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Prospect of Better Hours, Less Burnout Fuels Locum Tenens
Insane hours and work-driven burnout are increasingly pernicious forces in medical workplaces. They apparently also are helping steer more physicians toward locum tenens, or temporary, assignments.
In its “2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals,” Coppell, Texas–based staffing firm AMN Healthcare asked doctors, nurse practitioners, and physician assistants why they chose locum tenens work.
The reason chosen most often is improving work hours. Eighty-six percent of respondents said that was the “most important” or a “moderately important” factor. Next was addressing work burnout (80% of respondents), followed by unhappiness with compensation (75%), and dissatisfaction with being a full-time employee (71%).
“During the COVID pandemic, healthcare professionals began to rethink how, when, and where they work,” said Jeff Decker, president of AMN Healthcare’s physician solutions division, adding that he estimates about 52,000 US physicians now work on a locum tenens basis.
“Locum tenens offers relief from the long, inflexible work hours and onerous bureaucratic duties that often cause dissatisfaction and burnout among physicians and other healthcare providers.”
These feelings of dissatisfaction dovetail with findings in recent reports by this news organization based on surveys of physicians about burnout and employment. For example:
- Forty-nine percent of physicians acknowledged feeling burned out, up from 42% 6 years earlier.
- Eighty-three percent of doctors attributed their burnout and/or depression to the job entirely or most of the time.
- Flexibility in work schedules was one of the improvements chosen most often as a potential aid to burnout.
- The leading reasons cited for burnout were the number of bureaucratic tasks and too many hours at work.
Trying Locum Tenens Early in Career
According to AMN Healthcare, 81% of the physicians and APPs in its latest survey said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. Only 19% waited until after retiring from medicine compared with 36% in AMN Healthcare’s 2016 survey.
In the 2024 report, a strong plurality of respondents (47%) said they found locum tenens work more satisfying than permanent healthcare employment. Twelve percent said the opposite, and 30% found the choices about equal.
Even so, it doesn’t appear that locum tenens represents a permanent career path for many. About as many (45%) of physicians and APPs said they would return to full-time employment if progress were made with conditions like hours and burnout, as said they would not (43%).
“Many physicians and other healthcare professionals feel they are being pushed from permanent positions by unsatisfactory work conditions,” Mr. Decker said. “To get them back, employers should offer practice conditions that appeal to today’s providers.”
A version of this article appeared on Medscape.com.
Insane hours and work-driven burnout are increasingly pernicious forces in medical workplaces. They apparently also are helping steer more physicians toward locum tenens, or temporary, assignments.
In its “2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals,” Coppell, Texas–based staffing firm AMN Healthcare asked doctors, nurse practitioners, and physician assistants why they chose locum tenens work.
The reason chosen most often is improving work hours. Eighty-six percent of respondents said that was the “most important” or a “moderately important” factor. Next was addressing work burnout (80% of respondents), followed by unhappiness with compensation (75%), and dissatisfaction with being a full-time employee (71%).
“During the COVID pandemic, healthcare professionals began to rethink how, when, and where they work,” said Jeff Decker, president of AMN Healthcare’s physician solutions division, adding that he estimates about 52,000 US physicians now work on a locum tenens basis.
“Locum tenens offers relief from the long, inflexible work hours and onerous bureaucratic duties that often cause dissatisfaction and burnout among physicians and other healthcare providers.”
These feelings of dissatisfaction dovetail with findings in recent reports by this news organization based on surveys of physicians about burnout and employment. For example:
- Forty-nine percent of physicians acknowledged feeling burned out, up from 42% 6 years earlier.
- Eighty-three percent of doctors attributed their burnout and/or depression to the job entirely or most of the time.
- Flexibility in work schedules was one of the improvements chosen most often as a potential aid to burnout.
- The leading reasons cited for burnout were the number of bureaucratic tasks and too many hours at work.
Trying Locum Tenens Early in Career
According to AMN Healthcare, 81% of the physicians and APPs in its latest survey said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. Only 19% waited until after retiring from medicine compared with 36% in AMN Healthcare’s 2016 survey.
In the 2024 report, a strong plurality of respondents (47%) said they found locum tenens work more satisfying than permanent healthcare employment. Twelve percent said the opposite, and 30% found the choices about equal.
Even so, it doesn’t appear that locum tenens represents a permanent career path for many. About as many (45%) of physicians and APPs said they would return to full-time employment if progress were made with conditions like hours and burnout, as said they would not (43%).
“Many physicians and other healthcare professionals feel they are being pushed from permanent positions by unsatisfactory work conditions,” Mr. Decker said. “To get them back, employers should offer practice conditions that appeal to today’s providers.”
A version of this article appeared on Medscape.com.
Insane hours and work-driven burnout are increasingly pernicious forces in medical workplaces. They apparently also are helping steer more physicians toward locum tenens, or temporary, assignments.
In its “2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals,” Coppell, Texas–based staffing firm AMN Healthcare asked doctors, nurse practitioners, and physician assistants why they chose locum tenens work.
The reason chosen most often is improving work hours. Eighty-six percent of respondents said that was the “most important” or a “moderately important” factor. Next was addressing work burnout (80% of respondents), followed by unhappiness with compensation (75%), and dissatisfaction with being a full-time employee (71%).
“During the COVID pandemic, healthcare professionals began to rethink how, when, and where they work,” said Jeff Decker, president of AMN Healthcare’s physician solutions division, adding that he estimates about 52,000 US physicians now work on a locum tenens basis.
“Locum tenens offers relief from the long, inflexible work hours and onerous bureaucratic duties that often cause dissatisfaction and burnout among physicians and other healthcare providers.”
These feelings of dissatisfaction dovetail with findings in recent reports by this news organization based on surveys of physicians about burnout and employment. For example:
- Forty-nine percent of physicians acknowledged feeling burned out, up from 42% 6 years earlier.
- Eighty-three percent of doctors attributed their burnout and/or depression to the job entirely or most of the time.
- Flexibility in work schedules was one of the improvements chosen most often as a potential aid to burnout.
- The leading reasons cited for burnout were the number of bureaucratic tasks and too many hours at work.
Trying Locum Tenens Early in Career
According to AMN Healthcare, 81% of the physicians and APPs in its latest survey said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. Only 19% waited until after retiring from medicine compared with 36% in AMN Healthcare’s 2016 survey.
