MDedge Dermatology

TOPLINE:

A minority of Black dermatologists hold leadership positions in academia.

METHODOLOGY:

• To assess the prevalence of Black dermatologists in academic dermatology programs, researchers obtained an inventory of all 142 U.S.-accredited dermatology residency programs from the Accreditation Council for Graduate Medical Education.
• The researchers drew from institutional websites, the Black Derm Directory (an online repository of Black dermatologists), and other sources to identify full- and part-time Black faculty.
• Variables of interest for each Black dermatologist included gender, institution, department title, academic and nonacademic leadership roles, publication number, National Institutes of Health grant funding, degrees, subspecialties, medical school attended, place of residency, and fellowship training.
• The researchers used Pearson’s chi-squared testing to calculate associations.

TAKEAWAY:

• Of the 86 Black faculty identified, 81.4% were female; most (42.4%) were in the southern United States, followed by the Midwest (23.5%); and 83% held full-time positions.
• Slightly more than one-quarter (26.7%) of the Black faculty attended a top 10 medical school, 16.3% graduated from a historically Black college and university medical school, and 43.5% of those with 25 or more research publications had attended a top 10 medical school.
• Only three dermatology department chairs were Black, and all were female. In addition, more than half of Black faculty (59.2%) were assistant professors, 37.7% held leadership positions at their institutions, and 32.6% held outside leadership roles in dermatology (such as leadership titles at professional dermatology organizations or editorial positions at a journal).

IN PRACTICE:

“Greater efforts are needed to recruit Black dermatology graduates into academic faculty positions,” and “faculty development programs offered by academic institutions and dermatologic associations ... should continue to be expanded,” the authors conclude.

SOURCE:

Corresponding author Nada Elbuluk, MD, MSc, director of the skin of color and pigmentary disorders program and the diversity and inclusion program in the department of dermatology at the University of Southern California, Los Angeles, led the research. The study was published in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The process for identifying Black faculty and insufficient or outdated information on department websites were limitations.

DISCLOSURES:

Dr. Elbuluk disclosed that she has served as a consultant for Avita, Scientis, Incyte, VisualDx, La Roche Posay, Beiersdorf, and Unilever. She has served on advisory boards for Allergan, Eli Lilly, Galderma, Incyte, Pfizer, Janssen, La Roche Posay, L’Oreal, McGraw Hill, and Dior. She has been a speaker for La Roche Posay, Scientis, Medscape, Beiersdorf, and Dior, and has served as investigator for Avita. Another author is an investigator and speaker for Castle Biosciences.

A version of this article first appeared on Medscape.com.

TOPLINE:

A minority of Black dermatologists hold leadership positions in academia.

METHODOLOGY:

• To assess the prevalence of Black dermatologists in academic dermatology programs, researchers obtained an inventory of all 142 U.S.-accredited dermatology residency programs from the Accreditation Council for Graduate Medical Education.
• The researchers drew from institutional websites, the Black Derm Directory (an online repository of Black dermatologists), and other sources to identify full- and part-time Black faculty.
• Variables of interest for each Black dermatologist included gender, institution, department title, academic and nonacademic leadership roles, publication number, National Institutes of Health grant funding, degrees, subspecialties, medical school attended, place of residency, and fellowship training.
• The researchers used Pearson’s chi-squared testing to calculate associations.

TAKEAWAY:

• Of the 86 Black faculty identified, 81.4% were female; most (42.4%) were in the southern United States, followed by the Midwest (23.5%); and 83% held full-time positions.
• Slightly more than one-quarter (26.7%) of the Black faculty attended a top 10 medical school, 16.3% graduated from a historically Black college and university medical school, and 43.5% of those with 25 or more research publications had attended a top 10 medical school.
• Only three dermatology department chairs were Black, and all were female. In addition, more than half of Black faculty (59.2%) were assistant professors, 37.7% held leadership positions at their institutions, and 32.6% held outside leadership roles in dermatology (such as leadership titles at professional dermatology organizations or editorial positions at a journal).

IN PRACTICE:

“Greater efforts are needed to recruit Black dermatology graduates into academic faculty positions,” and “faculty development programs offered by academic institutions and dermatologic associations ... should continue to be expanded,” the authors conclude.

SOURCE:

Corresponding author Nada Elbuluk, MD, MSc, director of the skin of color and pigmentary disorders program and the diversity and inclusion program in the department of dermatology at the University of Southern California, Los Angeles, led the research. The study was published in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The process for identifying Black faculty and insufficient or outdated information on department websites were limitations.

DISCLOSURES:

Dr. Elbuluk disclosed that she has served as a consultant for Avita, Scientis, Incyte, VisualDx, La Roche Posay, Beiersdorf, and Unilever. She has served on advisory boards for Allergan, Eli Lilly, Galderma, Incyte, Pfizer, Janssen, La Roche Posay, L’Oreal, McGraw Hill, and Dior. She has been a speaker for La Roche Posay, Scientis, Medscape, Beiersdorf, and Dior, and has served as investigator for Avita. Another author is an investigator and speaker for Castle Biosciences.

A version of this article first appeared on Medscape.com.

TOPLINE:

A minority of Black dermatologists hold leadership positions in academia.

METHODOLOGY:

• To assess the prevalence of Black dermatologists in academic dermatology programs, researchers obtained an inventory of all 142 U.S.-accredited dermatology residency programs from the Accreditation Council for Graduate Medical Education.
• The researchers drew from institutional websites, the Black Derm Directory (an online repository of Black dermatologists), and other sources to identify full- and part-time Black faculty.
• Variables of interest for each Black dermatologist included gender, institution, department title, academic and nonacademic leadership roles, publication number, National Institutes of Health grant funding, degrees, subspecialties, medical school attended, place of residency, and fellowship training.
• The researchers used Pearson’s chi-squared testing to calculate associations.

TAKEAWAY:

• Of the 86 Black faculty identified, 81.4% were female; most (42.4%) were in the southern United States, followed by the Midwest (23.5%); and 83% held full-time positions.
• Slightly more than one-quarter (26.7%) of the Black faculty attended a top 10 medical school, 16.3% graduated from a historically Black college and university medical school, and 43.5% of those with 25 or more research publications had attended a top 10 medical school.
• Only three dermatology department chairs were Black, and all were female. In addition, more than half of Black faculty (59.2%) were assistant professors, 37.7% held leadership positions at their institutions, and 32.6% held outside leadership roles in dermatology (such as leadership titles at professional dermatology organizations or editorial positions at a journal).

IN PRACTICE:

“Greater efforts are needed to recruit Black dermatology graduates into academic faculty positions,” and “faculty development programs offered by academic institutions and dermatologic associations ... should continue to be expanded,” the authors conclude.

SOURCE:

Corresponding author Nada Elbuluk, MD, MSc, director of the skin of color and pigmentary disorders program and the diversity and inclusion program in the department of dermatology at the University of Southern California, Los Angeles, led the research. The study was published in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The process for identifying Black faculty and insufficient or outdated information on department websites were limitations.

DISCLOSURES:

Dr. Elbuluk disclosed that she has served as a consultant for Avita, Scientis, Incyte, VisualDx, La Roche Posay, Beiersdorf, and Unilever. She has served on advisory boards for Allergan, Eli Lilly, Galderma, Incyte, Pfizer, Janssen, La Roche Posay, L’Oreal, McGraw Hill, and Dior. She has been a speaker for La Roche Posay, Scientis, Medscape, Beiersdorf, and Dior, and has served as investigator for Avita. Another author is an investigator and speaker for Castle Biosciences.

A version of this article first appeared on Medscape.com.

TOPLINE:

Nearly three-quarters of adults with alopecia areata (AA) were not receiving treatment 1 year after diagnosis, according to a retrospective cohort study using data from more than 45,000 individuals.

METHODOLOGY:

• The study population included 45,483 adults aged 18 years and older with new diagnoses of AA between Oct. 15, 2015, and Feb. 28, 2020. Data were from a large U.S. health care database that included medical and pharmacy claims.
• The mean age of the participants was 43.8 years, and 65.7% were female.
• The researchers measured variables that might relate to AA and its treatment patterns within 1 year of starting the study and during the first year of the study, with data collected at 1, 42, 84, and 365 days after study entry.

TAKEAWAYS:

• During the first year after diagnosis, 66.4% of patients received at least one treatment for AA at one or more time points.
• At 1 year, 71.8% of patients were not receiving any active treatment for AA.
• Among those who received treatment, intralesional injections were the most often prescribed therapy (41.8% of patients), followed by topical corticosteroids (40.9%), intramuscular corticosteroids (38.1%), and oral corticosteroids (20.6%).
• Patients diagnosed with either alopecia totalis or alopecia universalis were significantly less likely to receive intralesional steroids and significantly more likely to receive topical corticosteroids than those without these diagnoses (11.1% vs. 44.1% and 25.4% vs. 42.1, respectively).

IN PRACTICE:

The results highlight the need to determine why so many alopecia patients with AA were no longer on treatment after 1 year, although treatment trends may change with the emergence of new therapies, such as JAK inhibitors and others, according to the authors.

SOURCE:

The lead author of the study was Hemin Lee, MD, MPH, Brigham and Women’s Hospital, Boston. The study was published online in JAMA Dermatology.

LIMITATIONS:

The use of insurance claims data did not allow analysis of over-the-counter medications and treatments, and the lack of a single ICD-10 code for defining AA could have resulted in misclassification of outcomes.

DISCLOSURES:

The study received no outside funding, and Dr. Lee had no disclosures. One author had disclosures that included receiving personal fees from Pfizer and Concert outside of the submitted study and participating in alopecia-related trials with Lilly, Concert, Aclaris, and Incyte. Another author’s disclosures included receiving personal fees from companies that included Pfizer, Concert, Lilly, and AbbVie. No other disclosures were reported.

A version of this article first appeared on Medscape.com.

TOPLINE:

Nearly three-quarters of adults with alopecia areata (AA) were not receiving treatment 1 year after diagnosis, according to a retrospective cohort study using data from more than 45,000 individuals.

METHODOLOGY:

• The study population included 45,483 adults aged 18 years and older with new diagnoses of AA between Oct. 15, 2015, and Feb. 28, 2020. Data were from a large U.S. health care database that included medical and pharmacy claims.
• The mean age of the participants was 43.8 years, and 65.7% were female.
• The researchers measured variables that might relate to AA and its treatment patterns within 1 year of starting the study and during the first year of the study, with data collected at 1, 42, 84, and 365 days after study entry.

TAKEAWAYS:

• During the first year after diagnosis, 66.4% of patients received at least one treatment for AA at one or more time points.
• At 1 year, 71.8% of patients were not receiving any active treatment for AA.
• Among those who received treatment, intralesional injections were the most often prescribed therapy (41.8% of patients), followed by topical corticosteroids (40.9%), intramuscular corticosteroids (38.1%), and oral corticosteroids (20.6%).
• Patients diagnosed with either alopecia totalis or alopecia universalis were significantly less likely to receive intralesional steroids and significantly more likely to receive topical corticosteroids than those without these diagnoses (11.1% vs. 44.1% and 25.4% vs. 42.1, respectively).

IN PRACTICE:

The results highlight the need to determine why so many alopecia patients with AA were no longer on treatment after 1 year, although treatment trends may change with the emergence of new therapies, such as JAK inhibitors and others, according to the authors.

SOURCE:

The lead author of the study was Hemin Lee, MD, MPH, Brigham and Women’s Hospital, Boston. The study was published online in JAMA Dermatology.

LIMITATIONS:

The use of insurance claims data did not allow analysis of over-the-counter medications and treatments, and the lack of a single ICD-10 code for defining AA could have resulted in misclassification of outcomes.

DISCLOSURES:

The study received no outside funding, and Dr. Lee had no disclosures. One author had disclosures that included receiving personal fees from Pfizer and Concert outside of the submitted study and participating in alopecia-related trials with Lilly, Concert, Aclaris, and Incyte. Another author’s disclosures included receiving personal fees from companies that included Pfizer, Concert, Lilly, and AbbVie. No other disclosures were reported.

A version of this article first appeared on Medscape.com.

TOPLINE:

Nearly three-quarters of adults with alopecia areata (AA) were not receiving treatment 1 year after diagnosis, according to a retrospective cohort study using data from more than 45,000 individuals.

METHODOLOGY:

• The study population included 45,483 adults aged 18 years and older with new diagnoses of AA between Oct. 15, 2015, and Feb. 28, 2020. Data were from a large U.S. health care database that included medical and pharmacy claims.
• The mean age of the participants was 43.8 years, and 65.7% were female.
• The researchers measured variables that might relate to AA and its treatment patterns within 1 year of starting the study and during the first year of the study, with data collected at 1, 42, 84, and 365 days after study entry.

TAKEAWAYS:

• During the first year after diagnosis, 66.4% of patients received at least one treatment for AA at one or more time points.
• At 1 year, 71.8% of patients were not receiving any active treatment for AA.
• Among those who received treatment, intralesional injections were the most often prescribed therapy (41.8% of patients), followed by topical corticosteroids (40.9%), intramuscular corticosteroids (38.1%), and oral corticosteroids (20.6%).
• Patients diagnosed with either alopecia totalis or alopecia universalis were significantly less likely to receive intralesional steroids and significantly more likely to receive topical corticosteroids than those without these diagnoses (11.1% vs. 44.1% and 25.4% vs. 42.1, respectively).

IN PRACTICE:

The results highlight the need to determine why so many alopecia patients with AA were no longer on treatment after 1 year, although treatment trends may change with the emergence of new therapies, such as JAK inhibitors and others, according to the authors.

SOURCE:

The lead author of the study was Hemin Lee, MD, MPH, Brigham and Women’s Hospital, Boston. The study was published online in JAMA Dermatology.

LIMITATIONS:

The use of insurance claims data did not allow analysis of over-the-counter medications and treatments, and the lack of a single ICD-10 code for defining AA could have resulted in misclassification of outcomes.

