study was supported by the British Skin Foundation Young Investigator Award. One investigator reported being a subinvestigator on an alopecia areata study funded by Pfizer. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
TOPLINE:
Investigators found that .
METHODOLOGY:
- OC use has been considered a possible factor behind the increased incidence of FFA because it was first documented in 1994, and a recent genome-wide association study of FFA identified a signal for an association with a variant in CYP1B1.
- The same researchers conducted a gene-environment interaction study with a case-control design involving 489 White female patients (mean age, 65.8 years) with FFA and 34,254 controls, matched for age and genetic ancestry.
- Data were collected from July 2015 to September 2017 and analyzed from October 2022 to December 2023.
- The study aimed to investigate the modulatory effect of OC use on the CYP1B1 variant’s impact on FFA risk, using logistic regression models for analysis.
TAKEAWAY:
- The use of OCs was associated with a 1.9 times greater risk for FFA in individuals with the specific CYP1B1 genetic variant, but there was no association among those with no history of OC use.
- The study suggests a significant gene-environment interaction, indicating that OC use may influence FFA risk in genetically predisposed individuals.
IN PRACTICE:
“This gene-environment interaction analysis suggests that the protective effect of the CYPIB1 missense variant on FFA risk might be mediated by exposure” to OCs, the authors wrote. The study, they added, “underscores the importance of considering genetic predispositions and environmental factors, such as oral contraceptive use, in understanding and managing frontal fibrosing alopecia.”
SOURCE:
Tuntas Rayinda, MD, MSc, PhD, of St. John’s Institute of Dermatology, King’s College London, led the study, which was published online May 29, 2024, in JAMA Dermatology.
LIMITATIONS:
The study’s reliance on self-reported OC use may have introduced recall and differences in ascertainment of OC use between patient and control groups and could have affected the study’s findings. The study also did not collect information on the type of OC used, which could have influenced the observed interaction.
DISCLOSURES:
The study was supported by the British Skin Foundation Young Investigator Award. One investigator reported being a subinvestigator on an alopecia areata study funded by Pfizer. No other disclosures were reported.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
A version of this article appeared on Medscape.com.
Plantar Hyperpigmentation
Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyper-pigmentation. We use the terms ethnic and racial interchangeably.
It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.1
There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.
Epidemiology
In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.2
The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.3 However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.1 In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.4 Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.4 Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.5-9
Key Clinical Features in Individuals With Darker Skin Tones
Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.7 The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.12 Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.2 Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.
It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.13 This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.
Worth noting
In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.14 Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.
Health disparity highlight
The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons15,16:
• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.17
Multi-institutional registries could improve understanding of acral melanoma in Black patients.4 More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.
1. Huang K, Fan J, Misra S. Acral lentiginous melanoma: incidence and survival in the United States, 2006-2015: an analysis of the SEER registry. J Surg Res. 2020;251:329-339. doi:10.1016/j.jss.2020.02.010
2. Coleman WP, Gately LE, Krementz AB, et al. Nevi, lentigines, and melanomas in blacks. Arch Dermatol. 1980;116:548-551.
3. Centers for Disease Control and Prevention. Melanoma Incidence and Mortality, United States: 2012-2016. USCS Data Brief, no. 9. Centers for Disease Control and Prevention, US Department of Health and Human Services; 2019. https://www.cdc.gov/cancer/uscs/about/data-briefs/no9-melanoma-incidence-mortality-UnitedStates-2012-2016.htm
4. Wix SN, Brown AB, Heberton M, et al. Clinical features and outcomes of black patients with melanoma. JAMA Dermatol. 2024;160:328-333. doi:10.1001/jamadermatol.2023.5789
5. Saida T, Koga H. Dermoscopic patterns of acral melanocytic nevi: their variations, changes, and significance. Arch Dermatol. 2007;143:1423-1426. doi:10.1001/archderm.143.11.1423
6. Saida T, Koga H, Uhara H. Key points in dermoscopic differentiation between early acral melanoma and acral nevus. J Dermatol. 2011;38:25-34. doi:10.1111/j.1346-8138.2010.01174.x
7. Saida T, Miyazaki A, Oguchi S. Significance of dermoscopic patterns in detecting malignant melanoma on acral volar skin: results of a multicenter study in Japan. Arch Dermatol. 2004;140:1233-1238. doi:10.1001/archderm.140.10.1233
8. Saida T, Koga H, Uhara H. Dermoscopy for acral melanocytic lesions: revision of the 3-step algorithm and refined definition of the regular and irregular fibrillar pattern. Dermatol Pract Concept. 2022;12:e2022123. doi:10.5826/dpc.1203a123