In the 2024 report, a strong plurality of respondents (47%) said they found locum tenens work more satisfying than permanent healthcare employment. Twelve percent said the opposite, and 30% found the choices about equal.
Even so, it doesn’t appear that locum tenens represents a permanent career path for many. About as many (45%) of physicians and APPs said they would return to full-time employment if progress were made with conditions like hours and burnout, as said they would not (43%).
“Many physicians and other healthcare professionals feel they are being pushed from permanent positions by unsatisfactory work conditions,” Mr. Decker said. “To get them back, employers should offer practice conditions that appeal to today’s providers.”
A version of this article appeared on Medscape.com.
This Tech Will Change Your Practice Sooner Than You Think
Medical innovations don’t happen overnight — but in today’s digital world, they happen pretty fast. Some are advancing faster than you think.
1. Artificial Intelligence (AI) Medical Scribes
You may already be using this or, at the very least, have heard about it.
Physician burnout is a growing problem, with many doctors spending 2 hours on paperwork for every hour with patients. But some doctors, such as Gregory Ator, MD, chief medical informatics officer at the University of Kansas Medical Center, Kansas City, Kansas, have found a better way.
“I have been using it for 9 months now, and it truly is a life changer,” Dr. Ator said of Abridge, an AI helper that transcribes and summarizes his conversations with patients. “Now, I go into the room, place my phone just about anywhere, and I can just listen.” He estimated that the tech saves him between 3 and 10 minutes per patient. “At 20 patients a day, that saves me around 2 hours,” he said.
Bonus: Patients “get a doctor’s full attention instead of just looking at the top of his head while they play with the computer,” Dr. Ator said. “I have yet to have a patient who didn’t think that was a positive thing.”
Several companies are already selling these AI devices, including Ambience Healthcare, Augmedix, Nuance, and Suki, and they offer more than just transcriptions, said John D. Halamka, MD, president of Mayo Clinic Platform, who oversees Mayo’s adoption of AI. They also generate notes for treatment and billing and update data in the electronic health record.
“It’s preparation of documentation based on ambient listening of doctor-patient conversations,” Dr. Halamka explained. “I’m very optimistic about the use of emerging AI technologies to enable every clinician to practice at the top of their license.”
Patricia Garcia, MD, associate clinical information officer for ambulatory care at Stanford Health Care, has spent much of the last year co-running the medical center’s pilot program for AI scribes, and she’s so impressed with the technology that she “expects it’ll become more widely available as an option for any clinician that wants to use it in the next 12-18 months.”
2. Three-Dimensional (3D) Printing
Although 3D-printed organs may not happen anytime soon, the future is here for some 3D-printed prosthetics and implants — everything from dentures to spinal implants to prosthetic fingers and noses.
“In the next few years, I see rapid growth in the use of 3D printing technology across orthopedic surgery,” said Rishin J. Kadakia, MD, an orthopedic surgeon in Atlanta. “It’s becoming more common not just at large academic institutions. More and more providers will turn to using 3D printing technology to help tackle challenging cases that previously did not have good solutions.”
Dr. Kadakia has experienced this firsthand with his patients at the Emory Orthopaedics & Spine Center. One female patient developed talar avascular necrosis due to a bone break she’d sustained in a serious car crash. An ankle and subtalar joint fusion would repair the damage but limit her mobility and change her gait. So instead, in August of 2021, Dr. Kadakia and fellow orthopedic surgeon Jason Bariteau, MD, created for her a 3D-printed cobalt chrome talus implant.
“It provided an opportunity for her to keep her ankle’s range of motion, and also mobilize faster than with a subtalar and ankle joint fusion,” said Dr. Kadakia.
The technology is also playing a role in customized medical devices — patient-specific tools for greater precision — and 3D-printed anatomical models, built to the exact specifications of individual patients. Mayo Clinic already has 3D modeling units in three states, and other hospitals are following suit. The models not only help doctors prepare for complicated surgeries but also can dramatically cut down on costs. A 2021 study from Durham University reported that 3D models helped reduce surgery time by between 1.5 and 2.5 hours in lengthy procedures.
3. Drones
For patients who can’t make it to a pharmacy to pick up their prescriptions, either because of distance or lack of transportation, drones — which can deliver medications onto a customer’s back yard or front porch — offer a compelling solution.
Several companies and hospitals are already experimenting with drones, like WellSpan Health in Pennsylvania, Amazon Pharmacy, and the Cleveland Clinic, which announced a partnership with drone delivery company Zipline and plans to begin prescription deliveries across Northeast Ohio by 2025.
Healthcare systems are just beginning to explore the potential of drone deliveries, for everything from lab samples to medical and surgical supplies — even defibrillators that could arrive at an ailing patient’s front door before an emergency medical technician arrives.
“For many providers, when you take a sample from a patient, that sample waits around for hours until a courier picks up all of the facility’s samples and drives them to an outside facility for processing,” said Hillary Brendzel, head of Zipline’s US Healthcare Practice.
According to a 2022 survey from American Nurse Journal, 71% of nurses said that medical courier delays and errors negatively affected their ability to provide patient care. But with drone delivery, “lab samples can be sent for processing immediately, on-demand, resulting in faster diagnosis, treatment, and ultimately better outcomes,” said Ms. Brendzel.
4. Portable Ultrasound
Within the next 2 years, portable ultrasound — pocket-sized devices that connect to a smartphone or tablet — will become the “21st-century stethoscope,” said Abhilash Hareendranathan, PhD, assistant professor in the Department of Radiology and Diagnostic Imaging at the University of Alberta, in Edmonton, Alberta, Canada.
AI can make these devices easy to use, allowing clinicians with minimal imaging training to capture clear images and understand the results. Dr. Hareendranathan developed the Ultrasound Arm Injury Detection tool, a portable ultrasound that uses AI to detect fracture.
“We plan to introduce this technology in emergency departments, where it could be used by triage nurses to perform quick examinations to detect fractures of the wrist, elbow, or shoulder,” he said.
More pocket-sized scanners like these could “reshape the way diagnostic care is provided in rural and remote communities,” Dr. Hareendranathan said, and will “reduce wait times in crowded emergency departments.” Bill Gates believes enough in portable ultrasound that last September, the Bill & Melinda Gates Foundation granted $44 million to GE HealthCare to develop the technology for under-resourced communities.