DISCLOSURES:

The study received no outside funding, and Dr. Lee had no disclosures. One author had disclosures that included receiving personal fees from Pfizer and Concert outside of the submitted study and participating in alopecia-related trials with Lilly, Concert, Aclaris, and Incyte. Another author’s disclosures included receiving personal fees from companies that included Pfizer, Concert, Lilly, and AbbVie. No other disclosures were reported.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study.

If you run into a health care provider these days and ask, “How are you doing?” you’re likely to get a response like this one: “You know, hanging in there.” You smile and move on. But it may be time to go a step further. If you ask that next question – “No, really, how are you doing?” Well, you might need to carve out some time.

It’s been a rough few years for those of us in the health care professions. Our lives, dominated by COVID-related concerns at home, were equally dominated by COVID concerns at work. On the job, there were fewer and fewer of us around as exploitation and COVID-related stressors led doctors, nurses, and others to leave the profession entirely or take early retirement. Even now, I’m not sure we’ve recovered. Staffing in the hospitals is still a huge problem, and the persistence of impersonal meetings via teleconference – which not only prevent any sort of human connection but, audaciously, run from one into another without a break – robs us of even the subtle joy of walking from one hallway to another for 5 minutes of reflection before sitting down to view the next hastily cobbled together PowerPoint.

I’m speaking in generalities, of course.

I’m talking about how bad things are now because, in truth, they’ve never been great. And that may be why health care workers – people with jobs focused on serving others – are nevertheless at substantially increased risk for suicide.

Analyses through the years have shown that physicians tend to have higher rates of death from suicide than the general population. There are reasons for this that may not entirely be because of work-related stress. Doctors’ suicide attempts are more often lethal – we know what is likely to work, after all.

But a focus on physicians fails to acknowledge the much larger population of people who work in health care, are less well-compensated, have less autonomy, and do not hold as respected a position in society. And, according to this paper in JAMA, it is those people who may be suffering most of all.

The study is a nationally representative sample based on the 2008 American Community Survey. Records were linked to the National Death Index through 2019.

Survey respondents were classified into five categories of health care worker, as you can see here. And 1,666,000 non–health care workers served as the control group.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

JAMA

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

A version of this article first appeared on Medscape.com.

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

A version of this article first appeared on Medscape.com.

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

A version of this article first appeared on Medscape.com.

The Diagnosis: Monilethrix

A diagnosis of monilethrix was rendered based on the clinical and trichoscopic findings. Simple surveillance of the patient’s condition and prevention of further hair trauma were proposed as management options.

Monilethrix is a hair shaft disorder that is inherited in a predominantly autosomal-dominant pattern with variable expressiveness and penetrance resulting from heterozygous mutations in hair keratin genes KRT81, KRT83, and KRT86 in a region of chromosome 12q13.13.^1,2 An autosomalrecessive form has been described with mutation in desmoglein 4, but it differs from the classical form by the variable periodicity of the region between the nodules.^3,4

The morphologic alteration consists of the formation of fusiform nodules of normal structure alternated with narrow and dystrophic constrictions (Figure). These internodes are fragile areas that cause breakage at constricted points.⁵ Clinically, monilethrix presents as areas of focal or diffuse alopecia with frequent involvement of the terminal follicles, mainly in areas of friction. The hair is normal at birth due to the predominance of lanugo in the neonatal period, but it subsequently is replaced by abnormal hairs in the first months of life.⁶ Initial clinical signs begin to appear when the terminal hairs begin to form.⁷ Although rarer, the eyebrows and eyelashes, as well as the axillary, pubic, and body hair, may be involved.⁵

Other hair shaft anomalies merit consideration in the differential diagnosis of monilethrix, including pseudomonilethrix, pressure alopecia, trichorrhexis invaginata, ectodermal dysplasia, tinea capitis, and trichothiodystrophy.⁶ The diagnosis is reached by clinical history and physical examination. Trichoscopy and light microscopy are used to confirm the diagnosis. Trichoscopic examination shows markedly higher rates of anagen hair. The shafts examined in our patient revealed 0.7- to 1-mm intervals between nodes. Hair can be better visualized under a polarized microscope, and the condition can be distinguished from pseudomonilethrix using this approach.^5,6 In our patient, the diagnosis was made based on light microscopy and trichoscopic findings with no genetic testing; however, genetic testing for the classic mutations of the keratin genes would be desirable to confirm the diagnosis but was not done in our patient.⁶ The prognosis of monilethrix is variable; most cases persist into adulthood, though spontaneous improvement may occur with advancing age, during summer, and during pregnancy.⁸

There is no definitive therapy for monilethrix. Although there have been reports of cases treated with systemic corticosteroids, oral retinoids, topical minoxidil, vitamins, and peeling ointments (desquamative oil), the cornerstone of management is protecting the hair against traumatic procedures such as excessive combing, brushing, and friction, as well as parent and patient education about the benign nature of the condition.9 Additionally, some cases have shown improvement with minoxidil solution at 2% and 5% concentrations, oral minoxidil, or acitretin.^7-9

The Diagnosis: Monilethrix

A diagnosis of monilethrix was rendered based on the clinical and trichoscopic findings. Simple surveillance of the patient’s condition and prevention of further hair trauma were proposed as management options.

Monilethrix is a hair shaft disorder that is inherited in a predominantly autosomal-dominant pattern with variable expressiveness and penetrance resulting from heterozygous mutations in hair keratin genes KRT81, KRT83, and KRT86 in a region of chromosome 12q13.13.^1,2 An autosomalrecessive form has been described with mutation in desmoglein 4, but it differs from the classical form by the variable periodicity of the region between the nodules.^3,4

The morphologic alteration consists of the formation of fusiform nodules of normal structure alternated with narrow and dystrophic constrictions (Figure). These internodes are fragile areas that cause breakage at constricted points.⁵ Clinically, monilethrix presents as areas of focal or diffuse alopecia with frequent involvement of the terminal follicles, mainly in areas of friction. The hair is normal at birth due to the predominance of lanugo in the neonatal period, but it subsequently is replaced by abnormal hairs in the first months of life.⁶ Initial clinical signs begin to appear when the terminal hairs begin to form.⁷ Although rarer, the eyebrows and eyelashes, as well as the axillary, pubic, and body hair, may be involved.⁵

Other hair shaft anomalies merit consideration in the differential diagnosis of monilethrix, including pseudomonilethrix, pressure alopecia, trichorrhexis invaginata, ectodermal dysplasia, tinea capitis, and trichothiodystrophy.⁶ The diagnosis is reached by clinical history and physical examination. Trichoscopy and light microscopy are used to confirm the diagnosis. Trichoscopic examination shows markedly higher rates of anagen hair. The shafts examined in our patient revealed 0.7- to 1-mm intervals between nodes. Hair can be better visualized under a polarized microscope, and the condition can be distinguished from pseudomonilethrix using this approach.^5,6 In our patient, the diagnosis was made based on light microscopy and trichoscopic findings with no genetic testing; however, genetic testing for the classic mutations of the keratin genes would be desirable to confirm the diagnosis but was not done in our patient.⁶ The prognosis of monilethrix is variable; most cases persist into adulthood, though spontaneous improvement may occur with advancing age, during summer, and during pregnancy.⁸

There is no definitive therapy for monilethrix. Although there have been reports of cases treated with systemic corticosteroids, oral retinoids, topical minoxidil, vitamins, and peeling ointments (desquamative oil), the cornerstone of management is protecting the hair against traumatic procedures such as excessive combing, brushing, and friction, as well as parent and patient education about the benign nature of the condition.9 Additionally, some cases have shown improvement with minoxidil solution at 2% and 5% concentrations, oral minoxidil, or acitretin.^7-9

The Diagnosis: Monilethrix

A diagnosis of monilethrix was rendered based on the clinical and trichoscopic findings. Simple surveillance of the patient’s condition and prevention of further hair trauma were proposed as management options.

Monilethrix is a hair shaft disorder that is inherited in a predominantly autosomal-dominant pattern with variable expressiveness and penetrance resulting from heterozygous mutations in hair keratin genes KRT81, KRT83, and KRT86 in a region of chromosome 12q13.13.^1,2 An autosomalrecessive form has been described with mutation in desmoglein 4, but it differs from the classical form by the variable periodicity of the region between the nodules.^3,4

The morphologic alteration consists of the formation of fusiform nodules of normal structure alternated with narrow and dystrophic constrictions (Figure). These internodes are fragile areas that cause breakage at constricted points.⁵ Clinically, monilethrix presents as areas of focal or diffuse alopecia with frequent involvement of the terminal follicles, mainly in areas of friction. The hair is normal at birth due to the predominance of lanugo in the neonatal period, but it subsequently is replaced by abnormal hairs in the first months of life.⁶ Initial clinical signs begin to appear when the terminal hairs begin to form.⁷ Although rarer, the eyebrows and eyelashes, as well as the axillary, pubic, and body hair, may be involved.⁵

Other hair shaft anomalies merit consideration in the differential diagnosis of monilethrix, including pseudomonilethrix, pressure alopecia, trichorrhexis invaginata, ectodermal dysplasia, tinea capitis, and trichothiodystrophy.⁶ The diagnosis is reached by clinical history and physical examination. Trichoscopy and light microscopy are used to confirm the diagnosis. Trichoscopic examination shows markedly higher rates of anagen hair. The shafts examined in our patient revealed 0.7- to 1-mm intervals between nodes. Hair can be better visualized under a polarized microscope, and the condition can be distinguished from pseudomonilethrix using this approach.^5,6 In our patient, the diagnosis was made based on light microscopy and trichoscopic findings with no genetic testing; however, genetic testing for the classic mutations of the keratin genes would be desirable to confirm the diagnosis but was not done in our patient.⁶ The prognosis of monilethrix is variable; most cases persist into adulthood, though spontaneous improvement may occur with advancing age, during summer, and during pregnancy.⁸

There is no definitive therapy for monilethrix. Although there have been reports of cases treated with systemic corticosteroids, oral retinoids, topical minoxidil, vitamins, and peeling ointments (desquamative oil), the cornerstone of management is protecting the hair against traumatic procedures such as excessive combing, brushing, and friction, as well as parent and patient education about the benign nature of the condition.9 Additionally, some cases have shown improvement with minoxidil solution at 2% and 5% concentrations, oral minoxidil, or acitretin.^7-9

SAN DIEGO – Despite the popularity of fractional lasers cleared for skin rejuvenation in the past decade, fully ablative laser resurfacing is still preferred by some patients because it usually requires only one treatment for reproducible results, according to Arisa E. Ortiz, MD.

Dr. Arisa E. Ortiz

“Fractional resurfacing is great because there is less downtime, but the results are not as dramatic as with fully ablative resurfacing,” Dr. Ortiz, director of laser and cosmetic dermatology at the University of California, San Diego, said at the annual Masters of Aesthetics Symposium. In her practice, she said, “we do a combination,” which can include “fully ablative around the mouth and eyes and fractional everywhere else.”

Key drawbacks to fully ablative laser resurfacing include significant downtime and extensive wound care, “so it’s not for everybody,” she said. Prolonged erythema following treatment is expected, “so patients need to plan for this. It can last 3-4 months, and it will continue to fade and can be covered up with makeup, but it does last a while,” she noted. “One of the things that made ablative resurfacing fall out of favor was the delayed and permanent hypopigmentation where there’s a stark line of demarcation because you can’t treat the neck [with this modality], so patients have this pearly white looking face that appears 6 months after the treatment,” she added.

Preoperatively, Dr. Ortiz asks patients what other cosmetic procedures they have had in the past. For example, if they have had a facelift, they might have neck skin on their jawline, which will react differently to fully ablative resurfacing than facial skin. “I don’t perform fully ablative resurfacing on the neck or body, or in patients with darker skin types,” she said.

To optimize results, she recommends pretreatment of the area with a neuromodulator a week or 2 before the procedure, “so that they’re not actively contracting and recreating creases,” she said. Studies, she noted, have shown that this approach results in better outcomes. She also asks patients to apply a tripeptide serum daily a week or 2 prior to their procedure to stimulate wound healing and collagen remodeling.

For antibiotic and antiviral prophylaxis, Dr. Ortiz typically prescribes doxycycline 100 mg b.i.d. for 7 days and valacyclovir 500 mg b.i.d. for 7 days and asks patients to start the course the night before the procedure. “If they break through the antiviral, I increase to zoster dosing,” she said. “I make sure they have my cell phone number and call me right away if that happens. I don’t routinely prescribe an antifungal, but you can if you want to.”

For anesthesia, Dr. Ortiz applies lidocaine 23%/tetracaine 7% an hour before the procedure and performs nerve blocks at the mentalis, infraorbital, supraorbital, and nasalis muscles. “I also do local infiltration with a three-pronged Mesoram adapter,” she said. “That has changed the comfort level for these patients. I don’t offer any sedation in my practice but that is an option if you have it available. If you’re going to be resurfacing within the orbital rim you need to know how to place corneal shields. Only use injectable lidocaine in this area because if topical lidocaine gets into the eye, it can cause a chemical corneal abrasion. Nothing happens to their vision permanently, but it’s extremely painful for 24-48 hours.”

Dr. Ortiz described postoperative wound care as “the hardest part” of fully ablative laser resurfacing treatments. The treated area will look “bloody and crusty” for 1-2 weeks. She instructs patients to do vinegar soaks four times per day for 2-3 weeks, “depending on how quickly they heal,” she said. She also counsels patients to apply petrolatum ointment to the area and provides them with a bottle of hypochlorous acid spray, an antiseptic – which also helps with the itching they may experience. “They need to avoid the sun, so I recommend full face visors,” she added.