9. Heath CR, Usatine RP. Melanoma. Cutis. 2022;109:284-285. doi:10.12788/cutis.0513.
10. Dinnes J, Deeks JJ, Chuchu N, et al; Cochrane Skin Cancer Diagnostic Test Accuracy Group. Visual inspection and dermoscopy, alone or in combination, for diagnosing keratinocyte skin cancers in adults. Cochrane Database Syst Rev. 2018; 12:CD011901. doi:10.1002/14651858.CD011901.pub2
11. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked-eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676. doi:10.1111/j.1365-2133.2008.08713.x
12. Phan A, Dalle S, Marcilly MC, et al. Benign dermoscopic parallel ridge pattern variants. Arch Dermatol. 2011;147:634. doi:10.1001/archdermatol.2011.47
13. Fracaroli TS, Lavorato FG, Maceira JP, et al. Parallel ridge pattern on dermoscopy: observation in non-melanoma cases. An Bras Dermatol. 2013;88:646-648. doi:10.1590/abd1806-4841.20132058
14. Manci RN, Dauscher M, Marchetti MA, et al. Features of skin cancer in black individuals: a single-institution retrospective cohort study. Dermatol Pract Concept. 2022;12:e2022075. doi:10.5826/dpc.1202a75
15. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dematol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
16. Ingrassia JP, Stein JA, Levine A, et al. Diagnosis and management of acral pigmented lesions. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 2023;49:926-931. doi:10.1097/DSS.0000000000003891
17. Hill L, Artiga S, Damico A. Health coverage by race and ethnicity, 2010-2022. Kaiser Family Foundation. Published January 11, 2024. Accessed May 9, 2024. https://www.kff.org/racial-equity-and-health-policy/issue-brief/health-coverage-by-race-and-ethnicity
Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyper-pigmentation. We use the terms ethnic and racial interchangeably.
It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.1
There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.
Epidemiology
In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.2
The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.3 However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.1 In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.4 Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.4 Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.5-9
Key Clinical Features in Individuals With Darker Skin Tones
Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.7 The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.12 Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.2 Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.
It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.13 This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.
Worth noting
In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.14 Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.
Health disparity highlight
The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons15,16:
• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.17
Multi-institutional registries could improve understanding of acral melanoma in Black patients.4 More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.
Plantar hyperpigmentation (also known as plantar melanosis [increased melanin], volar pigmented macules, benign racial melanosis, acral pigmentation, acral ethnic melanosis, or mottled hyperpigmentation of the plantar surface) is a benign finding in many individuals and is especially prevalent in those with darker skin tones. Acral refers to manifestation on the hands and feet, volar on the palms and soles, and plantar on the soles only. Here, we focus on plantar hyper-pigmentation. We use the terms ethnic and racial interchangeably.
It is critically important to differentiate benign hyperpigmentation, which is common in patients with skin of color, from melanoma. Although rare, Black patients in the United States experience high morbidity and mortality from acral melanoma, which often is diagnosed late in the disease course.1
There are many causes of hyperpigmentation on the plantar surfaces, including benign ethnic melanosis, nevi, melanoma, infections such as syphilis and tinea nigra, conditions such as Peutz-Jeghers syndrome and Laugier-Hunziker syndrome, and postinflammatory hyperpigmentation secondary to atopic dermatitis and psoriasis. We focus on the most common causes, ethnic melanosis and nevi, as well as melanoma, which is the deadliest cause.