5. Virtual Reality (VR)
When RelieVRx became the first US Food and Drug Administration (FDA)–approved VR therapy for chronic back pain in 2021, the technology was used in just a handful of Veterans Affairs (VA) facilities. But today, thousands of VR headsets have been deployed to more than 160 VA medical centers and clinics across the country.
“The VR experiences encompass pain neuroscience education, mindfulness, pleasant and relaxing distraction, and key skills to calm the nervous system,” said Beth Darnall, PhD, director of the Stanford Pain Relief Innovations Lab, who helped design the RelieVRx. She expects VR to go mainstream soon, not just because of increasing evidence that it works but also thanks to the Centers for Medicare & Medicaid Services, which recently issued a Healthcare Common Procedure Coding System code for VR. “This billing infrastructure will encourage adoption and uptake,” she said.
Hundreds of hospitals across the United States have already adopted the technology, for everything from childbirth pain to wound debridement, said Josh Sackman, the president and cofounder of AppliedVR, the company that developed RelieVRx.
“Over the next few years, we may see hundreds more deploy unique applications [for VR] that can handle multiple clinical indications,” he said. “Given the modality’s ability to scale and reduce reliance on pharmacological interventions, it has the power to improve the cost and quality of care.”
Hospital systems like Geisinger and Cedars-Sinai are already finding unique ways to implement the technology, he said, like using VR to reduce “scanxiety” during imaging service.
Other VR innovations are already being introduced, from the Smileyscope, a VR device for children that’s been proven to lessen the pain of a blood draw or intravenous insertion (it was cleared by the FDA last November) to several VR platforms launched by Cedars-Sinai in recent months, for applications that range from gastrointestinal issues to mental health therapy. “There may already be a thousand hospitals using VR in some capacity,” said Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai.
A version of this article appeared on Medscape.com.
Medical innovations don’t happen overnight — but in today’s digital world, they happen pretty fast. Some are advancing faster than you think.
1. Artificial Intelligence (AI) Medical Scribes
You may already be using this or, at the very least, have heard about it.
Physician burnout is a growing problem, with many doctors spending 2 hours on paperwork for every hour with patients. But some doctors, such as Gregory Ator, MD, chief medical informatics officer at the University of Kansas Medical Center, Kansas City, Kansas, have found a better way.
“I have been using it for 9 months now, and it truly is a life changer,” Dr. Ator said of Abridge, an AI helper that transcribes and summarizes his conversations with patients. “Now, I go into the room, place my phone just about anywhere, and I can just listen.” He estimated that the tech saves him between 3 and 10 minutes per patient. “At 20 patients a day, that saves me around 2 hours,” he said.
Bonus: Patients “get a doctor’s full attention instead of just looking at the top of his head while they play with the computer,” Dr. Ator said. “I have yet to have a patient who didn’t think that was a positive thing.”
Several companies are already selling these AI devices, including Ambience Healthcare, Augmedix, Nuance, and Suki, and they offer more than just transcriptions, said John D. Halamka, MD, president of Mayo Clinic Platform, who oversees Mayo’s adoption of AI. They also generate notes for treatment and billing and update data in the electronic health record.
“It’s preparation of documentation based on ambient listening of doctor-patient conversations,” Dr. Halamka explained. “I’m very optimistic about the use of emerging AI technologies to enable every clinician to practice at the top of their license.”
Patricia Garcia, MD, associate clinical information officer for ambulatory care at Stanford Health Care, has spent much of the last year co-running the medical center’s pilot program for AI scribes, and she’s so impressed with the technology that she “expects it’ll become more widely available as an option for any clinician that wants to use it in the next 12-18 months.”
2. Three-Dimensional (3D) Printing
Although 3D-printed organs may not happen anytime soon, the future is here for some 3D-printed prosthetics and implants — everything from dentures to spinal implants to prosthetic fingers and noses.
“In the next few years, I see rapid growth in the use of 3D printing technology across orthopedic surgery,” said Rishin J. Kadakia, MD, an orthopedic surgeon in Atlanta. “It’s becoming more common not just at large academic institutions. More and more providers will turn to using 3D printing technology to help tackle challenging cases that previously did not have good solutions.”
Dr. Kadakia has experienced this firsthand with his patients at the Emory Orthopaedics & Spine Center. One female patient developed talar avascular necrosis due to a bone break she’d sustained in a serious car crash. An ankle and subtalar joint fusion would repair the damage but limit her mobility and change her gait. So instead, in August of 2021, Dr. Kadakia and fellow orthopedic surgeon Jason Bariteau, MD, created for her a 3D-printed cobalt chrome talus implant.
“It provided an opportunity for her to keep her ankle’s range of motion, and also mobilize faster than with a subtalar and ankle joint fusion,” said Dr. Kadakia.
The technology is also playing a role in customized medical devices — patient-specific tools for greater precision — and 3D-printed anatomical models, built to the exact specifications of individual patients. Mayo Clinic already has 3D modeling units in three states, and other hospitals are following suit. The models not only help doctors prepare for complicated surgeries but also can dramatically cut down on costs. A 2021 study from Durham University reported that 3D models helped reduce surgery time by between 1.5 and 2.5 hours in lengthy procedures.
3. Drones
For patients who can’t make it to a pharmacy to pick up their prescriptions, either because of distance or lack of transportation, drones — which can deliver medications onto a customer’s back yard or front porch — offer a compelling solution.
Several companies and hospitals are already experimenting with drones, like WellSpan Health in Pennsylvania, Amazon Pharmacy, and the Cleveland Clinic, which announced a partnership with drone delivery company Zipline and plans to begin prescription deliveries across Northeast Ohio by 2025.
Healthcare systems are just beginning to explore the potential of drone deliveries, for everything from lab samples to medical and surgical supplies — even defibrillators that could arrive at an ailing patient’s front door before an emergency medical technician arrives.
“For many providers, when you take a sample from a patient, that sample waits around for hours until a courier picks up all of the facility’s samples and drives them to an outside facility for processing,” said Hillary Brendzel, head of Zipline’s US Healthcare Practice.
According to a 2022 survey from American Nurse Journal, 71% of nurses said that medical courier delays and errors negatively affected their ability to provide patient care. But with drone delivery, “lab samples can be sent for processing immediately, on-demand, resulting in faster diagnosis, treatment, and ultimately better outcomes,” said Ms. Brendzel.