In her clinical experience, postoperative pain medications are not required. “If the patient calls you on day 3 with increased pain, that’s usually a sign of infection; don’t ignore that,” said Dr. Ortiz, who is also president-elect of the American Society for Laser Medicine and Surgery. In a case of suspected infection, she asks the patient to come in right away, and obtains a bacterial culture. “If they break through the doxycycline, it’s usually a gram-negative infection, so I’ll treat them prophylactically for that,” she said.

“Significant itching may be a sign of Candida infection,” she noted. “Because the epidermis has been disrupted, if they have systemic symptoms then you want to consider IV antibiotics because the infection can spread rapidly.”

Dr. Ortiz disclosed having financial relationships with several pharmaceutical and device companies. She is also cochair of the MOAS.

SAN DIEGO – Despite the popularity of fractional lasers cleared for skin rejuvenation in the past decade, fully ablative laser resurfacing is still preferred by some patients because it usually requires only one treatment for reproducible results, according to Arisa E. Ortiz, MD.

Dr. Arisa E. Ortiz

“Fractional resurfacing is great because there is less downtime, but the results are not as dramatic as with fully ablative resurfacing,” Dr. Ortiz, director of laser and cosmetic dermatology at the University of California, San Diego, said at the annual Masters of Aesthetics Symposium. In her practice, she said, “we do a combination,” which can include “fully ablative around the mouth and eyes and fractional everywhere else.”

Key drawbacks to fully ablative laser resurfacing include significant downtime and extensive wound care, “so it’s not for everybody,” she said. Prolonged erythema following treatment is expected, “so patients need to plan for this. It can last 3-4 months, and it will continue to fade and can be covered up with makeup, but it does last a while,” she noted. “One of the things that made ablative resurfacing fall out of favor was the delayed and permanent hypopigmentation where there’s a stark line of demarcation because you can’t treat the neck [with this modality], so patients have this pearly white looking face that appears 6 months after the treatment,” she added.

Preoperatively, Dr. Ortiz asks patients what other cosmetic procedures they have had in the past. For example, if they have had a facelift, they might have neck skin on their jawline, which will react differently to fully ablative resurfacing than facial skin. “I don’t perform fully ablative resurfacing on the neck or body, or in patients with darker skin types,” she said.

To optimize results, she recommends pretreatment of the area with a neuromodulator a week or 2 before the procedure, “so that they’re not actively contracting and recreating creases,” she said. Studies, she noted, have shown that this approach results in better outcomes. She also asks patients to apply a tripeptide serum daily a week or 2 prior to their procedure to stimulate wound healing and collagen remodeling.

For antibiotic and antiviral prophylaxis, Dr. Ortiz typically prescribes doxycycline 100 mg b.i.d. for 7 days and valacyclovir 500 mg b.i.d. for 7 days and asks patients to start the course the night before the procedure. “If they break through the antiviral, I increase to zoster dosing,” she said. “I make sure they have my cell phone number and call me right away if that happens. I don’t routinely prescribe an antifungal, but you can if you want to.”

For anesthesia, Dr. Ortiz applies lidocaine 23%/tetracaine 7% an hour before the procedure and performs nerve blocks at the mentalis, infraorbital, supraorbital, and nasalis muscles. “I also do local infiltration with a three-pronged Mesoram adapter,” she said. “That has changed the comfort level for these patients. I don’t offer any sedation in my practice but that is an option if you have it available. If you’re going to be resurfacing within the orbital rim you need to know how to place corneal shields. Only use injectable lidocaine in this area because if topical lidocaine gets into the eye, it can cause a chemical corneal abrasion. Nothing happens to their vision permanently, but it’s extremely painful for 24-48 hours.”

Dr. Ortiz described postoperative wound care as “the hardest part” of fully ablative laser resurfacing treatments. The treated area will look “bloody and crusty” for 1-2 weeks. She instructs patients to do vinegar soaks four times per day for 2-3 weeks, “depending on how quickly they heal,” she said. She also counsels patients to apply petrolatum ointment to the area and provides them with a bottle of hypochlorous acid spray, an antiseptic – which also helps with the itching they may experience. “They need to avoid the sun, so I recommend full face visors,” she added.

In her clinical experience, postoperative pain medications are not required. “If the patient calls you on day 3 with increased pain, that’s usually a sign of infection; don’t ignore that,” said Dr. Ortiz, who is also president-elect of the American Society for Laser Medicine and Surgery. In a case of suspected infection, she asks the patient to come in right away, and obtains a bacterial culture. “If they break through the doxycycline, it’s usually a gram-negative infection, so I’ll treat them prophylactically for that,” she said.

“Significant itching may be a sign of Candida infection,” she noted. “Because the epidermis has been disrupted, if they have systemic symptoms then you want to consider IV antibiotics because the infection can spread rapidly.”

Dr. Ortiz disclosed having financial relationships with several pharmaceutical and device companies. She is also cochair of the MOAS.

SAN DIEGO – Despite the popularity of fractional lasers cleared for skin rejuvenation in the past decade, fully ablative laser resurfacing is still preferred by some patients because it usually requires only one treatment for reproducible results, according to Arisa E. Ortiz, MD.

Dr. Arisa E. Ortiz

“Fractional resurfacing is great because there is less downtime, but the results are not as dramatic as with fully ablative resurfacing,” Dr. Ortiz, director of laser and cosmetic dermatology at the University of California, San Diego, said at the annual Masters of Aesthetics Symposium. In her practice, she said, “we do a combination,” which can include “fully ablative around the mouth and eyes and fractional everywhere else.”

Key drawbacks to fully ablative laser resurfacing include significant downtime and extensive wound care, “so it’s not for everybody,” she said. Prolonged erythema following treatment is expected, “so patients need to plan for this. It can last 3-4 months, and it will continue to fade and can be covered up with makeup, but it does last a while,” she noted. “One of the things that made ablative resurfacing fall out of favor was the delayed and permanent hypopigmentation where there’s a stark line of demarcation because you can’t treat the neck [with this modality], so patients have this pearly white looking face that appears 6 months after the treatment,” she added.

Preoperatively, Dr. Ortiz asks patients what other cosmetic procedures they have had in the past. For example, if they have had a facelift, they might have neck skin on their jawline, which will react differently to fully ablative resurfacing than facial skin. “I don’t perform fully ablative resurfacing on the neck or body, or in patients with darker skin types,” she said.

To optimize results, she recommends pretreatment of the area with a neuromodulator a week or 2 before the procedure, “so that they’re not actively contracting and recreating creases,” she said. Studies, she noted, have shown that this approach results in better outcomes. She also asks patients to apply a tripeptide serum daily a week or 2 prior to their procedure to stimulate wound healing and collagen remodeling.

For antibiotic and antiviral prophylaxis, Dr. Ortiz typically prescribes doxycycline 100 mg b.i.d. for 7 days and valacyclovir 500 mg b.i.d. for 7 days and asks patients to start the course the night before the procedure. “If they break through the antiviral, I increase to zoster dosing,” she said. “I make sure they have my cell phone number and call me right away if that happens. I don’t routinely prescribe an antifungal, but you can if you want to.”

For anesthesia, Dr. Ortiz applies lidocaine 23%/tetracaine 7% an hour before the procedure and performs nerve blocks at the mentalis, infraorbital, supraorbital, and nasalis muscles. “I also do local infiltration with a three-pronged Mesoram adapter,” she said. “That has changed the comfort level for these patients. I don’t offer any sedation in my practice but that is an option if you have it available. If you’re going to be resurfacing within the orbital rim you need to know how to place corneal shields. Only use injectable lidocaine in this area because if topical lidocaine gets into the eye, it can cause a chemical corneal abrasion. Nothing happens to their vision permanently, but it’s extremely painful for 24-48 hours.”

Dr. Ortiz described postoperative wound care as “the hardest part” of fully ablative laser resurfacing treatments. The treated area will look “bloody and crusty” for 1-2 weeks. She instructs patients to do vinegar soaks four times per day for 2-3 weeks, “depending on how quickly they heal,” she said. She also counsels patients to apply petrolatum ointment to the area and provides them with a bottle of hypochlorous acid spray, an antiseptic – which also helps with the itching they may experience. “They need to avoid the sun, so I recommend full face visors,” she added.

In her clinical experience, postoperative pain medications are not required. “If the patient calls you on day 3 with increased pain, that’s usually a sign of infection; don’t ignore that,” said Dr. Ortiz, who is also president-elect of the American Society for Laser Medicine and Surgery. In a case of suspected infection, she asks the patient to come in right away, and obtains a bacterial culture. “If they break through the doxycycline, it’s usually a gram-negative infection, so I’ll treat them prophylactically for that,” she said.

“Significant itching may be a sign of Candida infection,” she noted. “Because the epidermis has been disrupted, if they have systemic symptoms then you want to consider IV antibiotics because the infection can spread rapidly.”

Dr. Ortiz disclosed having financial relationships with several pharmaceutical and device companies. She is also cochair of the MOAS.

It was just a routine checkup – or so she thought. But this time, Marnina Miller’s love interest came along. The pair headed to an STD clinic in Houston, where Ms. Miller worked, to get tested for syphilis and HIV. With an already compromised immune system because of an HIV diagnosis 9 years ago, it is critical for Ms. Miller to ensure she is clear of any other diseases. She tested negative for syphilis. Her partner, on the other hand, tested positive for latent (or stage 3) syphilis. 

Syphilis has been on the rise in the United States for more than 2 decades. From 2017 to 2021, the number of cases shot up 75% (to 176,713), according to the Centers for Disease Control and Prevention. Houston – the fourth-largest city in the United States – seems to be at the epicenter. Between 2019 and 2022, there was a 128% rise in syphilis cases there, particularly among women and people of color, according to the Houston Health Department. This summer, drugmaker Pfizer reported a widespread shortage of the antibiotic penicillin, which is used to cure early-stage syphilis and treat latent syphilis. 

“I was immediately scared,” Ms. Miller said. “I was nervous about what that meant for me because we did kiss before. And, although I am openly living with HIV, there is little education around syphilis and how it is contracted.”

The Houston Health Department has been warning Houstonites to take this public health crisis seriously by practicing safe sex and getting tested if they’re sexually active. There has also been a ninefold increase in congenital syphilis in Houston and Harris County, Tex. To help curb the spread, residents can now get free testing for sexually transmitted diseases at Houston health clinics. 

“It is crucial for pregnant women to seek prenatal care and syphilis testing to protect themselves from an infection that could result in the deaths of their babies,” said Marlene McNeese Ward, deputy assistant director of the Houston Health Department’s Bureau of HIV/STI and Viral Hepatitis Prevention. She said a pregnant woman needs to get tested for syphilis three times during her pregnancy.

There are four stages of syphilis: primary, secondary, latent, and tertiary. Oral, anal, and vaginal sex are some of the ways the disease can spread. Some people who contract syphilis never have symptoms and could have the disease for years without knowing.

Penicillin can cure both syphilis and congenital syphilis. The antibiotic cannot reverse damage done to organs via infection, especially if the disease has greatly progressed before treatment. 

Sergino Nicolas, MD, creates TikTok videos and Instagram reels to raise awareness about the outbreak. The Pittsburgh-based emergency medical doctor said there is often a “nonchalant” attitude toward STDs among some people in their 20s and 30s. Being unaware of the consequences of syphilis could drive that attitude. “With thoughts like ‘I can just get treated,’ I think there is danger in that, because when you have these infections, [irreversible] complications can occur,” he said.

Preconceived notions among this age group that oral sex is a safer alternative to vaginal or anal sex is also common, Dr. Nicolas said. “Any time you might have infected secretions or be exposed to mucosa, including the vaginal mucosa, that can result in spreading the infection.”

Women of color have been particularly impacted by the outbreak. Syphilis has a wide range of signs and symptoms, and that could play a major role, Dr. Nicolas said. Lack of education on the dangers of unprotected sex, particularly with multiple sexual partners, could be another reason, as this increases rates of yeast infections and STDs, he said.

Another potential factor: Sexually explicit music and entertainment can also cloud judgment on whether to engage in sexual activity, Dr. Nicolas said. Younger generations can especially fall prey to this. “There have been new artists over the past few months that have really been pushing for ‘female empowerment’ in a sense,” he said. “At the same time, they can also push a narrative more so pertaining to promiscuity, which could result in certain psychological effects” that could lead to unsafe sex practices.

Public health activists in Houston are spreading the word on the importance of getting tested for STDs. Kevin Anderson is the founder of the T.R.U.T.H. Project, a Houston-based nonprofit that educates and mobilizes LGBTQ communities of color through social arts that promote sexual, mental, and physical health.

While celebrating its 10th anniversary, T.R.U.T.H. Project is creatively promoting syphilis education and awareness. The organization’s recent events have included an open-mic night called “Heart and Soul,” with free STD testing on site for attendees. It also hosted a sex-positive night aiming to educate attendees about STDs and safe sex practices. Self-love, self-care, and self-awareness of one’s body is one of the group’s most prominent messages. “If something feels or looks different, love yourself enough to be proactive in following up to find out what’s going on – because avoidance leads to outbreaks,” Mr. Anderson said.

A version of this article first appeared on WebMD.com.

It was just a routine checkup – or so she thought. But this time, Marnina Miller’s love interest came along. The pair headed to an STD clinic in Houston, where Ms. Miller worked, to get tested for syphilis and HIV. With an already compromised immune system because of an HIV diagnosis 9 years ago, it is critical for Ms. Miller to ensure she is clear of any other diseases. She tested negative for syphilis. Her partner, on the other hand, tested positive for latent (or stage 3) syphilis. 

Syphilis has been on the rise in the United States for more than 2 decades. From 2017 to 2021, the number of cases shot up 75% (to 176,713), according to the Centers for Disease Control and Prevention. Houston – the fourth-largest city in the United States – seems to be at the epicenter. Between 2019 and 2022, there was a 128% rise in syphilis cases there, particularly among women and people of color, according to the Houston Health Department. This summer, drugmaker Pfizer reported a widespread shortage of the antibiotic penicillin, which is used to cure early-stage syphilis and treat latent syphilis. 