Epidemiology
In a 1980 study (N=251), Black Americans had a high incidence of plantar hyperpigmentation, with 52% of affected patients having dark brown skin and 31% having light brown skin.2
The epidemiology of melanoma varies by race/ethnicity. Melanoma in Black individuals is relatively rare, with an annual incidence of approximately 1 in 100,000 individuals.3 However, when individuals with skin of color develop melanoma, they are more likely than their White counterparts to have acral melanoma (acral lentiginous melanoma), one of the deadliest types.1 In a case series of Black patients with melanoma (N=48) from 2 tertiary care centers in Texas, 30 of 40 primary cutaneous melanomas (75%) were located on acral skin.4 Overall, 13 patients developed stage IV disease and 12 died due to disease progression. All patients who developed distant metastases or died of melanoma had acral melanoma.4 Individuals of Asian descent also have a high incidence of acral melanoma, as shown in research from Japan.5-9
Key Clinical Features in Individuals With Darker Skin Tones
Dermoscopy is an evidence-based clinical examination method for earlier diagnosis of cutaneous melanoma, including on acral skin.10,11 Benign nevi on the volar skin as well as the palms and soles tend to have one of these 3 dermoscopic patterns: parallel furrow, lattice, or irregular fibrillar. The pattern that is most predictive of volar melanoma is the parallel ridge pattern (PRP) (Figures A and B [insets]), which showed a high specificity (99.0%) and very high negative predictive value (97.7%) for malignant melanoma in a Japanese population.7 The PRP data from this study cannot be applied reliably to Black individuals, especially because benign ethnic melanosis and other benign conditions can demonstrate PRP.12 Reliance on the PRP as a diagnostic clue could result in unneccessary biopsies in as many as 50% of Black patients with benign plantar hyperpigmentation.2 Furthermore, biopsies of the plantar surface can be painful and cause pain while walking.
It has been suggested that PRP seen on dermoscopy in benign hyperpigmentation such as ethnic melanosis and nevi may preserve the acrosyringia (eccrine gland openings on the ridge), whereas PRP in melanoma may obliterate the acrosyringia.13 This observation is based on case reports only and needs further study. However, if validated, it could be a useful diagnostic clue.
Worth noting
In a retrospective cohort study of skin cancer in Black individuals (n=165) at a New York City–based cancer center from 2000 to 2020, 68% of patients were diagnosed with melanomas—80% were the acral subtype and 75% displayed a PRP. However, the surrounding uninvolved background skin, which was visible in most cases, also demonstrated a PRP.14 Because of the high morbidity and mortality rates of acral melanoma, clinicians should biopsy or immediately refer patients with concerning plantar hyperpigmentation to a dermatologist.
Health disparity highlight
The mortality rate for acral melanoma in Black patients is disproportionately high for the following reasons15,16:
• Patients and health care providers do not expect to see melanoma in Black patients (it truly is rare!), so screening and education on sun protection are limited.
• Benign ethnic melanosis makes it more difficult to distinguish between early acral melanoma and benign skin changes.
• Black patients and other US patient populations with skin of color may be less likely to have health insurance, which contributes to inequities in access to health care. As of 2022, the uninsured rates for nonelderly American Indian and Alaska Native, Hispanic, Native Hawaiian and Other Pacific Islander, Black, and White individuals were 19.1%, 18.0%, 12.7%, 10.0%, and 6.6%, respectively.17
Multi-institutional registries could improve understanding of acral melanoma in Black patients.4 More studies are needed to help differentiate between the dermoscopic finding of PRP in benign ethnic melanosis vs malignant melanoma.
1. Huang K, Fan J, Misra S. Acral lentiginous melanoma: incidence and survival in the United States, 2006-2015: an analysis of the SEER registry. J Surg Res. 2020;251:329-339. doi:10.1016/j.jss.2020.02.010
2. Coleman WP, Gately LE, Krementz AB, et al. Nevi, lentigines, and melanomas in blacks. Arch Dermatol. 1980;116:548-551.
3. Centers for Disease Control and Prevention. Melanoma Incidence and Mortality, United States: 2012-2016. USCS Data Brief, no. 9. Centers for Disease Control and Prevention, US Department of Health and Human Services; 2019. https://www.cdc.gov/cancer/uscs/about/data-briefs/no9-melanoma-incidence-mortality-UnitedStates-2012-2016.htm
4. Wix SN, Brown AB, Heberton M, et al. Clinical features and outcomes of black patients with melanoma. JAMA Dermatol. 2024;160:328-333. doi:10.1001/jamadermatol.2023.5789
5. Saida T, Koga H. Dermoscopic patterns of acral melanocytic nevi: their variations, changes, and significance. Arch Dermatol. 2007;143:1423-1426. doi:10.1001/archderm.143.11.1423
6. Saida T, Koga H, Uhara H. Key points in dermoscopic differentiation between early acral melanoma and acral nevus. J Dermatol. 2011;38:25-34. doi:10.1111/j.1346-8138.2010.01174.x
7. Saida T, Miyazaki A, Oguchi S. Significance of dermoscopic patterns in detecting malignant melanoma on acral volar skin: results of a multicenter study in Japan. Arch Dermatol. 2004;140:1233-1238. doi:10.1001/archderm.140.10.1233
8. Saida T, Koga H, Uhara H. Dermoscopy for acral melanocytic lesions: revision of the 3-step algorithm and refined definition of the regular and irregular fibrillar pattern. Dermatol Pract Concept. 2022;12:e2022123. doi:10.5826/dpc.1203a123