4. Portable Ultrasound
Within the next 2 years, portable ultrasound — pocket-sized devices that connect to a smartphone or tablet — will become the “21st-century stethoscope,” said Abhilash Hareendranathan, PhD, assistant professor in the Department of Radiology and Diagnostic Imaging at the University of Alberta, in Edmonton, Alberta, Canada.
AI can make these devices easy to use, allowing clinicians with minimal imaging training to capture clear images and understand the results. Dr. Hareendranathan developed the Ultrasound Arm Injury Detection tool, a portable ultrasound that uses AI to detect fracture.
“We plan to introduce this technology in emergency departments, where it could be used by triage nurses to perform quick examinations to detect fractures of the wrist, elbow, or shoulder,” he said.
More pocket-sized scanners like these could “reshape the way diagnostic care is provided in rural and remote communities,” Dr. Hareendranathan said, and will “reduce wait times in crowded emergency departments.” Bill Gates believes enough in portable ultrasound that last September, the Bill & Melinda Gates Foundation granted $44 million to GE HealthCare to develop the technology for under-resourced communities.
5. Virtual Reality (VR)
When RelieVRx became the first US Food and Drug Administration (FDA)–approved VR therapy for chronic back pain in 2021, the technology was used in just a handful of Veterans Affairs (VA) facilities. But today, thousands of VR headsets have been deployed to more than 160 VA medical centers and clinics across the country.
“The VR experiences encompass pain neuroscience education, mindfulness, pleasant and relaxing distraction, and key skills to calm the nervous system,” said Beth Darnall, PhD, director of the Stanford Pain Relief Innovations Lab, who helped design the RelieVRx. She expects VR to go mainstream soon, not just because of increasing evidence that it works but also thanks to the Centers for Medicare & Medicaid Services, which recently issued a Healthcare Common Procedure Coding System code for VR. “This billing infrastructure will encourage adoption and uptake,” she said.
Hundreds of hospitals across the United States have already adopted the technology, for everything from childbirth pain to wound debridement, said Josh Sackman, the president and cofounder of AppliedVR, the company that developed RelieVRx.
“Over the next few years, we may see hundreds more deploy unique applications [for VR] that can handle multiple clinical indications,” he said. “Given the modality’s ability to scale and reduce reliance on pharmacological interventions, it has the power to improve the cost and quality of care.”
Hospital systems like Geisinger and Cedars-Sinai are already finding unique ways to implement the technology, he said, like using VR to reduce “scanxiety” during imaging service.
Other VR innovations are already being introduced, from the Smileyscope, a VR device for children that’s been proven to lessen the pain of a blood draw or intravenous insertion (it was cleared by the FDA last November) to several VR platforms launched by Cedars-Sinai in recent months, for applications that range from gastrointestinal issues to mental health therapy. “There may already be a thousand hospitals using VR in some capacity,” said Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai.
A version of this article appeared on Medscape.com.
Medical innovations don’t happen overnight — but in today’s digital world, they happen pretty fast. Some are advancing faster than you think.
1. Artificial Intelligence (AI) Medical Scribes
You may already be using this or, at the very least, have heard about it.
Physician burnout is a growing problem, with many doctors spending 2 hours on paperwork for every hour with patients. But some doctors, such as Gregory Ator, MD, chief medical informatics officer at the University of Kansas Medical Center, Kansas City, Kansas, have found a better way.
“I have been using it for 9 months now, and it truly is a life changer,” Dr. Ator said of Abridge, an AI helper that transcribes and summarizes his conversations with patients. “Now, I go into the room, place my phone just about anywhere, and I can just listen.” He estimated that the tech saves him between 3 and 10 minutes per patient. “At 20 patients a day, that saves me around 2 hours,” he said.
Bonus: Patients “get a doctor’s full attention instead of just looking at the top of his head while they play with the computer,” Dr. Ator said. “I have yet to have a patient who didn’t think that was a positive thing.”
Several companies are already selling these AI devices, including Ambience Healthcare, Augmedix, Nuance, and Suki, and they offer more than just transcriptions, said John D. Halamka, MD, president of Mayo Clinic Platform, who oversees Mayo’s adoption of AI. They also generate notes for treatment and billing and update data in the electronic health record.
“It’s preparation of documentation based on ambient listening of doctor-patient conversations,” Dr. Halamka explained. “I’m very optimistic about the use of emerging AI technologies to enable every clinician to practice at the top of their license.”
Patricia Garcia, MD, associate clinical information officer for ambulatory care at Stanford Health Care, has spent much of the last year co-running the medical center’s pilot program for AI scribes, and she’s so impressed with the technology that she “expects it’ll become more widely available as an option for any clinician that wants to use it in the next 12-18 months.”
2. Three-Dimensional (3D) Printing
Although 3D-printed organs may not happen anytime soon, the future is here for some 3D-printed prosthetics and implants — everything from dentures to spinal implants to prosthetic fingers and noses.
“In the next few years, I see rapid growth in the use of 3D printing technology across orthopedic surgery,” said Rishin J. Kadakia, MD, an orthopedic surgeon in Atlanta. “It’s becoming more common not just at large academic institutions. More and more providers will turn to using 3D printing technology to help tackle challenging cases that previously did not have good solutions.”
Dr. Kadakia has experienced this firsthand with his patients at the Emory Orthopaedics & Spine Center. One female patient developed talar avascular necrosis due to a bone break she’d sustained in a serious car crash. An ankle and subtalar joint fusion would repair the damage but limit her mobility and change her gait. So instead, in August of 2021, Dr. Kadakia and fellow orthopedic surgeon Jason Bariteau, MD, created for her a 3D-printed cobalt chrome talus implant.
“It provided an opportunity for her to keep her ankle’s range of motion, and also mobilize faster than with a subtalar and ankle joint fusion,” said Dr. Kadakia.
The technology is also playing a role in customized medical devices — patient-specific tools for greater precision — and 3D-printed anatomical models, built to the exact specifications of individual patients. Mayo Clinic already has 3D modeling units in three states, and other hospitals are following suit. The models not only help doctors prepare for complicated surgeries but also can dramatically cut down on costs. A 2021 study from Durham University reported that 3D models helped reduce surgery time by between 1.5 and 2.5 hours in lengthy procedures.
3. Drones
For patients who can’t make it to a pharmacy to pick up their prescriptions, either because of distance or lack of transportation, drones — which can deliver medications onto a customer’s back yard or front porch — offer a compelling solution.