“I was immediately scared,” Ms. Miller said. “I was nervous about what that meant for me because we did kiss before. And, although I am openly living with HIV, there is little education around syphilis and how it is contracted.”

The Houston Health Department has been warning Houstonites to take this public health crisis seriously by practicing safe sex and getting tested if they’re sexually active. There has also been a ninefold increase in congenital syphilis in Houston and Harris County, Tex. To help curb the spread, residents can now get free testing for sexually transmitted diseases at Houston health clinics. 

“It is crucial for pregnant women to seek prenatal care and syphilis testing to protect themselves from an infection that could result in the deaths of their babies,” said Marlene McNeese Ward, deputy assistant director of the Houston Health Department’s Bureau of HIV/STI and Viral Hepatitis Prevention. She said a pregnant woman needs to get tested for syphilis three times during her pregnancy.

There are four stages of syphilis: primary, secondary, latent, and tertiary. Oral, anal, and vaginal sex are some of the ways the disease can spread. Some people who contract syphilis never have symptoms and could have the disease for years without knowing.

Penicillin can cure both syphilis and congenital syphilis. The antibiotic cannot reverse damage done to organs via infection, especially if the disease has greatly progressed before treatment. 

Sergino Nicolas, MD, creates TikTok videos and Instagram reels to raise awareness about the outbreak. The Pittsburgh-based emergency medical doctor said there is often a “nonchalant” attitude toward STDs among some people in their 20s and 30s. Being unaware of the consequences of syphilis could drive that attitude. “With thoughts like ‘I can just get treated,’ I think there is danger in that, because when you have these infections, [irreversible] complications can occur,” he said.

Preconceived notions among this age group that oral sex is a safer alternative to vaginal or anal sex is also common, Dr. Nicolas said. “Any time you might have infected secretions or be exposed to mucosa, including the vaginal mucosa, that can result in spreading the infection.”

Women of color have been particularly impacted by the outbreak. Syphilis has a wide range of signs and symptoms, and that could play a major role, Dr. Nicolas said. Lack of education on the dangers of unprotected sex, particularly with multiple sexual partners, could be another reason, as this increases rates of yeast infections and STDs, he said.

Another potential factor: Sexually explicit music and entertainment can also cloud judgment on whether to engage in sexual activity, Dr. Nicolas said. Younger generations can especially fall prey to this. “There have been new artists over the past few months that have really been pushing for ‘female empowerment’ in a sense,” he said. “At the same time, they can also push a narrative more so pertaining to promiscuity, which could result in certain psychological effects” that could lead to unsafe sex practices.

Public health activists in Houston are spreading the word on the importance of getting tested for STDs. Kevin Anderson is the founder of the T.R.U.T.H. Project, a Houston-based nonprofit that educates and mobilizes LGBTQ communities of color through social arts that promote sexual, mental, and physical health.

While celebrating its 10th anniversary, T.R.U.T.H. Project is creatively promoting syphilis education and awareness. The organization’s recent events have included an open-mic night called “Heart and Soul,” with free STD testing on site for attendees. It also hosted a sex-positive night aiming to educate attendees about STDs and safe sex practices. Self-love, self-care, and self-awareness of one’s body is one of the group’s most prominent messages. “If something feels or looks different, love yourself enough to be proactive in following up to find out what’s going on – because avoidance leads to outbreaks,” Mr. Anderson said.

A version of this article first appeared on WebMD.com.

It was just a routine checkup – or so she thought. But this time, Marnina Miller’s love interest came along. The pair headed to an STD clinic in Houston, where Ms. Miller worked, to get tested for syphilis and HIV. With an already compromised immune system because of an HIV diagnosis 9 years ago, it is critical for Ms. Miller to ensure she is clear of any other diseases. She tested negative for syphilis. Her partner, on the other hand, tested positive for latent (or stage 3) syphilis. 

Syphilis has been on the rise in the United States for more than 2 decades. From 2017 to 2021, the number of cases shot up 75% (to 176,713), according to the Centers for Disease Control and Prevention. Houston – the fourth-largest city in the United States – seems to be at the epicenter. Between 2019 and 2022, there was a 128% rise in syphilis cases there, particularly among women and people of color, according to the Houston Health Department. This summer, drugmaker Pfizer reported a widespread shortage of the antibiotic penicillin, which is used to cure early-stage syphilis and treat latent syphilis. 

“I was immediately scared,” Ms. Miller said. “I was nervous about what that meant for me because we did kiss before. And, although I am openly living with HIV, there is little education around syphilis and how it is contracted.”

The Houston Health Department has been warning Houstonites to take this public health crisis seriously by practicing safe sex and getting tested if they’re sexually active. There has also been a ninefold increase in congenital syphilis in Houston and Harris County, Tex. To help curb the spread, residents can now get free testing for sexually transmitted diseases at Houston health clinics. 

“It is crucial for pregnant women to seek prenatal care and syphilis testing to protect themselves from an infection that could result in the deaths of their babies,” said Marlene McNeese Ward, deputy assistant director of the Houston Health Department’s Bureau of HIV/STI and Viral Hepatitis Prevention. She said a pregnant woman needs to get tested for syphilis three times during her pregnancy.

There are four stages of syphilis: primary, secondary, latent, and tertiary. Oral, anal, and vaginal sex are some of the ways the disease can spread. Some people who contract syphilis never have symptoms and could have the disease for years without knowing.

Penicillin can cure both syphilis and congenital syphilis. The antibiotic cannot reverse damage done to organs via infection, especially if the disease has greatly progressed before treatment. 

Sergino Nicolas, MD, creates TikTok videos and Instagram reels to raise awareness about the outbreak. The Pittsburgh-based emergency medical doctor said there is often a “nonchalant” attitude toward STDs among some people in their 20s and 30s. Being unaware of the consequences of syphilis could drive that attitude. “With thoughts like ‘I can just get treated,’ I think there is danger in that, because when you have these infections, [irreversible] complications can occur,” he said.

Preconceived notions among this age group that oral sex is a safer alternative to vaginal or anal sex is also common, Dr. Nicolas said. “Any time you might have infected secretions or be exposed to mucosa, including the vaginal mucosa, that can result in spreading the infection.”

Women of color have been particularly impacted by the outbreak. Syphilis has a wide range of signs and symptoms, and that could play a major role, Dr. Nicolas said. Lack of education on the dangers of unprotected sex, particularly with multiple sexual partners, could be another reason, as this increases rates of yeast infections and STDs, he said.

Another potential factor: Sexually explicit music and entertainment can also cloud judgment on whether to engage in sexual activity, Dr. Nicolas said. Younger generations can especially fall prey to this. “There have been new artists over the past few months that have really been pushing for ‘female empowerment’ in a sense,” he said. “At the same time, they can also push a narrative more so pertaining to promiscuity, which could result in certain psychological effects” that could lead to unsafe sex practices.

Public health activists in Houston are spreading the word on the importance of getting tested for STDs. Kevin Anderson is the founder of the T.R.U.T.H. Project, a Houston-based nonprofit that educates and mobilizes LGBTQ communities of color through social arts that promote sexual, mental, and physical health.

While celebrating its 10th anniversary, T.R.U.T.H. Project is creatively promoting syphilis education and awareness. The organization’s recent events have included an open-mic night called “Heart and Soul,” with free STD testing on site for attendees. It also hosted a sex-positive night aiming to educate attendees about STDs and safe sex practices. Self-love, self-care, and self-awareness of one’s body is one of the group’s most prominent messages. “If something feels or looks different, love yourself enough to be proactive in following up to find out what’s going on – because avoidance leads to outbreaks,” Mr. Anderson said.

A version of this article first appeared on WebMD.com.

SAN DIEGO – The use of absorbable threads to improve skin laxity is safe and effective, but their long-term aesthetic effects remain unclear, according to Catherine M. DiGiorgio, MD, MS.

In the 1990s, clinicians used nonabsorbable sutures for thread lifts, including polypropylene-barbed threads, which caused adverse events ranging from extrusion and migration to thread expulsion, dimpling, granuloma formation, and prolonged pain, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. As a result, the Food and Drug Administration withdrew its approval of contour thread aesthetic procedures in 2009. Since then, the development of absorbable threads made from a hybrid of poly-l-lactic acid (PLLA) and polyglycolide/l-lactide (PLGA), and from polydioxanone (PDO) has led to renewed interest in thread lift procedures.

Dr. DiGiorgio

While a surgical facelift remains the gold standard, “we have some options to offer patients for noninvasive tightening,” Dr. DiGiorgio said. “We have devices that provide minimal downtime and are less costly, but results are inconsistent. Thread lifts, or suspension sutures, also have minimal downtime and are less costly, but the [results are] subtle and not long lasting.”

PLGA/PLLA threads consist of an 18% PLGA and 82% PLLA monofilament with bidirectional cones that shift the tissue. They are available in 8, 12, or 16 cones spaced 5-8 mm apart on either side of a 2-cm central cone-free area. “There is a 12-cm, 23-gauge needle on either side of the thread, to allow for insertion,” she explained. “These cones stimulate types I and II collagen, which results in collagenesis. The skin encapsulates the cones, resulting in lasting volume and contour.”

PDO threads, meanwhile, are biodegradable by hydrolysis over 4-8 months. They are inserted with a cannula or a needle and vary based on length, diameter, twined vs. braided, coned vs. barbed, and twisted vs. smooth. “The barbed PDO threads are what I use the most,” Dr. DiGiorgio said. “They provide slight tissue repositioning by anchoring and gripping.”

In 2019, researchers in Korea published results of a study that evaluated the collagen-producing effects of powdered PDO injection, compared with PLLA injection, in a murine model. They found that while both PDO and PLLA induced granulomatous reactions and collagen formation, PDO resulted in slightly more collagen formation than PLLA.

Dr. DiGiorgio, who transitioned to using PDO threads after first using the PLLA/PLGA threads, said that both are effective. “I find PDO threads to be easier. They’re less costly for me, they’re less costly for the patient, and the results are about equivalent.”

Absorbable threads are indicated for the cheek, jawline, neck, lips, forehead, and brow. She finds them most useful “for the lower face, below the nasolabial fold down to the jawline, for improvement of the jowls,” she said. “I don’t think they really work on the neck.”

As with any cosmetic procedure, patient selection is key. According to Dr. DiGiorgio, the patient should have specific and segmental areas of facial laxity amenable to lifting and recontouring along a straight-line vector, adequate dermal thickness, and appropriate expectations for the level of correction. “I like to re-volumize with filler before performing thread lifts to make sure that volume is restored, because you can’t really provide lift to someone with significant volume loss,” she said.
 

Procedural tips

Prior to the procedure, Dr. DiGiorgio marks the area to be treated while the patient is seated upright and holding a mirror. Then, she pulls back the amount of skin laxity the thread is going to correct. The plane of insertion for barbed threads is at the superficial musculoaponeurotic system (SMAS), and she typically uses 3-4 threads on each side of the face.

“How do you know you’re in the right plane?” If the patient is experiencing significant pain, “you’re too deep, and it’s not going to work,” she said. “You can see if the thread is too superficial as you do more of these.”

After the procedure she asks the patient to sit up prior to trimming the threads. “I take a look in the mirror with them and have them smile and make funny faces to see if there is any dimpling or crimpling, which is probably the most common side effect,” she said. “If I see that, I will pull the thread immediately, so we don’t have a problem. It’s a little uncomfortable to pull the thread but not more uncomfortable than the procedure itself, but I think it’s worth doing to avoid having a dimple or a crimple that can last up to a year.”

In her clinical experience, thread lifts last about 8-10 months. “I find that my patients will come in about once a year for this procedure, and the treated area feels tight afterward,” Dr. DiGiorgio said. “I think that sensation of feeling tight also provides satisfaction to the patient. Results are very subtle. It’s tissue repositioning; it is not a facelift. There’s not really any downtime, but further studies are required to see if threads are safe and effective in the long-term.”

In an interview after the meeting, she noted that the learning curve for thread lifts is variable, as with any new procedure a physician chooses to add to his or her practice. “It’s important to see these patients in follow-up 2 weeks after the procedure consistently, especially when someone first starts performing the procedure,” she recommended. “These patients are usually coming in to see me for other treatments, so I see them at regular 3-month intervals regardless. You begin to get a feel for what angles work and why and how to optimize the results. As with any procedure, the more experience you have performing the procedure will result in improved outcomes and improved management.”

Dr. DiGiorgio disclosed that she has been an advisory board member for Quthero and she holds stock options in the company. She is a consultant for Revelle and has received equipment from Acclaro.

SAN DIEGO – The use of absorbable threads to improve skin laxity is safe and effective, but their long-term aesthetic effects remain unclear, according to Catherine M. DiGiorgio, MD, MS.

In the 1990s, clinicians used nonabsorbable sutures for thread lifts, including polypropylene-barbed threads, which caused adverse events ranging from extrusion and migration to thread expulsion, dimpling, granuloma formation, and prolonged pain, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. As a result, the Food and Drug Administration withdrew its approval of contour thread aesthetic procedures in 2009. Since then, the development of absorbable threads made from a hybrid of poly-l-lactic acid (PLLA) and polyglycolide/l-lactide (PLGA), and from polydioxanone (PDO) has led to renewed interest in thread lift procedures.

Dr. DiGiorgio

While a surgical facelift remains the gold standard, “we have some options to offer patients for noninvasive tightening,” Dr. DiGiorgio said. “We have devices that provide minimal downtime and are less costly, but results are inconsistent. Thread lifts, or suspension sutures, also have minimal downtime and are less costly, but the [results are] subtle and not long lasting.”