9. Heath CR, Usatine RP. Melanoma. Cutis. 2022;109:284-285. doi:10.12788/cutis.0513.
10. Dinnes J, Deeks JJ, Chuchu N, et al; Cochrane Skin Cancer Diagnostic Test Accuracy Group. Visual inspection and dermoscopy, alone or in combination, for diagnosing keratinocyte skin cancers in adults. Cochrane Database Syst Rev. 2018; 12:CD011901. doi:10.1002/14651858.CD011901.pub2
11. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked-eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676. doi:10.1111/j.1365-2133.2008.08713.x
12. Phan A, Dalle S, Marcilly MC, et al. Benign dermoscopic parallel ridge pattern variants. Arch Dermatol. 2011;147:634. doi:10.1001/archdermatol.2011.47
13. Fracaroli TS, Lavorato FG, Maceira JP, et al. Parallel ridge pattern on dermoscopy: observation in non-melanoma cases. An Bras Dermatol. 2013;88:646-648. doi:10.1590/abd1806-4841.20132058
14. Manci RN, Dauscher M, Marchetti MA, et al. Features of skin cancer in black individuals: a single-institution retrospective cohort study. Dermatol Pract Concept. 2022;12:e2022075. doi:10.5826/dpc.1202a75
15. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dematol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
16. Ingrassia JP, Stein JA, Levine A, et al. Diagnosis and management of acral pigmented lesions. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 2023;49:926-931. doi:10.1097/DSS.0000000000003891
17. Hill L, Artiga S, Damico A. Health coverage by race and ethnicity, 2010-2022. Kaiser Family Foundation. Published January 11, 2024. Accessed May 9, 2024. https://www.kff.org/racial-equity-and-health-policy/issue-brief/health-coverage-by-race-and-ethnicity
1. Huang K, Fan J, Misra S. Acral lentiginous melanoma: incidence and survival in the United States, 2006-2015: an analysis of the SEER registry. J Surg Res. 2020;251:329-339. doi:10.1016/j.jss.2020.02.010
2. Coleman WP, Gately LE, Krementz AB, et al. Nevi, lentigines, and melanomas in blacks. Arch Dermatol. 1980;116:548-551.
3. Centers for Disease Control and Prevention. Melanoma Incidence and Mortality, United States: 2012-2016. USCS Data Brief, no. 9. Centers for Disease Control and Prevention, US Department of Health and Human Services; 2019. https://www.cdc.gov/cancer/uscs/about/data-briefs/no9-melanoma-incidence-mortality-UnitedStates-2012-2016.htm
4. Wix SN, Brown AB, Heberton M, et al. Clinical features and outcomes of black patients with melanoma. JAMA Dermatol. 2024;160:328-333. doi:10.1001/jamadermatol.2023.5789
5. Saida T, Koga H. Dermoscopic patterns of acral melanocytic nevi: their variations, changes, and significance. Arch Dermatol. 2007;143:1423-1426. doi:10.1001/archderm.143.11.1423
6. Saida T, Koga H, Uhara H. Key points in dermoscopic differentiation between early acral melanoma and acral nevus. J Dermatol. 2011;38:25-34. doi:10.1111/j.1346-8138.2010.01174.x
7. Saida T, Miyazaki A, Oguchi S. Significance of dermoscopic patterns in detecting malignant melanoma on acral volar skin: results of a multicenter study in Japan. Arch Dermatol. 2004;140:1233-1238. doi:10.1001/archderm.140.10.1233
8. Saida T, Koga H, Uhara H. Dermoscopy for acral melanocytic lesions: revision of the 3-step algorithm and refined definition of the regular and irregular fibrillar pattern. Dermatol Pract Concept. 2022;12:e2022123. doi:10.5826/dpc.1203a123