Several companies and hospitals are already experimenting with drones, like WellSpan Health in Pennsylvania, Amazon Pharmacy, and the Cleveland Clinic, which announced a partnership with drone delivery company Zipline and plans to begin prescription deliveries across Northeast Ohio by 2025.
Healthcare systems are just beginning to explore the potential of drone deliveries, for everything from lab samples to medical and surgical supplies — even defibrillators that could arrive at an ailing patient’s front door before an emergency medical technician arrives.
“For many providers, when you take a sample from a patient, that sample waits around for hours until a courier picks up all of the facility’s samples and drives them to an outside facility for processing,” said Hillary Brendzel, head of Zipline’s US Healthcare Practice.
According to a 2022 survey from American Nurse Journal, 71% of nurses said that medical courier delays and errors negatively affected their ability to provide patient care. But with drone delivery, “lab samples can be sent for processing immediately, on-demand, resulting in faster diagnosis, treatment, and ultimately better outcomes,” said Ms. Brendzel.
4. Portable Ultrasound
Within the next 2 years, portable ultrasound — pocket-sized devices that connect to a smartphone or tablet — will become the “21st-century stethoscope,” said Abhilash Hareendranathan, PhD, assistant professor in the Department of Radiology and Diagnostic Imaging at the University of Alberta, in Edmonton, Alberta, Canada.
AI can make these devices easy to use, allowing clinicians with minimal imaging training to capture clear images and understand the results. Dr. Hareendranathan developed the Ultrasound Arm Injury Detection tool, a portable ultrasound that uses AI to detect fracture.
“We plan to introduce this technology in emergency departments, where it could be used by triage nurses to perform quick examinations to detect fractures of the wrist, elbow, or shoulder,” he said.
More pocket-sized scanners like these could “reshape the way diagnostic care is provided in rural and remote communities,” Dr. Hareendranathan said, and will “reduce wait times in crowded emergency departments.” Bill Gates believes enough in portable ultrasound that last September, the Bill & Melinda Gates Foundation granted $44 million to GE HealthCare to develop the technology for under-resourced communities.
5. Virtual Reality (VR)
When RelieVRx became the first US Food and Drug Administration (FDA)–approved VR therapy for chronic back pain in 2021, the technology was used in just a handful of Veterans Affairs (VA) facilities. But today, thousands of VR headsets have been deployed to more than 160 VA medical centers and clinics across the country.
“The VR experiences encompass pain neuroscience education, mindfulness, pleasant and relaxing distraction, and key skills to calm the nervous system,” said Beth Darnall, PhD, director of the Stanford Pain Relief Innovations Lab, who helped design the RelieVRx. She expects VR to go mainstream soon, not just because of increasing evidence that it works but also thanks to the Centers for Medicare & Medicaid Services, which recently issued a Healthcare Common Procedure Coding System code for VR. “This billing infrastructure will encourage adoption and uptake,” she said.
Hundreds of hospitals across the United States have already adopted the technology, for everything from childbirth pain to wound debridement, said Josh Sackman, the president and cofounder of AppliedVR, the company that developed RelieVRx.
“Over the next few years, we may see hundreds more deploy unique applications [for VR] that can handle multiple clinical indications,” he said. “Given the modality’s ability to scale and reduce reliance on pharmacological interventions, it has the power to improve the cost and quality of care.”
Hospital systems like Geisinger and Cedars-Sinai are already finding unique ways to implement the technology, he said, like using VR to reduce “scanxiety” during imaging service.
Other VR innovations are already being introduced, from the Smileyscope, a VR device for children that’s been proven to lessen the pain of a blood draw or intravenous insertion (it was cleared by the FDA last November) to several VR platforms launched by Cedars-Sinai in recent months, for applications that range from gastrointestinal issues to mental health therapy. “There may already be a thousand hospitals using VR in some capacity,” said Brennan Spiegel, MD, director of Health Services Research at Cedars-Sinai.
A version of this article appeared on Medscape.com.
Gene Therapy for Dystrophic EB: Extension Study Results Reported
The results were presented by Amy S. Paller, MD, during a late-breaking session at the annual meeting of the American Academy of Dermatology.
In May 2023, beremagene geperpavec, marketed as Vyjuvek (formerly known as B-VEC) was approved by the US Food and Drug Administration (FDA) for the treatment of wounds in patients 6 months of age and older with DEB, a rare genetic blistering disorder caused by COL7A1 gene variants. The therapy uses a nonreplicating herpes simplex virus type 1 (HSV-1) vector to deliver the COL7A1 gene directly to skin cells, restoring the COL7 protein fibrils that stabilize skin structure. It is designed to be used repetitively, to heal a single wound, or on more than one wound.
In the pivotal study of patients with DEB, the gene therapy, delivered in a topical gel, was administered once a week for 6 months to one wound and placebo was applied to another wound for each participant. The proportion of wounds treated with beremagene geperpavec that healed was significantly higher than among placebo-treated wounds at 3 and 6 months (68% vs. 23% at 3 months, P = .003) and 65% vs. 26% at 6 months (P = .012), with no serious adverse events related to treatment.
The prospective, open label, uncontrolled extension study included 24 patients from the phase 3 study and 23 treatment-naive patients from five US sites. Their mean age was 16 years (range, 6 months to 46 years).
Of the 47 patients, 29 (62%) were on treatment for more than 1 year (the longest was about 2 years), and the mean duration of treatment was 475 days; 5 patients withdrew from the study for reasons not related to treatment.
Their types of adverse events (AEs) were similar to those seen in the phase 3 study and were consistent with what would be expected in patients with DEB, said Dr. Paller, professor and chair of dermatology, Northwestern University, Chicago. One patient experienced two wound hemorrhages that were possibly related to treatment, but there were no treatment-related AEs, no deaths or treatment discontinuations because of an AE, and no serious AEs thought to be related to treatment.
Wounds that were evaluated in the phase 3 study showed “a high durability of closure with continued treatment,” according to Dr. Paller. There were enough data on 19 of the 24 patients who had been in the phase 3 trial to evaluate wound closure, defined as “complete wound closure based on comparison to the exact wound area selected at baseline” at the beginning of the phase 3 study.
In the extension study, wound closure rates were almost 90% at baseline, 84.2% at 3 months, 61.1% at 6 months, 82.4% at 9 months, and 62.5% at 12 months, which was comparable to the rates observed in the third (86.4%) and sixth (73.7%) months of the phase 3 study, Dr. Paller said.