PLGA/PLLA threads consist of an 18% PLGA and 82% PLLA monofilament with bidirectional cones that shift the tissue. They are available in 8, 12, or 16 cones spaced 5-8 mm apart on either side of a 2-cm central cone-free area. “There is a 12-cm, 23-gauge needle on either side of the thread, to allow for insertion,” she explained. “These cones stimulate types I and II collagen, which results in collagenesis. The skin encapsulates the cones, resulting in lasting volume and contour.”

PDO threads, meanwhile, are biodegradable by hydrolysis over 4-8 months. They are inserted with a cannula or a needle and vary based on length, diameter, twined vs. braided, coned vs. barbed, and twisted vs. smooth. “The barbed PDO threads are what I use the most,” Dr. DiGiorgio said. “They provide slight tissue repositioning by anchoring and gripping.”

In 2019, researchers in Korea published results of a study that evaluated the collagen-producing effects of powdered PDO injection, compared with PLLA injection, in a murine model. They found that while both PDO and PLLA induced granulomatous reactions and collagen formation, PDO resulted in slightly more collagen formation than PLLA.

Dr. DiGiorgio, who transitioned to using PDO threads after first using the PLLA/PLGA threads, said that both are effective. “I find PDO threads to be easier. They’re less costly for me, they’re less costly for the patient, and the results are about equivalent.”

Absorbable threads are indicated for the cheek, jawline, neck, lips, forehead, and brow. She finds them most useful “for the lower face, below the nasolabial fold down to the jawline, for improvement of the jowls,” she said. “I don’t think they really work on the neck.”

As with any cosmetic procedure, patient selection is key. According to Dr. DiGiorgio, the patient should have specific and segmental areas of facial laxity amenable to lifting and recontouring along a straight-line vector, adequate dermal thickness, and appropriate expectations for the level of correction. “I like to re-volumize with filler before performing thread lifts to make sure that volume is restored, because you can’t really provide lift to someone with significant volume loss,” she said.
 

Procedural tips

Prior to the procedure, Dr. DiGiorgio marks the area to be treated while the patient is seated upright and holding a mirror. Then, she pulls back the amount of skin laxity the thread is going to correct. The plane of insertion for barbed threads is at the superficial musculoaponeurotic system (SMAS), and she typically uses 3-4 threads on each side of the face.

“How do you know you’re in the right plane?” If the patient is experiencing significant pain, “you’re too deep, and it’s not going to work,” she said. “You can see if the thread is too superficial as you do more of these.”

After the procedure she asks the patient to sit up prior to trimming the threads. “I take a look in the mirror with them and have them smile and make funny faces to see if there is any dimpling or crimpling, which is probably the most common side effect,” she said. “If I see that, I will pull the thread immediately, so we don’t have a problem. It’s a little uncomfortable to pull the thread but not more uncomfortable than the procedure itself, but I think it’s worth doing to avoid having a dimple or a crimple that can last up to a year.”

In her clinical experience, thread lifts last about 8-10 months. “I find that my patients will come in about once a year for this procedure, and the treated area feels tight afterward,” Dr. DiGiorgio said. “I think that sensation of feeling tight also provides satisfaction to the patient. Results are very subtle. It’s tissue repositioning; it is not a facelift. There’s not really any downtime, but further studies are required to see if threads are safe and effective in the long-term.”

In an interview after the meeting, she noted that the learning curve for thread lifts is variable, as with any new procedure a physician chooses to add to his or her practice. “It’s important to see these patients in follow-up 2 weeks after the procedure consistently, especially when someone first starts performing the procedure,” she recommended. “These patients are usually coming in to see me for other treatments, so I see them at regular 3-month intervals regardless. You begin to get a feel for what angles work and why and how to optimize the results. As with any procedure, the more experience you have performing the procedure will result in improved outcomes and improved management.”

Dr. DiGiorgio disclosed that she has been an advisory board member for Quthero and she holds stock options in the company. She is a consultant for Revelle and has received equipment from Acclaro.

SAN DIEGO – The use of absorbable threads to improve skin laxity is safe and effective, but their long-term aesthetic effects remain unclear, according to Catherine M. DiGiorgio, MD, MS.

In the 1990s, clinicians used nonabsorbable sutures for thread lifts, including polypropylene-barbed threads, which caused adverse events ranging from extrusion and migration to thread expulsion, dimpling, granuloma formation, and prolonged pain, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. As a result, the Food and Drug Administration withdrew its approval of contour thread aesthetic procedures in 2009. Since then, the development of absorbable threads made from a hybrid of poly-l-lactic acid (PLLA) and polyglycolide/l-lactide (PLGA), and from polydioxanone (PDO) has led to renewed interest in thread lift procedures.

Dr. DiGiorgio

While a surgical facelift remains the gold standard, “we have some options to offer patients for noninvasive tightening,” Dr. DiGiorgio said. “We have devices that provide minimal downtime and are less costly, but results are inconsistent. Thread lifts, or suspension sutures, also have minimal downtime and are less costly, but the [results are] subtle and not long lasting.”

PLGA/PLLA threads consist of an 18% PLGA and 82% PLLA monofilament with bidirectional cones that shift the tissue. They are available in 8, 12, or 16 cones spaced 5-8 mm apart on either side of a 2-cm central cone-free area. “There is a 12-cm, 23-gauge needle on either side of the thread, to allow for insertion,” she explained. “These cones stimulate types I and II collagen, which results in collagenesis. The skin encapsulates the cones, resulting in lasting volume and contour.”

PDO threads, meanwhile, are biodegradable by hydrolysis over 4-8 months. They are inserted with a cannula or a needle and vary based on length, diameter, twined vs. braided, coned vs. barbed, and twisted vs. smooth. “The barbed PDO threads are what I use the most,” Dr. DiGiorgio said. “They provide slight tissue repositioning by anchoring and gripping.”

In 2019, researchers in Korea published results of a study that evaluated the collagen-producing effects of powdered PDO injection, compared with PLLA injection, in a murine model. They found that while both PDO and PLLA induced granulomatous reactions and collagen formation, PDO resulted in slightly more collagen formation than PLLA.

Dr. DiGiorgio, who transitioned to using PDO threads after first using the PLLA/PLGA threads, said that both are effective. “I find PDO threads to be easier. They’re less costly for me, they’re less costly for the patient, and the results are about equivalent.”

Absorbable threads are indicated for the cheek, jawline, neck, lips, forehead, and brow. She finds them most useful “for the lower face, below the nasolabial fold down to the jawline, for improvement of the jowls,” she said. “I don’t think they really work on the neck.”

As with any cosmetic procedure, patient selection is key. According to Dr. DiGiorgio, the patient should have specific and segmental areas of facial laxity amenable to lifting and recontouring along a straight-line vector, adequate dermal thickness, and appropriate expectations for the level of correction. “I like to re-volumize with filler before performing thread lifts to make sure that volume is restored, because you can’t really provide lift to someone with significant volume loss,” she said.
 

Procedural tips

Prior to the procedure, Dr. DiGiorgio marks the area to be treated while the patient is seated upright and holding a mirror. Then, she pulls back the amount of skin laxity the thread is going to correct. The plane of insertion for barbed threads is at the superficial musculoaponeurotic system (SMAS), and she typically uses 3-4 threads on each side of the face.

“How do you know you’re in the right plane?” If the patient is experiencing significant pain, “you’re too deep, and it’s not going to work,” she said. “You can see if the thread is too superficial as you do more of these.”

After the procedure she asks the patient to sit up prior to trimming the threads. “I take a look in the mirror with them and have them smile and make funny faces to see if there is any dimpling or crimpling, which is probably the most common side effect,” she said. “If I see that, I will pull the thread immediately, so we don’t have a problem. It’s a little uncomfortable to pull the thread but not more uncomfortable than the procedure itself, but I think it’s worth doing to avoid having a dimple or a crimple that can last up to a year.”

In her clinical experience, thread lifts last about 8-10 months. “I find that my patients will come in about once a year for this procedure, and the treated area feels tight afterward,” Dr. DiGiorgio said. “I think that sensation of feeling tight also provides satisfaction to the patient. Results are very subtle. It’s tissue repositioning; it is not a facelift. There’s not really any downtime, but further studies are required to see if threads are safe and effective in the long-term.”

In an interview after the meeting, she noted that the learning curve for thread lifts is variable, as with any new procedure a physician chooses to add to his or her practice. “It’s important to see these patients in follow-up 2 weeks after the procedure consistently, especially when someone first starts performing the procedure,” she recommended. “These patients are usually coming in to see me for other treatments, so I see them at regular 3-month intervals regardless. You begin to get a feel for what angles work and why and how to optimize the results. As with any procedure, the more experience you have performing the procedure will result in improved outcomes and improved management.”

Dr. DiGiorgio disclosed that she has been an advisory board member for Quthero and she holds stock options in the company. She is a consultant for Revelle and has received equipment from Acclaro.

To the Editor:

Granulomatous dermatitis (GD) has been described as a rare side effect of MEK and BRAF inhibitor use in the treatment of BRAF V600E mutation–positive metastatic melanoma. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation. We present the case of a 52-year-old woman who developed GD while being treated with vemurafenib and cobimetinib for BRAF V600E mutation–positive metastatic cholangiocarcinoma.

A 52-year-old White woman presented with faint patches of nonpalpable violaceous mottling that extended distally to proximally from the ankles to the thighs on the medial aspects of both legs. She was diagnosed with cholangiocarcinoma 10 months prior, with metastases to the lung, liver, and sternum. She underwent treatment with gemcitabine and cisplatin therapy. Computed tomography after several treatment cycles revealed progressive disease with multiple pulmonary nodules as well as metastatic intrathoracic and abdominal adenopathy. Treatment with gemcitabine and cisplatin failed to produce a favorable response and was discontinued after 6 treatment cycles.

Genomic testing performed at the time of diagnosis revealed a positive mutation for BRAF V600E. The patient subsequently enrolled in a clinical trial and started treatment with the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib. She developed sun sensitivity and multiple sunburns after starting these therapies. The patient tolerated the next few cycles of therapy well with only moderate concerns of dry sensitive skin.

During the sixth cycle of therapy, she presented to dermatology after developing a rash. Over the next 2 weeks, similar lesions appeared on the arms. The patient denied the use of any new lotions, soaps, or other medications. Punch biopsies of the right forearm and right medial thigh revealed nonnecrotizing granulomas in the superficial dermis that extended into the subcutaneous adipose tissue (Figure 1). Surrounding chronic inflammation was scant, and the presence of rare eosinophils was noted (Figure 2). The histiocytes were highlighted by a CD68 immunohistochemical stain. An auramine-O special stain test was negative for acid-fast bacilli, and a Grocott methenamine-silver special stain test for fungal organisms was negative. These findings were consistent with GD. Computed tomography of the chest performed 2 months prior and 1 month after biopsy of the skin lesions revealed no axillary, mediastinal, or hilar lymphadenopathy. The calcium level at the time of skin biopsy was within reference range.

A topical steroid was prescribed; however, it was not utilized by the patient. Within 2 months of onset, the GD lesions resolved with no treatment. The GD lesions did not affect the patient’s enrollment in the clinical trial, and no dose reductions were made. Due to progressive disease with metastases to the brain, the patient eventually discontinued the clinical trial.

BRAF inhibitors are US Food and Drug Administration approved for the treatment of metastatic melanoma to deactivate the serine-threonine kinase BRAF gene mutation, which leads to decreased generation and survival of melanoma cells.^1,2 Vemurafenib, dabrafenib, and encorafenib are the only BRAF inhibitors approved in the United States.³ The most common side effects of vemurafenib include arthralgia, fatigue, rash, and photosensitivity.^1,4 There are 4 MEK inhibitors currently available in the United States: cobimetinib, trametinib, selumetinib and binimetinib. The addition of a MEK inhibitor to BRAF inhibitor therapy has shown increased patient response rates and prolonged survival in 3 phase 3 studies.^5-10

Response rates remain low in the treatment of advanced cholangiocarcinoma with standard chemotherapy. Recent research has explored if targeted therapies at the molecular level would be of benefit.¹¹ Our patient was enrolled in the American Society of Clinical Oncology Targeted Agent and Profiling Utilization Registry (TAPUR) trial, a phase 2, prospective, nonrandomized trial that matches eligible participants to US Food and Drug Administration–approved study medications based on specific data from their molecular testing results.¹² Some of the most common mutations in intrahepatic cholangiocarcinoma include HER2, KRAS, MET, and BRAF.^13-17 Our patient’s molecular test results were positive for a BRAF V600E–positive mutation, and she subsequently started therapy with vemurafenib and cobimetinib. The use of personalized genomic treatment approaches for BRAF V600E mutation–positive cholangiocarcinoma has produced a dramatic patient response to BRAF and MEK inhibitor combination therapies.^11,18-20

Drug-induced GD most likely is caused by vascular insults that lead to deposition of immune complexes in vessels causing inflammation and a consequent granulomatous infiltrate.^21,22 Although cordlike lesions in the subcutaneous tissue on the trunk commonly are reported, the presentation of GD can vary considerably. Other presentations include areas of violaceous or erythematous patches or plaques on the limbs, intertriginous areas, and upper trunk. Diffuse macular erythema or small flesh-colored papules also can be observed.²³

Granulomatous dermatitis secondary to drug reactions can have varying morphologies. The infiltrate often can have an interstitial appearance with the presence of lymphocytes, plasma cells, histiocytes, eosinophils, and multinucleated giant cells.²⁴ These findings can be confused with interstitial granuloma annulare. Other cases, such as in our patient, can have discrete granulomata formation with a sarcoidlike appearance. These naked granulomas lack surrounding inflammation and suggest a differential diagnosis of sarcoidosis and infection. Use of immune checkpoint inhibitors (CIs) and kinase inhibitors has been proven to cause sarcoidosislike reactions.²⁵ The development of granulomatous/sarcoidlike lesions associated with the use of BRAF and MEK inhibitors may clinically and radiographically mimic disease recurrence. An awareness of this type of reaction by clinicians and pathologists is important to ensure appropriate management in patients who develop GD.²⁶

Checkpoint inhibitor–induced GD that remains asymptomatic does not necessarily warrant treatment; however, corticosteroid use and elimination of CI therapies have resolved GD in prior cases. Responsiveness of the cancer to CI therapy and severity of GD symptoms should be considered before discontinuation of a CI trial.²⁵

One case report described complete resolution of a GD eruption without interruption of the scheduled BRAF and MEK inhibitor therapies for the treatment of metastatic melanoma. There was no reported use of a steroidal cream or other topical medication to aid in controlling the eruption.²⁷ The exact mechanism of how GD resolves while continuing therapy is unknown; however, it has been suggested that a GD eruption may be the consequence of a BRAF and MEK inhibitor–mediated immune response against a subclinical area of metastatic melanoma.²⁸ If the immune response successfully eliminates the subclinical tumor, one could postulate that the inflammatory response and granulomatous eruption would resolve. Future studies are necessary to further elucidate the exact mechanisms involved.