9. Heath CR, Usatine RP. Melanoma. Cutis. 2022;109:284-285. doi:10.12788/cutis.0513.
10. Dinnes J, Deeks JJ, Chuchu N, et al; Cochrane Skin Cancer Diagnostic Test Accuracy Group. Visual inspection and dermoscopy, alone or in combination, for diagnosing keratinocyte skin cancers in adults. Cochrane Database Syst Rev. 2018; 12:CD011901. doi:10.1002/14651858.CD011901.pub2
11. Vestergaard ME, Macaskill P, Holt PE, et al. Dermoscopy compared with naked-eye examination for the diagnosis of primary melanoma: a meta-analysis of studies performed in a clinical setting. Br J Dermatol. 2008;159:669-676. doi:10.1111/j.1365-2133.2008.08713.x
12. Phan A, Dalle S, Marcilly MC, et al. Benign dermoscopic parallel ridge pattern variants. Arch Dermatol. 2011;147:634. doi:10.1001/archdermatol.2011.47
13. Fracaroli TS, Lavorato FG, Maceira JP, et al. Parallel ridge pattern on dermoscopy: observation in non-melanoma cases. An Bras Dermatol. 2013;88:646-648. doi:10.1590/abd1806-4841.20132058
14. Manci RN, Dauscher M, Marchetti MA, et al. Features of skin cancer in black individuals: a single-institution retrospective cohort study. Dermatol Pract Concept. 2022;12:e2022075. doi:10.5826/dpc.1202a75
15. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dematol. 2016;75:983-991. doi:10.1016/j.jaad.2016.06.006
16. Ingrassia JP, Stein JA, Levine A, et al. Diagnosis and management of acral pigmented lesions. Dermatol Surg Off Publ Am Soc Dermatol Surg Al. 2023;49:926-931. doi:10.1097/DSS.0000000000003891
17. Hill L, Artiga S, Damico A. Health coverage by race and ethnicity, 2010-2022. Kaiser Family Foundation. Published January 11, 2024. Accessed May 9, 2024. https://www.kff.org/racial-equity-and-health-policy/issue-brief/health-coverage-by-race-and-ethnicity
EASI, Other Instruments Recommended to Evaluate Patients With Atopic Dermatitis
recommended.
These include the Eczema Area and Severity Index (EASI), the Validated Investigator Global Assessment for AD (vIGAAD), and the Investigator’s Global Assessment (IGA) multiplied by or measured concurrently with a body surface area (BSA) assessment.
The recommendations are part of a consensus statement based on an updated systematic review conducted by the Harmonizing Outcome Measures for Eczema Clinical Practice (HOME-CP) initiative, whose goal is to identify validated, feasible outcome instruments designed to measure AD in the clinical setting. In the statement, which was published in JAMA Dermatology on May 22, 2024, corresponding author Eric L. Simpson, MD, MCR, professor of dermatology at Oregon Health & Science University, Portland, and coauthors described HOME-CP as “a ‘pick-and-choose’ list of valid and feasible OMIs [outcome measure instruments] that can be incorporated into the practice setting depending on the particular need of that clinic or health system.”
For the effort, the authors implemented a mixed methods design and incorporated systematic reviews and qualitative consensus methods modeled after the HOME core outcome set initiative, which developed a set of consensus-based core outcome sets for clinical trials and clinical practice. In October of 2022, a daylong in-person consensus exercise was held in Montreal, Canada, where attendees met to reach consensus on recommended instruments to measure AD clinical signs in clinical practice, based on an updated systematic review evaluating the validity of clinical signs instruments.
The review included 22 studies describing 16 instruments that assessed AD clinical signs and an additional 12 variants of instruments. The meeting was attended by 34 individuals from 13 countries, including patient and patient advocate research partners, health care professionals, researchers, methodologists, and industry representatives. Consensus was defined as less than 30% disagreement.
Following their daylong consensus exercise, the stakeholders reached consensus on recommendations to use the EASI, the vIGAAD, and an IGA multiplied or measured alongside a BSA measurement to measure the domain of clinical signs of AD in the clinical practice setting. “The use of multiple IGAs, most with insufficient validation, and the diverse methods used to assess BSA prevented participants from making specific recommendations for the exact IGA/BSA instrument,” the authors wrote. “We recommend that clinicians include at least one of the recommended instruments in their clinical practices and in documentation.”
They explained that the ideal method of measuring BSA was difficult to assess “because multiple techniques exist for its measurement, including regional percentages, the Rule of Nines, or the handprint method. Most studies did not report which method was performed, and to our knowledge, no studies have been performed in patients with AD that have formally compared them.”