Patient-reported outcomes indicated that quality of life and satisfaction with treatment were preserved with continued treatment.The extension study was terminated in July 2023, after FDA approval, when patients could be transitioned to the commercially available treatment.Dr. Paller disclosed being an investigator (funds to institution) for multiple pharmaceutical companies, including the manufacturer of beremagene geperpavec, Krystal Biotech, which funded the study.
The results were presented by Amy S. Paller, MD, during a late-breaking session at the annual meeting of the American Academy of Dermatology.
In May 2023, beremagene geperpavec, marketed as Vyjuvek (formerly known as B-VEC) was approved by the US Food and Drug Administration (FDA) for the treatment of wounds in patients 6 months of age and older with DEB, a rare genetic blistering disorder caused by COL7A1 gene variants. The therapy uses a nonreplicating herpes simplex virus type 1 (HSV-1) vector to deliver the COL7A1 gene directly to skin cells, restoring the COL7 protein fibrils that stabilize skin structure. It is designed to be used repetitively, to heal a single wound, or on more than one wound.
In the pivotal study of patients with DEB, the gene therapy, delivered in a topical gel, was administered once a week for 6 months to one wound and placebo was applied to another wound for each participant. The proportion of wounds treated with beremagene geperpavec that healed was significantly higher than among placebo-treated wounds at 3 and 6 months (68% vs. 23% at 3 months, P = .003) and 65% vs. 26% at 6 months (P = .012), with no serious adverse events related to treatment.
The prospective, open label, uncontrolled extension study included 24 patients from the phase 3 study and 23 treatment-naive patients from five US sites. Their mean age was 16 years (range, 6 months to 46 years).
Of the 47 patients, 29 (62%) were on treatment for more than 1 year (the longest was about 2 years), and the mean duration of treatment was 475 days; 5 patients withdrew from the study for reasons not related to treatment.
Their types of adverse events (AEs) were similar to those seen in the phase 3 study and were consistent with what would be expected in patients with DEB, said Dr. Paller, professor and chair of dermatology, Northwestern University, Chicago. One patient experienced two wound hemorrhages that were possibly related to treatment, but there were no treatment-related AEs, no deaths or treatment discontinuations because of an AE, and no serious AEs thought to be related to treatment.
Wounds that were evaluated in the phase 3 study showed “a high durability of closure with continued treatment,” according to Dr. Paller. There were enough data on 19 of the 24 patients who had been in the phase 3 trial to evaluate wound closure, defined as “complete wound closure based on comparison to the exact wound area selected at baseline” at the beginning of the phase 3 study.
In the extension study, wound closure rates were almost 90% at baseline, 84.2% at 3 months, 61.1% at 6 months, 82.4% at 9 months, and 62.5% at 12 months, which was comparable to the rates observed in the third (86.4%) and sixth (73.7%) months of the phase 3 study, Dr. Paller said.
Patient-reported outcomes indicated that quality of life and satisfaction with treatment were preserved with continued treatment.The extension study was terminated in July 2023, after FDA approval, when patients could be transitioned to the commercially available treatment.Dr. Paller disclosed being an investigator (funds to institution) for multiple pharmaceutical companies, including the manufacturer of beremagene geperpavec, Krystal Biotech, which funded the study.
The results were presented by Amy S. Paller, MD, during a late-breaking session at the annual meeting of the American Academy of Dermatology.
In May 2023, beremagene geperpavec, marketed as Vyjuvek (formerly known as B-VEC) was approved by the US Food and Drug Administration (FDA) for the treatment of wounds in patients 6 months of age and older with DEB, a rare genetic blistering disorder caused by COL7A1 gene variants. The therapy uses a nonreplicating herpes simplex virus type 1 (HSV-1) vector to deliver the COL7A1 gene directly to skin cells, restoring the COL7 protein fibrils that stabilize skin structure. It is designed to be used repetitively, to heal a single wound, or on more than one wound.
In the pivotal study of patients with DEB, the gene therapy, delivered in a topical gel, was administered once a week for 6 months to one wound and placebo was applied to another wound for each participant. The proportion of wounds treated with beremagene geperpavec that healed was significantly higher than among placebo-treated wounds at 3 and 6 months (68% vs. 23% at 3 months, P = .003) and 65% vs. 26% at 6 months (P = .012), with no serious adverse events related to treatment.
The prospective, open label, uncontrolled extension study included 24 patients from the phase 3 study and 23 treatment-naive patients from five US sites. Their mean age was 16 years (range, 6 months to 46 years).
Of the 47 patients, 29 (62%) were on treatment for more than 1 year (the longest was about 2 years), and the mean duration of treatment was 475 days; 5 patients withdrew from the study for reasons not related to treatment.
Their types of adverse events (AEs) were similar to those seen in the phase 3 study and were consistent with what would be expected in patients with DEB, said Dr. Paller, professor and chair of dermatology, Northwestern University, Chicago. One patient experienced two wound hemorrhages that were possibly related to treatment, but there were no treatment-related AEs, no deaths or treatment discontinuations because of an AE, and no serious AEs thought to be related to treatment.
Wounds that were evaluated in the phase 3 study showed “a high durability of closure with continued treatment,” according to Dr. Paller. There were enough data on 19 of the 24 patients who had been in the phase 3 trial to evaluate wound closure, defined as “complete wound closure based on comparison to the exact wound area selected at baseline” at the beginning of the phase 3 study.
In the extension study, wound closure rates were almost 90% at baseline, 84.2% at 3 months, 61.1% at 6 months, 82.4% at 9 months, and 62.5% at 12 months, which was comparable to the rates observed in the third (86.4%) and sixth (73.7%) months of the phase 3 study, Dr. Paller said.
Patient-reported outcomes indicated that quality of life and satisfaction with treatment were preserved with continued treatment.The extension study was terminated in July 2023, after FDA approval, when patients could be transitioned to the commercially available treatment.Dr. Paller disclosed being an investigator (funds to institution) for multiple pharmaceutical companies, including the manufacturer of beremagene geperpavec, Krystal Biotech, which funded the study.
FROM AAD 2024
Positive Phase 2 Results Reported for TYK2 Inhibitor for Patients With Moderate to Severe Psoriasis
, in a phase 2 study presented during a late breaker presentation at the annual meeting of the American Academy of Dermatology.
ESK-001 is a highly-selective TYK2 inhibitor that “reduces signaling through several cytokine receptors including receptors for interleukin (IL)-12, IL-23, and interferon (IFN)-alpha,” according to Alumis, the company developing ESK-001.