There have been several case reports of GD with vemurafenib treatment,^29,30 1 report of GD and erythema induratum with vemurafenib and cobimetinib treatment,³¹ 2 reports of GD with dabrafenib treatment,^27,30 and a few reports of GD with the BRAF inhibitor dabrafenib combined with the MEK inhibitor trametinib,^28,32,33 all for the treatment of metastatic melanoma. Additionally, a report described a 3-year-old boy who developed GD secondary to vemurafenib for the treatment of Langerhans cell histiocytosis.³⁴ We present a unique case of BRAF and MEK inhibitor therapy–induced GD in the treatment of metastatic cholangiocarcinoma with vemurafenib and cobimetinib.

BRAF and MEK inhibitor therapy is used in patients with metastatic melanomas with a positive BRAF V600E mutation. Due to advancements in next-generation DNA sequencing, these therapies also are being tested in clinical trials for use in the treatment of other cancers with the same checkpoint mutation, such as metastatic cholangiocarcinoma. Cutaneous reactions frequently are documented side effects that occur during treatment with BRAF and MEK inhibitors; GD is an uncommon finding. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of other cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation.

To the Editor:

Granulomatous dermatitis (GD) has been described as a rare side effect of MEK and BRAF inhibitor use in the treatment of BRAF V600E mutation–positive metastatic melanoma. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation. We present the case of a 52-year-old woman who developed GD while being treated with vemurafenib and cobimetinib for BRAF V600E mutation–positive metastatic cholangiocarcinoma.

A 52-year-old White woman presented with faint patches of nonpalpable violaceous mottling that extended distally to proximally from the ankles to the thighs on the medial aspects of both legs. She was diagnosed with cholangiocarcinoma 10 months prior, with metastases to the lung, liver, and sternum. She underwent treatment with gemcitabine and cisplatin therapy. Computed tomography after several treatment cycles revealed progressive disease with multiple pulmonary nodules as well as metastatic intrathoracic and abdominal adenopathy. Treatment with gemcitabine and cisplatin failed to produce a favorable response and was discontinued after 6 treatment cycles.

Genomic testing performed at the time of diagnosis revealed a positive mutation for BRAF V600E. The patient subsequently enrolled in a clinical trial and started treatment with the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib. She developed sun sensitivity and multiple sunburns after starting these therapies. The patient tolerated the next few cycles of therapy well with only moderate concerns of dry sensitive skin.

During the sixth cycle of therapy, she presented to dermatology after developing a rash. Over the next 2 weeks, similar lesions appeared on the arms. The patient denied the use of any new lotions, soaps, or other medications. Punch biopsies of the right forearm and right medial thigh revealed nonnecrotizing granulomas in the superficial dermis that extended into the subcutaneous adipose tissue (Figure 1). Surrounding chronic inflammation was scant, and the presence of rare eosinophils was noted (Figure 2). The histiocytes were highlighted by a CD68 immunohistochemical stain. An auramine-O special stain test was negative for acid-fast bacilli, and a Grocott methenamine-silver special stain test for fungal organisms was negative. These findings were consistent with GD. Computed tomography of the chest performed 2 months prior and 1 month after biopsy of the skin lesions revealed no axillary, mediastinal, or hilar lymphadenopathy. The calcium level at the time of skin biopsy was within reference range.

A topical steroid was prescribed; however, it was not utilized by the patient. Within 2 months of onset, the GD lesions resolved with no treatment. The GD lesions did not affect the patient’s enrollment in the clinical trial, and no dose reductions were made. Due to progressive disease with metastases to the brain, the patient eventually discontinued the clinical trial.

BRAF inhibitors are US Food and Drug Administration approved for the treatment of metastatic melanoma to deactivate the serine-threonine kinase BRAF gene mutation, which leads to decreased generation and survival of melanoma cells.^1,2 Vemurafenib, dabrafenib, and encorafenib are the only BRAF inhibitors approved in the United States.³ The most common side effects of vemurafenib include arthralgia, fatigue, rash, and photosensitivity.^1,4 There are 4 MEK inhibitors currently available in the United States: cobimetinib, trametinib, selumetinib and binimetinib. The addition of a MEK inhibitor to BRAF inhibitor therapy has shown increased patient response rates and prolonged survival in 3 phase 3 studies.^5-10

Response rates remain low in the treatment of advanced cholangiocarcinoma with standard chemotherapy. Recent research has explored if targeted therapies at the molecular level would be of benefit.¹¹ Our patient was enrolled in the American Society of Clinical Oncology Targeted Agent and Profiling Utilization Registry (TAPUR) trial, a phase 2, prospective, nonrandomized trial that matches eligible participants to US Food and Drug Administration–approved study medications based on specific data from their molecular testing results.¹² Some of the most common mutations in intrahepatic cholangiocarcinoma include HER2, KRAS, MET, and BRAF.^13-17 Our patient’s molecular test results were positive for a BRAF V600E–positive mutation, and she subsequently started therapy with vemurafenib and cobimetinib. The use of personalized genomic treatment approaches for BRAF V600E mutation–positive cholangiocarcinoma has produced a dramatic patient response to BRAF and MEK inhibitor combination therapies.^11,18-20

Drug-induced GD most likely is caused by vascular insults that lead to deposition of immune complexes in vessels causing inflammation and a consequent granulomatous infiltrate.^21,22 Although cordlike lesions in the subcutaneous tissue on the trunk commonly are reported, the presentation of GD can vary considerably. Other presentations include areas of violaceous or erythematous patches or plaques on the limbs, intertriginous areas, and upper trunk. Diffuse macular erythema or small flesh-colored papules also can be observed.²³

Granulomatous dermatitis secondary to drug reactions can have varying morphologies. The infiltrate often can have an interstitial appearance with the presence of lymphocytes, plasma cells, histiocytes, eosinophils, and multinucleated giant cells.²⁴ These findings can be confused with interstitial granuloma annulare. Other cases, such as in our patient, can have discrete granulomata formation with a sarcoidlike appearance. These naked granulomas lack surrounding inflammation and suggest a differential diagnosis of sarcoidosis and infection. Use of immune checkpoint inhibitors (CIs) and kinase inhibitors has been proven to cause sarcoidosislike reactions.²⁵ The development of granulomatous/sarcoidlike lesions associated with the use of BRAF and MEK inhibitors may clinically and radiographically mimic disease recurrence. An awareness of this type of reaction by clinicians and pathologists is important to ensure appropriate management in patients who develop GD.²⁶

Checkpoint inhibitor–induced GD that remains asymptomatic does not necessarily warrant treatment; however, corticosteroid use and elimination of CI therapies have resolved GD in prior cases. Responsiveness of the cancer to CI therapy and severity of GD symptoms should be considered before discontinuation of a CI trial.²⁵

One case report described complete resolution of a GD eruption without interruption of the scheduled BRAF and MEK inhibitor therapies for the treatment of metastatic melanoma. There was no reported use of a steroidal cream or other topical medication to aid in controlling the eruption.²⁷ The exact mechanism of how GD resolves while continuing therapy is unknown; however, it has been suggested that a GD eruption may be the consequence of a BRAF and MEK inhibitor–mediated immune response against a subclinical area of metastatic melanoma.²⁸ If the immune response successfully eliminates the subclinical tumor, one could postulate that the inflammatory response and granulomatous eruption would resolve. Future studies are necessary to further elucidate the exact mechanisms involved.

There have been several case reports of GD with vemurafenib treatment,^29,30 1 report of GD and erythema induratum with vemurafenib and cobimetinib treatment,³¹ 2 reports of GD with dabrafenib treatment,^27,30 and a few reports of GD with the BRAF inhibitor dabrafenib combined with the MEK inhibitor trametinib,^28,32,33 all for the treatment of metastatic melanoma. Additionally, a report described a 3-year-old boy who developed GD secondary to vemurafenib for the treatment of Langerhans cell histiocytosis.³⁴ We present a unique case of BRAF and MEK inhibitor therapy–induced GD in the treatment of metastatic cholangiocarcinoma with vemurafenib and cobimetinib.

BRAF and MEK inhibitor therapy is used in patients with metastatic melanomas with a positive BRAF V600E mutation. Due to advancements in next-generation DNA sequencing, these therapies also are being tested in clinical trials for use in the treatment of other cancers with the same checkpoint mutation, such as metastatic cholangiocarcinoma. Cutaneous reactions frequently are documented side effects that occur during treatment with BRAF and MEK inhibitors; GD is an uncommon finding. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of other cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation.

To the Editor:

Granulomatous dermatitis (GD) has been described as a rare side effect of MEK and BRAF inhibitor use in the treatment of BRAF V600E mutation–positive metastatic melanoma. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation. We present the case of a 52-year-old woman who developed GD while being treated with vemurafenib and cobimetinib for BRAF V600E mutation–positive metastatic cholangiocarcinoma.

A 52-year-old White woman presented with faint patches of nonpalpable violaceous mottling that extended distally to proximally from the ankles to the thighs on the medial aspects of both legs. She was diagnosed with cholangiocarcinoma 10 months prior, with metastases to the lung, liver, and sternum. She underwent treatment with gemcitabine and cisplatin therapy. Computed tomography after several treatment cycles revealed progressive disease with multiple pulmonary nodules as well as metastatic intrathoracic and abdominal adenopathy. Treatment with gemcitabine and cisplatin failed to produce a favorable response and was discontinued after 6 treatment cycles.

Genomic testing performed at the time of diagnosis revealed a positive mutation for BRAF V600E. The patient subsequently enrolled in a clinical trial and started treatment with the BRAF inhibitor vemurafenib and the MEK inhibitor cobimetinib. She developed sun sensitivity and multiple sunburns after starting these therapies. The patient tolerated the next few cycles of therapy well with only moderate concerns of dry sensitive skin.

During the sixth cycle of therapy, she presented to dermatology after developing a rash. Over the next 2 weeks, similar lesions appeared on the arms. The patient denied the use of any new lotions, soaps, or other medications. Punch biopsies of the right forearm and right medial thigh revealed nonnecrotizing granulomas in the superficial dermis that extended into the subcutaneous adipose tissue (Figure 1). Surrounding chronic inflammation was scant, and the presence of rare eosinophils was noted (Figure 2). The histiocytes were highlighted by a CD68 immunohistochemical stain. An auramine-O special stain test was negative for acid-fast bacilli, and a Grocott methenamine-silver special stain test for fungal organisms was negative. These findings were consistent with GD. Computed tomography of the chest performed 2 months prior and 1 month after biopsy of the skin lesions revealed no axillary, mediastinal, or hilar lymphadenopathy. The calcium level at the time of skin biopsy was within reference range.

A topical steroid was prescribed; however, it was not utilized by the patient. Within 2 months of onset, the GD lesions resolved with no treatment. The GD lesions did not affect the patient’s enrollment in the clinical trial, and no dose reductions were made. Due to progressive disease with metastases to the brain, the patient eventually discontinued the clinical trial.

BRAF inhibitors are US Food and Drug Administration approved for the treatment of metastatic melanoma to deactivate the serine-threonine kinase BRAF gene mutation, which leads to decreased generation and survival of melanoma cells.^1,2 Vemurafenib, dabrafenib, and encorafenib are the only BRAF inhibitors approved in the United States.³ The most common side effects of vemurafenib include arthralgia, fatigue, rash, and photosensitivity.^1,4 There are 4 MEK inhibitors currently available in the United States: cobimetinib, trametinib, selumetinib and binimetinib. The addition of a MEK inhibitor to BRAF inhibitor therapy has shown increased patient response rates and prolonged survival in 3 phase 3 studies.^5-10

Response rates remain low in the treatment of advanced cholangiocarcinoma with standard chemotherapy. Recent research has explored if targeted therapies at the molecular level would be of benefit.¹¹ Our patient was enrolled in the American Society of Clinical Oncology Targeted Agent and Profiling Utilization Registry (TAPUR) trial, a phase 2, prospective, nonrandomized trial that matches eligible participants to US Food and Drug Administration–approved study medications based on specific data from their molecular testing results.¹² Some of the most common mutations in intrahepatic cholangiocarcinoma include HER2, KRAS, MET, and BRAF.^13-17 Our patient’s molecular test results were positive for a BRAF V600E–positive mutation, and she subsequently started therapy with vemurafenib and cobimetinib. The use of personalized genomic treatment approaches for BRAF V600E mutation–positive cholangiocarcinoma has produced a dramatic patient response to BRAF and MEK inhibitor combination therapies.^11,18-20

Drug-induced GD most likely is caused by vascular insults that lead to deposition of immune complexes in vessels causing inflammation and a consequent granulomatous infiltrate.^21,22 Although cordlike lesions in the subcutaneous tissue on the trunk commonly are reported, the presentation of GD can vary considerably. Other presentations include areas of violaceous or erythematous patches or plaques on the limbs, intertriginous areas, and upper trunk. Diffuse macular erythema or small flesh-colored papules also can be observed.²³

Granulomatous dermatitis secondary to drug reactions can have varying morphologies. The infiltrate often can have an interstitial appearance with the presence of lymphocytes, plasma cells, histiocytes, eosinophils, and multinucleated giant cells.²⁴ These findings can be confused with interstitial granuloma annulare. Other cases, such as in our patient, can have discrete granulomata formation with a sarcoidlike appearance. These naked granulomas lack surrounding inflammation and suggest a differential diagnosis of sarcoidosis and infection. Use of immune checkpoint inhibitors (CIs) and kinase inhibitors has been proven to cause sarcoidosislike reactions.²⁵ The development of granulomatous/sarcoidlike lesions associated with the use of BRAF and MEK inhibitors may clinically and radiographically mimic disease recurrence. An awareness of this type of reaction by clinicians and pathologists is important to ensure appropriate management in patients who develop GD.²⁶

Checkpoint inhibitor–induced GD that remains asymptomatic does not necessarily warrant treatment; however, corticosteroid use and elimination of CI therapies have resolved GD in prior cases. Responsiveness of the cancer to CI therapy and severity of GD symptoms should be considered before discontinuation of a CI trial.²⁵

One case report described complete resolution of a GD eruption without interruption of the scheduled BRAF and MEK inhibitor therapies for the treatment of metastatic melanoma. There was no reported use of a steroidal cream or other topical medication to aid in controlling the eruption.²⁷ The exact mechanism of how GD resolves while continuing therapy is unknown; however, it has been suggested that a GD eruption may be the consequence of a BRAF and MEK inhibitor–mediated immune response against a subclinical area of metastatic melanoma.²⁸ If the immune response successfully eliminates the subclinical tumor, one could postulate that the inflammatory response and granulomatous eruption would resolve. Future studies are necessary to further elucidate the exact mechanisms involved.