During the consensus exercise, the authors noted, several clinicians “expressed concern whether the EASI was feasible for universal use in clinical practice given its complexity, long completion time, and documentation/calculation requirements.” But clinicians who commonly perform the EASI in clinical practice said that the time it takes to complete this measure “has dropped substantially and now is not a considerable burden,” they wrote, adding that, “studies have shown that with trained investigators, EASI completion times can be as low as nearly 2 minutes.”
The authors acknowledged certain limitations of their recommendations, including the lack of input from primary care clinicians. “It is unknown whether ClinROMs [clinician-reported outcome measures] for AD clinical signs are used in the primary care setting, especially given the large amount of conditions that are managed simultaneously and the ever-increasing number of primary care documentation requirements,” they wrote.
Robert Sidbury, MD, MPH, chief of the division of dermatology at Seattle Children’s Hospital, who was asked to comment on the consensus statement, said that with the advent of new, improved, and more expensive medications for AD, “it is ever more important that [the clinical] assessment is reliable and reproducible.”
Insurers “are understandably less willing to rubber-stamp approval of more expensive medications without a reliable standard by which to justify such decisions,” he added. “This is even more important in a disease state like atopic dermatitis that lacks a reliable biomarker. Therefore, one or several practical, reliable, validated severity metrics will help standardize and improve AD care.”
Dr. Sidbury, who cochaired the 2023 American Academy of Dermatology guidelines of care for the management of AD in adults with phototherapy and systemic therapies, added that the instruments evaluated in the review “can be challenging for anyone,” not just primary care providers. “The EASI isn’t that easy, and while there is a learning curve and it ultimately does, like anything, become more efficient in the gathering, it is unclear if non-AD researchers will be willing to invest the time” to routinely use it, he said.
Dr. Simpson and several coauthors reported receiving grants and personal fees from multiple pharmaceutical companies. Dr. Sidbury reported that he serves as an investigator for Regeneron, Galderma, UCB, Castle, and Pfizer; is a consultant for LEO, Lilly, Arcutis, Dermavant, and Pierre Fabre; and a speaker for Beiersdorf.
A version of this article appeared on Medscape.com .
recommended.
These include the Eczema Area and Severity Index (EASI), the Validated Investigator Global Assessment for AD (vIGAAD), and the Investigator’s Global Assessment (IGA) multiplied by or measured concurrently with a body surface area (BSA) assessment.
The recommendations are part of a consensus statement based on an updated systematic review conducted by the Harmonizing Outcome Measures for Eczema Clinical Practice (HOME-CP) initiative, whose goal is to identify validated, feasible outcome instruments designed to measure AD in the clinical setting. In the statement, which was published in JAMA Dermatology on May 22, 2024, corresponding author Eric L. Simpson, MD, MCR, professor of dermatology at Oregon Health & Science University, Portland, and coauthors described HOME-CP as “a ‘pick-and-choose’ list of valid and feasible OMIs [outcome measure instruments] that can be incorporated into the practice setting depending on the particular need of that clinic or health system.”
For the effort, the authors implemented a mixed methods design and incorporated systematic reviews and qualitative consensus methods modeled after the HOME core outcome set initiative, which developed a set of consensus-based core outcome sets for clinical trials and clinical practice. In October of 2022, a daylong in-person consensus exercise was held in Montreal, Canada, where attendees met to reach consensus on recommended instruments to measure AD clinical signs in clinical practice, based on an updated systematic review evaluating the validity of clinical signs instruments.
The review included 22 studies describing 16 instruments that assessed AD clinical signs and an additional 12 variants of instruments. The meeting was attended by 34 individuals from 13 countries, including patient and patient advocate research partners, health care professionals, researchers, methodologists, and industry representatives. Consensus was defined as less than 30% disagreement.
Following their daylong consensus exercise, the stakeholders reached consensus on recommendations to use the EASI, the vIGAAD, and an IGA multiplied or measured alongside a BSA measurement to measure the domain of clinical signs of AD in the clinical practice setting. “The use of multiple IGAs, most with insufficient validation, and the diverse methods used to assess BSA prevented participants from making specific recommendations for the exact IGA/BSA instrument,” the authors wrote. “We recommend that clinicians include at least one of the recommended instruments in their clinical practices and in documentation.”