The STRIDE trial enrolled 228 adults (mean age, 48 years) with a mean PASI score of 17.8 at baseline, randomized to one of five doses of ESK-001, or placebo. Nearly 70% of those enrolled were men, 82.5% were White, nearly 6% were Asian, and about 4% were Black.
The proportion of patients achieving at least a PASI-75 at 12 weeks, the primary endpoint, ranged from 19.4% among those on the lower dose (10 mg a day) to 56.4% among those on 20 mg twice a day and those on 40 mg once a day, and 64.1% among those on 40 mg twice a day, the highest dose evaluated, compared with 0% of those on placebo.
In addition, 38.5% and 15.4% of those on the highest dose achieved a PASI 90 and PASI 100, respectively, at 12 weeks, according to results presented at the meeting by Kim A. Papp, MD.
Improvements in static Physician’s Global Assessment (sPGA) scores, a secondary endpoint, at 12 weeks were also observed; including 59% of those on the highest dose (40 mg twice a day) achieving an sPGA of 0/1 at 12 weeks, according to Dr. Papp, president of Probity Medical Research, in Waterloo, Ontario, and a study investigator.
Treatment was “generally safe and well tolerated” at all doses, and most treatment-emergent adverse events were “mild to moderate” and self-limited, he said.
The most frequent treatment emergent adverse events included headache and nasopharyngitis (also reported in the placebo group), and upper respiratory tract infections. No cases of treatment-related serious adverse events were reported, and there were no cases of MACE (major adverse cardiovascular events), serious infections, thromboses related to treatment, or lab or ECG findings of concern.
In an ongoing open label extension study, 165 patients on 40 mg once a day and those on 40 mg twice a day are continuing to be evaluated, and at week 16, have continued to show significant efficacy, with a favorable risk-benefit profile to date, according to Dr. Papp.
ESK-001 is also being evaluated in a phase 2b study of patients with systemic lupus erythematosus, and a phase 2 proof-of-concept study of patients with non-infectious uveitis, according to Alumis.
In addition to being an investigator for Alumis, Dr. Papp disclosed serving as an adviser, consultant, investigator, and/or speaker for multiple other pharmaceutical companies.
, in a phase 2 study presented during a late breaker presentation at the annual meeting of the American Academy of Dermatology.
ESK-001 is a highly-selective TYK2 inhibitor that “reduces signaling through several cytokine receptors including receptors for interleukin (IL)-12, IL-23, and interferon (IFN)-alpha,” according to Alumis, the company developing ESK-001.
The STRIDE trial enrolled 228 adults (mean age, 48 years) with a mean PASI score of 17.8 at baseline, randomized to one of five doses of ESK-001, or placebo. Nearly 70% of those enrolled were men, 82.5% were White, nearly 6% were Asian, and about 4% were Black.
The proportion of patients achieving at least a PASI-75 at 12 weeks, the primary endpoint, ranged from 19.4% among those on the lower dose (10 mg a day) to 56.4% among those on 20 mg twice a day and those on 40 mg once a day, and 64.1% among those on 40 mg twice a day, the highest dose evaluated, compared with 0% of those on placebo.
In addition, 38.5% and 15.4% of those on the highest dose achieved a PASI 90 and PASI 100, respectively, at 12 weeks, according to results presented at the meeting by Kim A. Papp, MD.
Improvements in static Physician’s Global Assessment (sPGA) scores, a secondary endpoint, at 12 weeks were also observed; including 59% of those on the highest dose (40 mg twice a day) achieving an sPGA of 0/1 at 12 weeks, according to Dr. Papp, president of Probity Medical Research, in Waterloo, Ontario, and a study investigator.
Treatment was “generally safe and well tolerated” at all doses, and most treatment-emergent adverse events were “mild to moderate” and self-limited, he said.
The most frequent treatment emergent adverse events included headache and nasopharyngitis (also reported in the placebo group), and upper respiratory tract infections. No cases of treatment-related serious adverse events were reported, and there were no cases of MACE (major adverse cardiovascular events), serious infections, thromboses related to treatment, or lab or ECG findings of concern.
In an ongoing open label extension study, 165 patients on 40 mg once a day and those on 40 mg twice a day are continuing to be evaluated, and at week 16, have continued to show significant efficacy, with a favorable risk-benefit profile to date, according to Dr. Papp.
ESK-001 is also being evaluated in a phase 2b study of patients with systemic lupus erythematosus, and a phase 2 proof-of-concept study of patients with non-infectious uveitis, according to Alumis.
In addition to being an investigator for Alumis, Dr. Papp disclosed serving as an adviser, consultant, investigator, and/or speaker for multiple other pharmaceutical companies.
, in a phase 2 study presented during a late breaker presentation at the annual meeting of the American Academy of Dermatology.
ESK-001 is a highly-selective TYK2 inhibitor that “reduces signaling through several cytokine receptors including receptors for interleukin (IL)-12, IL-23, and interferon (IFN)-alpha,” according to Alumis, the company developing ESK-001.
The STRIDE trial enrolled 228 adults (mean age, 48 years) with a mean PASI score of 17.8 at baseline, randomized to one of five doses of ESK-001, or placebo. Nearly 70% of those enrolled were men, 82.5% were White, nearly 6% were Asian, and about 4% were Black.
The proportion of patients achieving at least a PASI-75 at 12 weeks, the primary endpoint, ranged from 19.4% among those on the lower dose (10 mg a day) to 56.4% among those on 20 mg twice a day and those on 40 mg once a day, and 64.1% among those on 40 mg twice a day, the highest dose evaluated, compared with 0% of those on placebo.
In addition, 38.5% and 15.4% of those on the highest dose achieved a PASI 90 and PASI 100, respectively, at 12 weeks, according to results presented at the meeting by Kim A. Papp, MD.
Improvements in static Physician’s Global Assessment (sPGA) scores, a secondary endpoint, at 12 weeks were also observed; including 59% of those on the highest dose (40 mg twice a day) achieving an sPGA of 0/1 at 12 weeks, according to Dr. Papp, president of Probity Medical Research, in Waterloo, Ontario, and a study investigator.
Treatment was “generally safe and well tolerated” at all doses, and most treatment-emergent adverse events were “mild to moderate” and self-limited, he said.