There have been several case reports of GD with vemurafenib treatment,^29,30 1 report of GD and erythema induratum with vemurafenib and cobimetinib treatment,³¹ 2 reports of GD with dabrafenib treatment,^27,30 and a few reports of GD with the BRAF inhibitor dabrafenib combined with the MEK inhibitor trametinib,^28,32,33 all for the treatment of metastatic melanoma. Additionally, a report described a 3-year-old boy who developed GD secondary to vemurafenib for the treatment of Langerhans cell histiocytosis.³⁴ We present a unique case of BRAF and MEK inhibitor therapy–induced GD in the treatment of metastatic cholangiocarcinoma with vemurafenib and cobimetinib.

BRAF and MEK inhibitor therapy is used in patients with metastatic melanomas with a positive BRAF V600E mutation. Due to advancements in next-generation DNA sequencing, these therapies also are being tested in clinical trials for use in the treatment of other cancers with the same checkpoint mutation, such as metastatic cholangiocarcinoma. Cutaneous reactions frequently are documented side effects that occur during treatment with BRAF and MEK inhibitors; GD is an uncommon finding. As the utilization of BRAF and MEK inhibitors increases for the treatment of a variety of other cancers, it is essential that clinicians and pathologists recognize GD as a potential cutaneous manifestation.

Atopic dermatitis (AD) and psoriasis are common skin diseases in which dysfunction of the epidermal barrier leads to skin inflammation and altered expression of proinflammatory cytokines.¹ There often is overlap in the clinical and histopathologic features of AD and psoriasis, which can make diagnosis a challenge. Persistent late-stage AD can present with psoriasiform lichenified changes, and psoriasis lesions in the acute stage can have an eczematous appearance.² Histologically, chronic psoriasis lesions share many overlapping features with AD, and some subsets of AD with IL-17 predominance (ie, intrinsic, pediatric, presentation in Asian patients) exhibit a psoriasiform appearance.^3,4

Atopic dermatitis and psoriasis are considered 2 distinct conditions because AD is a helper T cell (T_H2)–driven disease with subsequent overproduction of IL-4 and IL-13 and psoriasis is a T_H17 cell–driven disease with overproduction of IL-17³; however, the shared features of AD and psoriasis represent an underlying immunopathological spectrum^2,5,6 in which one condition can develop following treatment of the other condition (immunological shift in pathways), both conditions can occur at different times in a patient’s life with alternating cycles of disease flares, or both conditions can coexist as an overlapping syndrome.^1,2 A retrospective study from 2012 to 2019 estimated the prevalence of concomitant AD and psoriasis in the United States at 1.3%, with AD following the diagnosis of psoriasis in 67% of cases.¹ Concurrent AD and psoriasis—when both diseases flaresimultaneously—is the rarest scenario.^2,5

Treatment modalities for AD include topical corticosteroids, which act on immune cells to suppress the release of proinflammatory cytokines, as well as dupilumab, which offers targeted blockade of involved cytokines IL-4 and IL-13. Psoriasis can be treated with multiple immune modulators, including topical corticosteroids and vitamin D analogs, as well as systemic medications that reduce T-cell activation and inflammatory cytokines through targeting of IFN-γ, IL-2, tumor necrosis factor α, IL-17, and IL-23.^7,8

We present the case of a patient with long-standing concurrent, treatment-resistant AD and psoriasis who was successfully treated with dual biologic therapy with guselkumab and dupilumab.

Case Report

A 62-year-old woman presented to our dermatology clinic with red itchy scales and painful fissures on the palms, hands, and soles of more than 12 years’ duration. Her medical history included an allergy to amoxicillin-clavulanate as well as an allergy to both dog and cat dander on prick testing. Her family history included dyshidrotic eczema in her mother. A complete blood cell count with differential was within reference range. A shave biopsy of the right dorsal hand performed at the onset of symptoms at an outside facility revealed hyperkeratotic acanthotic epidermis with a mild perivascular lymphocytic infiltrate.

Results of patch testing indicated contact hypersensitivity to the botanical rosin colophonium (or colophony); carba mix (1, 3-diphenylguanidine, zinc dibutyldithiocarbamate, and zinc diethydithiocarbamate); thiuram mix (tetramethylthiuram disulfide, tetramethylthiuram monosulfide, and tetraethylthiuram disulfide); n,n-diphenylguanidine; and tixocortol-21-pivalate. Our patient was given guidance on avoiding these agents, as it was suspected that exposure may be exacerbating the psoriasis. The psoriasis was treated with topical corticosteroids, keratolytics, and calcineurin inhibitors, all of which offered minimal or no relief. Trials of systemic agents, including methotrexate (discontinued because transaminitis developed), etanercept, adalimumab, and apremilast for 6 to 10 months did not provide improvement.

Two years prior to the current presentation, our patient had been treated with the IL-23 inhibitor guselkumab, which provided moderate improvement. When she presented to our clinic, physical examination while she was taking guselkumab demonstrated prurigo with excoriations of the extremities, hyperkeratosis with scaling and fissures of the soles, erythematous scaly plaques on the palms and dorsal surface of the hands, and mild onycholysis of the nails (Figures 1 and 2). Because we were concerned about concomitant intrinsic AD, dupilumab was initiated in conjunction with guselkumab. A second biopsy was considered but deferred in favor of clinical monitoring.

After 1 year of dual biologic therapy, the patient experienced near-complete resolution of symptoms. The psoriasis completely resolved from an initial body surface area of 5%, and the AD body surface area decreased from 30% to 2% (Figure 3). The patient reported no adverse effects from treatment.

Comment

Atopic dermatitis and psoriasis involve complex immunopathology and a spectrum of cytokines that might explain the overlap in their clinical and histopathologic presentations.

Atopic dermatitis—Atopic dermatitis involves T_H1, T_H2, T_H9, T_H17, and T_H22 cells; T_H2 cells release IL-4, IL-5, and IL-13, all of which are key cytokines in the inflammatory pathway of AD.^9,10 Activation of the helper T-cell subset and the release of cytokines differ slightly based on the subcategory of AD and the stage of exacerbation. In addition to T_H2-cell activation, T_H1 cells and T_H22 cells—which release IL-12 and IL-22, respectively—are active in both intrinsic and extrinsic AD. T_H17 cells and T_H9 cells—which release IL-17 and IL-9, respectively—are more prominent in the intrinsic pathway than in the extrinsic pathway.⁹ Intrinsic AD is recognized by a lack of eosinophilia, female predominance, and delayed onset compared to extrinsic AD; there also is a lack of history of atopy.¹ Extrinsic AD is characterized by eosinophilia as well as a personal and family history of atopy.¹¹ Our patient—a female with onset in older adulthood, lack of eosinophilia, and a family history of atopy—displayed features of both intrinsic and extrinsic AD.

Psoriasis—The immunopathology of psoriasis involves stimulation of dendritic cells, which activate T_H17 cells through IL-23. T_H17 cells then release IL-17 and IL-22. Therefore, both AD and psoriasis involve activation of T_H22 and T_H1 cells, with increased IL-17 and IL-22 production.^3,10,12 IL-17 and IL-22 induce epidermal hyperplasia; IL-22 also contributes to skin barrier dysfunction.¹² Therefore, it might be reasonable to consider psoriasis and AD as diseases that exist across a T-cell axis spectrum, thereby accounting for some overlap in disease characteristics.³

Dual Biologic Therapy—Dupilumab blocks the IL-4 receptor α subunit, a receptor for IL-4 and IL-13, which are key cytokines in the pathogenesis of AD.¹⁰ Guselkumab inhibits IL-23, thus blocking the inflammatory cascade of T_H17 cell activation and release of IL-17 and IL-22 in the psoriasis pathway.¹³ Although an immunopathological spectrum exists between the 2 diseases, the continued presence of AD symptoms after blocking the IL-23 cascade suggests that additional blockade of T_H2 cells is required to control AD in patients with true concurrent disease.

Accurate diagnosis of AD and/or psoriasis is important when considering targeted treatment of these conditions with biologics. The use of dual biologics is limited by a paucity of data regarding the safety of these agents when given in combination. A recent meta-analysis of dual biologic therapy in patients with inflammatory bowel disease demonstrated acceptable safety results with a pooled adverse reaction rate of 31%.¹⁴

Anchoring Bias—Anchoring bias can occur when a clinician’s decisions are influenced by a particular event or reference point, which might cause them to disregard subsequent evidence. Our case illustrates the importance of critically assessing the response to treatment and being mindful of the potential influence of anchoring bias on the differential diagnosis. Although overcoming biases in conditions with clinical overlap can be challenging, it is important to consider coexisting AD and psoriasis in patients with extensive hand involvement when multiple treatments have failed and only a partial response to targeted pathways has been achieved. In our case, the patient also had contact hypersensitivity to tixocortol-21-pivalate, which indicates hypersensitivity to many prescription topical corticosteroids, oral prednisone, and over-the-counter hydrocortisone; however, topical corticosteroids continued to be prescribed for her, which might have contributed to the lack of improvement and even exacerbated the rash.

Future Considerations—A consideration for the future in this case is discontinuing guselkumab to observe whether symptoms recur. We discussed this option with the patient, but she opted to continue treatment with dupilumab and guselkumab because of the symptom resolution.

Conclusion

Concomitant disease can present as an overlapping pattern in the same area, whereas other regions might have geographically isolated disease. Our patient’s overlap of symptoms, the failure of multiple treatments, and the partial improvement she experienced on guselkumab made diagnosis and management challenging; however, dual biologic therapy was successful.

Atopic dermatitis (AD) and psoriasis are common skin diseases in which dysfunction of the epidermal barrier leads to skin inflammation and altered expression of proinflammatory cytokines.¹ There often is overlap in the clinical and histopathologic features of AD and psoriasis, which can make diagnosis a challenge. Persistent late-stage AD can present with psoriasiform lichenified changes, and psoriasis lesions in the acute stage can have an eczematous appearance.² Histologically, chronic psoriasis lesions share many overlapping features with AD, and some subsets of AD with IL-17 predominance (ie, intrinsic, pediatric, presentation in Asian patients) exhibit a psoriasiform appearance.^3,4

Atopic dermatitis and psoriasis are considered 2 distinct conditions because AD is a helper T cell (T_H2)–driven disease with subsequent overproduction of IL-4 and IL-13 and psoriasis is a T_H17 cell–driven disease with overproduction of IL-17³; however, the shared features of AD and psoriasis represent an underlying immunopathological spectrum^2,5,6 in which one condition can develop following treatment of the other condition (immunological shift in pathways), both conditions can occur at different times in a patient’s life with alternating cycles of disease flares, or both conditions can coexist as an overlapping syndrome.^1,2 A retrospective study from 2012 to 2019 estimated the prevalence of concomitant AD and psoriasis in the United States at 1.3%, with AD following the diagnosis of psoriasis in 67% of cases.¹ Concurrent AD and psoriasis—when both diseases flaresimultaneously—is the rarest scenario.^2,5

Treatment modalities for AD include topical corticosteroids, which act on immune cells to suppress the release of proinflammatory cytokines, as well as dupilumab, which offers targeted blockade of involved cytokines IL-4 and IL-13. Psoriasis can be treated with multiple immune modulators, including topical corticosteroids and vitamin D analogs, as well as systemic medications that reduce T-cell activation and inflammatory cytokines through targeting of IFN-γ, IL-2, tumor necrosis factor α, IL-17, and IL-23.^7,8

We present the case of a patient with long-standing concurrent, treatment-resistant AD and psoriasis who was successfully treated with dual biologic therapy with guselkumab and dupilumab.

Case Report

A 62-year-old woman presented to our dermatology clinic with red itchy scales and painful fissures on the palms, hands, and soles of more than 12 years’ duration. Her medical history included an allergy to amoxicillin-clavulanate as well as an allergy to both dog and cat dander on prick testing. Her family history included dyshidrotic eczema in her mother. A complete blood cell count with differential was within reference range. A shave biopsy of the right dorsal hand performed at the onset of symptoms at an outside facility revealed hyperkeratotic acanthotic epidermis with a mild perivascular lymphocytic infiltrate.