They explained that the ideal method of measuring BSA was difficult to assess “because multiple techniques exist for its measurement, including regional percentages, the Rule of Nines, or the handprint method. Most studies did not report which method was performed, and to our knowledge, no studies have been performed in patients with AD that have formally compared them.”
During the consensus exercise, the authors noted, several clinicians “expressed concern whether the EASI was feasible for universal use in clinical practice given its complexity, long completion time, and documentation/calculation requirements.” But clinicians who commonly perform the EASI in clinical practice said that the time it takes to complete this measure “has dropped substantially and now is not a considerable burden,” they wrote, adding that, “studies have shown that with trained investigators, EASI completion times can be as low as nearly 2 minutes.”
The authors acknowledged certain limitations of their recommendations, including the lack of input from primary care clinicians. “It is unknown whether ClinROMs [clinician-reported outcome measures] for AD clinical signs are used in the primary care setting, especially given the large amount of conditions that are managed simultaneously and the ever-increasing number of primary care documentation requirements,” they wrote.
Robert Sidbury, MD, MPH, chief of the division of dermatology at Seattle Children’s Hospital, who was asked to comment on the consensus statement, said that with the advent of new, improved, and more expensive medications for AD, “it is ever more important that [the clinical] assessment is reliable and reproducible.”
Insurers “are understandably less willing to rubber-stamp approval of more expensive medications without a reliable standard by which to justify such decisions,” he added. “This is even more important in a disease state like atopic dermatitis that lacks a reliable biomarker. Therefore, one or several practical, reliable, validated severity metrics will help standardize and improve AD care.”
Dr. Sidbury, who cochaired the 2023 American Academy of Dermatology guidelines of care for the management of AD in adults with phototherapy and systemic therapies, added that the instruments evaluated in the review “can be challenging for anyone,” not just primary care providers. “The EASI isn’t that easy, and while there is a learning curve and it ultimately does, like anything, become more efficient in the gathering, it is unclear if non-AD researchers will be willing to invest the time” to routinely use it, he said.
Dr. Simpson and several coauthors reported receiving grants and personal fees from multiple pharmaceutical companies. Dr. Sidbury reported that he serves as an investigator for Regeneron, Galderma, UCB, Castle, and Pfizer; is a consultant for LEO, Lilly, Arcutis, Dermavant, and Pierre Fabre; and a speaker for Beiersdorf.
A version of this article appeared on Medscape.com .
recommended.
These include the Eczema Area and Severity Index (EASI), the Validated Investigator Global Assessment for AD (vIGAAD), and the Investigator’s Global Assessment (IGA) multiplied by or measured concurrently with a body surface area (BSA) assessment.
The recommendations are part of a consensus statement based on an updated systematic review conducted by the Harmonizing Outcome Measures for Eczema Clinical Practice (HOME-CP) initiative, whose goal is to identify validated, feasible outcome instruments designed to measure AD in the clinical setting. In the statement, which was published in JAMA Dermatology on May 22, 2024, corresponding author Eric L. Simpson, MD, MCR, professor of dermatology at Oregon Health & Science University, Portland, and coauthors described HOME-CP as “a ‘pick-and-choose’ list of valid and feasible OMIs [outcome measure instruments] that can be incorporated into the practice setting depending on the particular need of that clinic or health system.”
For the effort, the authors implemented a mixed methods design and incorporated systematic reviews and qualitative consensus methods modeled after the HOME core outcome set initiative, which developed a set of consensus-based core outcome sets for clinical trials and clinical practice. In October of 2022, a daylong in-person consensus exercise was held in Montreal, Canada, where attendees met to reach consensus on recommended instruments to measure AD clinical signs in clinical practice, based on an updated systematic review evaluating the validity of clinical signs instruments.
The review included 22 studies describing 16 instruments that assessed AD clinical signs and an additional 12 variants of instruments. The meeting was attended by 34 individuals from 13 countries, including patient and patient advocate research partners, health care professionals, researchers, methodologists, and industry representatives. Consensus was defined as less than 30% disagreement.
Following their daylong consensus exercise, the stakeholders reached consensus on recommendations to use the EASI, the vIGAAD, and an IGA multiplied or measured alongside a BSA measurement to measure the domain of clinical signs of AD in the clinical practice setting. “The use of multiple IGAs, most with insufficient validation, and the diverse methods used to assess BSA prevented participants from making specific recommendations for the exact IGA/BSA instrument,” the authors wrote. “We recommend that clinicians include at least one of the recommended instruments in their clinical practices and in documentation.”