Results of patch testing indicated contact hypersensitivity to the botanical rosin colophonium (or colophony); carba mix (1, 3-diphenylguanidine, zinc dibutyldithiocarbamate, and zinc diethydithiocarbamate); thiuram mix (tetramethylthiuram disulfide, tetramethylthiuram monosulfide, and tetraethylthiuram disulfide); n,n-diphenylguanidine; and tixocortol-21-pivalate. Our patient was given guidance on avoiding these agents, as it was suspected that exposure may be exacerbating the psoriasis. The psoriasis was treated with topical corticosteroids, keratolytics, and calcineurin inhibitors, all of which offered minimal or no relief. Trials of systemic agents, including methotrexate (discontinued because transaminitis developed), etanercept, adalimumab, and apremilast for 6 to 10 months did not provide improvement.

Two years prior to the current presentation, our patient had been treated with the IL-23 inhibitor guselkumab, which provided moderate improvement. When she presented to our clinic, physical examination while she was taking guselkumab demonstrated prurigo with excoriations of the extremities, hyperkeratosis with scaling and fissures of the soles, erythematous scaly plaques on the palms and dorsal surface of the hands, and mild onycholysis of the nails (Figures 1 and 2). Because we were concerned about concomitant intrinsic AD, dupilumab was initiated in conjunction with guselkumab. A second biopsy was considered but deferred in favor of clinical monitoring.

After 1 year of dual biologic therapy, the patient experienced near-complete resolution of symptoms. The psoriasis completely resolved from an initial body surface area of 5%, and the AD body surface area decreased from 30% to 2% (Figure 3). The patient reported no adverse effects from treatment.

Comment

Atopic dermatitis and psoriasis involve complex immunopathology and a spectrum of cytokines that might explain the overlap in their clinical and histopathologic presentations.

Atopic dermatitis—Atopic dermatitis involves T_H1, T_H2, T_H9, T_H17, and T_H22 cells; T_H2 cells release IL-4, IL-5, and IL-13, all of which are key cytokines in the inflammatory pathway of AD.^9,10 Activation of the helper T-cell subset and the release of cytokines differ slightly based on the subcategory of AD and the stage of exacerbation. In addition to T_H2-cell activation, T_H1 cells and T_H22 cells—which release IL-12 and IL-22, respectively—are active in both intrinsic and extrinsic AD. T_H17 cells and T_H9 cells—which release IL-17 and IL-9, respectively—are more prominent in the intrinsic pathway than in the extrinsic pathway.⁹ Intrinsic AD is recognized by a lack of eosinophilia, female predominance, and delayed onset compared to extrinsic AD; there also is a lack of history of atopy.¹ Extrinsic AD is characterized by eosinophilia as well as a personal and family history of atopy.¹¹ Our patient—a female with onset in older adulthood, lack of eosinophilia, and a family history of atopy—displayed features of both intrinsic and extrinsic AD.

Psoriasis—The immunopathology of psoriasis involves stimulation of dendritic cells, which activate T_H17 cells through IL-23. T_H17 cells then release IL-17 and IL-22. Therefore, both AD and psoriasis involve activation of T_H22 and T_H1 cells, with increased IL-17 and IL-22 production.^3,10,12 IL-17 and IL-22 induce epidermal hyperplasia; IL-22 also contributes to skin barrier dysfunction.¹² Therefore, it might be reasonable to consider psoriasis and AD as diseases that exist across a T-cell axis spectrum, thereby accounting for some overlap in disease characteristics.³

Dual Biologic Therapy—Dupilumab blocks the IL-4 receptor α subunit, a receptor for IL-4 and IL-13, which are key cytokines in the pathogenesis of AD.¹⁰ Guselkumab inhibits IL-23, thus blocking the inflammatory cascade of T_H17 cell activation and release of IL-17 and IL-22 in the psoriasis pathway.¹³ Although an immunopathological spectrum exists between the 2 diseases, the continued presence of AD symptoms after blocking the IL-23 cascade suggests that additional blockade of T_H2 cells is required to control AD in patients with true concurrent disease.

Accurate diagnosis of AD and/or psoriasis is important when considering targeted treatment of these conditions with biologics. The use of dual biologics is limited by a paucity of data regarding the safety of these agents when given in combination. A recent meta-analysis of dual biologic therapy in patients with inflammatory bowel disease demonstrated acceptable safety results with a pooled adverse reaction rate of 31%.¹⁴

Anchoring Bias—Anchoring bias can occur when a clinician’s decisions are influenced by a particular event or reference point, which might cause them to disregard subsequent evidence. Our case illustrates the importance of critically assessing the response to treatment and being mindful of the potential influence of anchoring bias on the differential diagnosis. Although overcoming biases in conditions with clinical overlap can be challenging, it is important to consider coexisting AD and psoriasis in patients with extensive hand involvement when multiple treatments have failed and only a partial response to targeted pathways has been achieved. In our case, the patient also had contact hypersensitivity to tixocortol-21-pivalate, which indicates hypersensitivity to many prescription topical corticosteroids, oral prednisone, and over-the-counter hydrocortisone; however, topical corticosteroids continued to be prescribed for her, which might have contributed to the lack of improvement and even exacerbated the rash.

Future Considerations—A consideration for the future in this case is discontinuing guselkumab to observe whether symptoms recur. We discussed this option with the patient, but she opted to continue treatment with dupilumab and guselkumab because of the symptom resolution.

Conclusion

Concomitant disease can present as an overlapping pattern in the same area, whereas other regions might have geographically isolated disease. Our patient’s overlap of symptoms, the failure of multiple treatments, and the partial improvement she experienced on guselkumab made diagnosis and management challenging; however, dual biologic therapy was successful.

Atopic dermatitis (AD) and psoriasis are common skin diseases in which dysfunction of the epidermal barrier leads to skin inflammation and altered expression of proinflammatory cytokines.¹ There often is overlap in the clinical and histopathologic features of AD and psoriasis, which can make diagnosis a challenge. Persistent late-stage AD can present with psoriasiform lichenified changes, and psoriasis lesions in the acute stage can have an eczematous appearance.² Histologically, chronic psoriasis lesions share many overlapping features with AD, and some subsets of AD with IL-17 predominance (ie, intrinsic, pediatric, presentation in Asian patients) exhibit a psoriasiform appearance.^3,4

Atopic dermatitis and psoriasis are considered 2 distinct conditions because AD is a helper T cell (T_H2)–driven disease with subsequent overproduction of IL-4 and IL-13 and psoriasis is a T_H17 cell–driven disease with overproduction of IL-17³; however, the shared features of AD and psoriasis represent an underlying immunopathological spectrum^2,5,6 in which one condition can develop following treatment of the other condition (immunological shift in pathways), both conditions can occur at different times in a patient’s life with alternating cycles of disease flares, or both conditions can coexist as an overlapping syndrome.^1,2 A retrospective study from 2012 to 2019 estimated the prevalence of concomitant AD and psoriasis in the United States at 1.3%, with AD following the diagnosis of psoriasis in 67% of cases.¹ Concurrent AD and psoriasis—when both diseases flaresimultaneously—is the rarest scenario.^2,5

Treatment modalities for AD include topical corticosteroids, which act on immune cells to suppress the release of proinflammatory cytokines, as well as dupilumab, which offers targeted blockade of involved cytokines IL-4 and IL-13. Psoriasis can be treated with multiple immune modulators, including topical corticosteroids and vitamin D analogs, as well as systemic medications that reduce T-cell activation and inflammatory cytokines through targeting of IFN-γ, IL-2, tumor necrosis factor α, IL-17, and IL-23.^7,8

We present the case of a patient with long-standing concurrent, treatment-resistant AD and psoriasis who was successfully treated with dual biologic therapy with guselkumab and dupilumab.

Case Report

A 62-year-old woman presented to our dermatology clinic with red itchy scales and painful fissures on the palms, hands, and soles of more than 12 years’ duration. Her medical history included an allergy to amoxicillin-clavulanate as well as an allergy to both dog and cat dander on prick testing. Her family history included dyshidrotic eczema in her mother. A complete blood cell count with differential was within reference range. A shave biopsy of the right dorsal hand performed at the onset of symptoms at an outside facility revealed hyperkeratotic acanthotic epidermis with a mild perivascular lymphocytic infiltrate.

Results of patch testing indicated contact hypersensitivity to the botanical rosin colophonium (or colophony); carba mix (1, 3-diphenylguanidine, zinc dibutyldithiocarbamate, and zinc diethydithiocarbamate); thiuram mix (tetramethylthiuram disulfide, tetramethylthiuram monosulfide, and tetraethylthiuram disulfide); n,n-diphenylguanidine; and tixocortol-21-pivalate. Our patient was given guidance on avoiding these agents, as it was suspected that exposure may be exacerbating the psoriasis. The psoriasis was treated with topical corticosteroids, keratolytics, and calcineurin inhibitors, all of which offered minimal or no relief. Trials of systemic agents, including methotrexate (discontinued because transaminitis developed), etanercept, adalimumab, and apremilast for 6 to 10 months did not provide improvement.

Two years prior to the current presentation, our patient had been treated with the IL-23 inhibitor guselkumab, which provided moderate improvement. When she presented to our clinic, physical examination while she was taking guselkumab demonstrated prurigo with excoriations of the extremities, hyperkeratosis with scaling and fissures of the soles, erythematous scaly plaques on the palms and dorsal surface of the hands, and mild onycholysis of the nails (Figures 1 and 2). Because we were concerned about concomitant intrinsic AD, dupilumab was initiated in conjunction with guselkumab. A second biopsy was considered but deferred in favor of clinical monitoring.

After 1 year of dual biologic therapy, the patient experienced near-complete resolution of symptoms. The psoriasis completely resolved from an initial body surface area of 5%, and the AD body surface area decreased from 30% to 2% (Figure 3). The patient reported no adverse effects from treatment.

Comment

Atopic dermatitis and psoriasis involve complex immunopathology and a spectrum of cytokines that might explain the overlap in their clinical and histopathologic presentations.

Atopic dermatitis—Atopic dermatitis involves T_H1, T_H2, T_H9, T_H17, and T_H22 cells; T_H2 cells release IL-4, IL-5, and IL-13, all of which are key cytokines in the inflammatory pathway of AD.^9,10 Activation of the helper T-cell subset and the release of cytokines differ slightly based on the subcategory of AD and the stage of exacerbation. In addition to T_H2-cell activation, T_H1 cells and T_H22 cells—which release IL-12 and IL-22, respectively—are active in both intrinsic and extrinsic AD. T_H17 cells and T_H9 cells—which release IL-17 and IL-9, respectively—are more prominent in the intrinsic pathway than in the extrinsic pathway.⁹ Intrinsic AD is recognized by a lack of eosinophilia, female predominance, and delayed onset compared to extrinsic AD; there also is a lack of history of atopy.¹ Extrinsic AD is characterized by eosinophilia as well as a personal and family history of atopy.¹¹ Our patient—a female with onset in older adulthood, lack of eosinophilia, and a family history of atopy—displayed features of both intrinsic and extrinsic AD.

Psoriasis—The immunopathology of psoriasis involves stimulation of dendritic cells, which activate T_H17 cells through IL-23. T_H17 cells then release IL-17 and IL-22. Therefore, both AD and psoriasis involve activation of T_H22 and T_H1 cells, with increased IL-17 and IL-22 production.^3,10,12 IL-17 and IL-22 induce epidermal hyperplasia; IL-22 also contributes to skin barrier dysfunction.¹² Therefore, it might be reasonable to consider psoriasis and AD as diseases that exist across a T-cell axis spectrum, thereby accounting for some overlap in disease characteristics.³

Dual Biologic Therapy—Dupilumab blocks the IL-4 receptor α subunit, a receptor for IL-4 and IL-13, which are key cytokines in the pathogenesis of AD.¹⁰ Guselkumab inhibits IL-23, thus blocking the inflammatory cascade of T_H17 cell activation and release of IL-17 and IL-22 in the psoriasis pathway.¹³ Although an immunopathological spectrum exists between the 2 diseases, the continued presence of AD symptoms after blocking the IL-23 cascade suggests that additional blockade of T_H2 cells is required to control AD in patients with true concurrent disease.

Accurate diagnosis of AD and/or psoriasis is important when considering targeted treatment of these conditions with biologics. The use of dual biologics is limited by a paucity of data regarding the safety of these agents when given in combination. A recent meta-analysis of dual biologic therapy in patients with inflammatory bowel disease demonstrated acceptable safety results with a pooled adverse reaction rate of 31%.¹⁴

Anchoring Bias—Anchoring bias can occur when a clinician’s decisions are influenced by a particular event or reference point, which might cause them to disregard subsequent evidence. Our case illustrates the importance of critically assessing the response to treatment and being mindful of the potential influence of anchoring bias on the differential diagnosis. Although overcoming biases in conditions with clinical overlap can be challenging, it is important to consider coexisting AD and psoriasis in patients with extensive hand involvement when multiple treatments have failed and only a partial response to targeted pathways has been achieved. In our case, the patient also had contact hypersensitivity to tixocortol-21-pivalate, which indicates hypersensitivity to many prescription topical corticosteroids, oral prednisone, and over-the-counter hydrocortisone; however, topical corticosteroids continued to be prescribed for her, which might have contributed to the lack of improvement and even exacerbated the rash.

Future Considerations—A consideration for the future in this case is discontinuing guselkumab to observe whether symptoms recur. We discussed this option with the patient, but she opted to continue treatment with dupilumab and guselkumab because of the symptom resolution.

Conclusion

Concomitant disease can present as an overlapping pattern in the same area, whereas other regions might have geographically isolated disease. Our patient’s overlap of symptoms, the failure of multiple treatments, and the partial improvement she experienced on guselkumab made diagnosis and management challenging; however, dual biologic therapy was successful.