They explained that the ideal method of measuring BSA was difficult to assess “because multiple techniques exist for its measurement, including regional percentages, the Rule of Nines, or the handprint method. Most studies did not report which method was performed, and to our knowledge, no studies have been performed in patients with AD that have formally compared them.”
During the consensus exercise, the authors noted, several clinicians “expressed concern whether the EASI was feasible for universal use in clinical practice given its complexity, long completion time, and documentation/calculation requirements.” But clinicians who commonly perform the EASI in clinical practice said that the time it takes to complete this measure “has dropped substantially and now is not a considerable burden,” they wrote, adding that, “studies have shown that with trained investigators, EASI completion times can be as low as nearly 2 minutes.”
The authors acknowledged certain limitations of their recommendations, including the lack of input from primary care clinicians. “It is unknown whether ClinROMs [clinician-reported outcome measures] for AD clinical signs are used in the primary care setting, especially given the large amount of conditions that are managed simultaneously and the ever-increasing number of primary care documentation requirements,” they wrote.
Robert Sidbury, MD, MPH, chief of the division of dermatology at Seattle Children’s Hospital, who was asked to comment on the consensus statement, said that with the advent of new, improved, and more expensive medications for AD, “it is ever more important that [the clinical] assessment is reliable and reproducible.”
Insurers “are understandably less willing to rubber-stamp approval of more expensive medications without a reliable standard by which to justify such decisions,” he added. “This is even more important in a disease state like atopic dermatitis that lacks a reliable biomarker. Therefore, one or several practical, reliable, validated severity metrics will help standardize and improve AD care.”
Dr. Sidbury, who cochaired the 2023 American Academy of Dermatology guidelines of care for the management of AD in adults with phototherapy and systemic therapies, added that the instruments evaluated in the review “can be challenging for anyone,” not just primary care providers. “The EASI isn’t that easy, and while there is a learning curve and it ultimately does, like anything, become more efficient in the gathering, it is unclear if non-AD researchers will be willing to invest the time” to routinely use it, he said.
Dr. Simpson and several coauthors reported receiving grants and personal fees from multiple pharmaceutical companies. Dr. Sidbury reported that he serves as an investigator for Regeneron, Galderma, UCB, Castle, and Pfizer; is a consultant for LEO, Lilly, Arcutis, Dermavant, and Pierre Fabre; and a speaker for Beiersdorf.
A version of this article appeared on Medscape.com .
FROM JAMA DERMATOLOGY
Parental e-Cigarette Use Linked to Atopic Dermatitis Risk in Children
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- AD is one of the most common inflammatory conditions in children and is linked to environmental risk factors, such as exposure to secondhand smoke and prenatal exposure to tobacco.
- To address the effect of e-cigarettes use on children, researchers conducted a cross-sectional analysis of data from the 2014-2018 National Health Interview Survey, a nationally representative sample of the US population.
- The analysis included 48,637,111 individuals (mean age, 8.4 years), with 6,354,515 (13%) indicating a history of AD (mean age, 8 years).
TAKEAWAY:
- The prevalence of parental e-cigarette use was 18.0% among individuals with AD, compared with 14.4% among those without AD.
- This corresponded to a 24% higher risk for AD associated with parental e-cigarette use (adjusted odds ratio, 1.24; 95% CI, 1.08-1.42).
- The association between e-cigarette use and AD in children held regardless of parent’s sex.
IN PRACTICE:
“Our results suggest that parental e-cigarette use was associated with pediatric AD,” the authors concluded. They noted that the authors of a previous study that associated e-cigarette use with AD in adults postulated that the cause was “the inflammatory state created by” e-cigarettes.
SOURCE:
This study, led by Gun Min Youn, Department of Dermatology, Stanford University School of Medicine, Stanford, California, was published online in JAMA Dermatology.
LIMITATIONS:
The cross-sectional survey design limited the ability to draw causal inferences. Defining e-cigarette use as a single past instance could affect the strength of the findings. Only past-year e-cigarette use was considered. Furthermore, data on pediatric cigarette or e-cigarette use, a potential confounder, were unavailable.
DISCLOSURES:
The study did not disclose funding information. One author reported receiving consultation fees outside the submitted work. No other disclosures were reported.
A version of this article appeared on Medscape.com.