The most frequent treatment emergent adverse events included headache and nasopharyngitis (also reported in the placebo group), and upper respiratory tract infections. No cases of treatment-related serious adverse events were reported, and there were no cases of MACE (major adverse cardiovascular events), serious infections, thromboses related to treatment, or lab or ECG findings of concern.
In an ongoing open label extension study, 165 patients on 40 mg once a day and those on 40 mg twice a day are continuing to be evaluated, and at week 16, have continued to show significant efficacy, with a favorable risk-benefit profile to date, according to Dr. Papp.
ESK-001 is also being evaluated in a phase 2b study of patients with systemic lupus erythematosus, and a phase 2 proof-of-concept study of patients with non-infectious uveitis, according to Alumis.
In addition to being an investigator for Alumis, Dr. Papp disclosed serving as an adviser, consultant, investigator, and/or speaker for multiple other pharmaceutical companies.
FROM AAD 2024
FDA Requests More Information for RDEB Rx Under Review
The Food and Drug Administration
(RDEB), requesting more information from the manufacturer.Pz-cel, which comprises autologous, COL7A1 gene–corrected epidermal sheets, is being evaluated for its ability to enable normal type VII collagen expression in a patient’s skin cells and to facilitate wound healing and pain reduction in wounds in patients with RDEB after a one-time application procedure. The cause of RDEB is a defect in the COL7A1 gene that “results in the inability to produce type VII collagen,” a press release from the manufacturer noted.
On April 22, 2024, the manufacturer Abeona Therapeutics announced that following a meeting with the FDA in March and in a subsequent request for information, the agency requires additional information to satisfy certain Chemistry Manufacturing and Controls requirements before the BLA for pz-cel can be approved. According to a press release from the company, the information pertains to validation requirements for certain manufacturing and release testing methods, including some that were observed during the FDA’s pre-licensing inspection.
The complete response letter did not identify any issues related to the clinical efficacy or safety data in the BLA, and the FDA did not request any new clinical trials or clinical data to support approval, according to the company.
The company anticipates completing the BLA resubmission in the third quarter of 2024. The application is supported by clinical efficacy and safety data from the pivotal phase 3 VIITAL study and a phase 1/2a study in patients with RDEB.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration
(RDEB), requesting more information from the manufacturer.Pz-cel, which comprises autologous, COL7A1 gene–corrected epidermal sheets, is being evaluated for its ability to enable normal type VII collagen expression in a patient’s skin cells and to facilitate wound healing and pain reduction in wounds in patients with RDEB after a one-time application procedure. The cause of RDEB is a defect in the COL7A1 gene that “results in the inability to produce type VII collagen,” a press release from the manufacturer noted.
On April 22, 2024, the manufacturer Abeona Therapeutics announced that following a meeting with the FDA in March and in a subsequent request for information, the agency requires additional information to satisfy certain Chemistry Manufacturing and Controls requirements before the BLA for pz-cel can be approved. According to a press release from the company, the information pertains to validation requirements for certain manufacturing and release testing methods, including some that were observed during the FDA’s pre-licensing inspection.
The complete response letter did not identify any issues related to the clinical efficacy or safety data in the BLA, and the FDA did not request any new clinical trials or clinical data to support approval, according to the company.
The company anticipates completing the BLA resubmission in the third quarter of 2024. The application is supported by clinical efficacy and safety data from the pivotal phase 3 VIITAL study and a phase 1/2a study in patients with RDEB.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration
(RDEB), requesting more information from the manufacturer.Pz-cel, which comprises autologous, COL7A1 gene–corrected epidermal sheets, is being evaluated for its ability to enable normal type VII collagen expression in a patient’s skin cells and to facilitate wound healing and pain reduction in wounds in patients with RDEB after a one-time application procedure. The cause of RDEB is a defect in the COL7A1 gene that “results in the inability to produce type VII collagen,” a press release from the manufacturer noted.
On April 22, 2024, the manufacturer Abeona Therapeutics announced that following a meeting with the FDA in March and in a subsequent request for information, the agency requires additional information to satisfy certain Chemistry Manufacturing and Controls requirements before the BLA for pz-cel can be approved. According to a press release from the company, the information pertains to validation requirements for certain manufacturing and release testing methods, including some that were observed during the FDA’s pre-licensing inspection.
The complete response letter did not identify any issues related to the clinical efficacy or safety data in the BLA, and the FDA did not request any new clinical trials or clinical data to support approval, according to the company.
The company anticipates completing the BLA resubmission in the third quarter of 2024. The application is supported by clinical efficacy and safety data from the pivotal phase 3 VIITAL study and a phase 1/2a study in patients with RDEB.
A version of this article first appeared on Medscape.com.
Clinical Manifestation of Degos Disease: Painful Penile Ulcers
To the Editor:
A 56-year-old man was referred to our Grand Rounds by another dermatologist in our health system for evaluation of a red scaly rash on the trunk that had been present for more than a year. More recently, over the course of approximately 9 months he experienced recurrent painful penile ulcers that lasted for approximately 4 weeks and then self-resolved. He had a medical history of central retinal vein occlusion, primary hyperparathyroidism, and nonspecific colitis. A family history was notable for lung cancer in the patient’s father and myelodysplastic syndrome and breast cancer in his mother; however, there was no family history of a similar rash. A bacterial culture of the penile ulcer was negative. Testing for antibodies against HIV and herpes simplex virus (HSV) types 1 and 2 was negative. Results of a serum VDRL test were nonreactive, which ruled out syphilis. The patient was treated by the referring dermatologist with azithromycin for possible chancroid without relief.
The patient was being followed by the referring dermatologist who initially was concerned for Degos disease based on clinical examination findings, prompting biopsy of a lesion on the back, which revealed vacuolar interface dermatitis, a sparse superficial perivascular lymphocytic infiltrate, and increased mucin—all highly suspicious for connective tissue disease (Figure 1). An antinuclear antibody test was positive, with a titer of 1:640. The patient was started on prednisone and referred to rheumatology; however, further evaluation by rheumatology for an autoimmune process—including anticardiolipin antibodies—was unremarkable. A few months prior to the current presentation, he also had mildly elevated liver function test results. A colonoscopy was performed, and a biopsy revealed nonspecific colitis. A biopsy of the penile ulcer also was nonspecific, showing only ulceration and acute and chronic inflammation. No epidermal interface change was seen. Results from a Grocott-Gomori methenamine-silver stain, Treponema pallidum immunostain, and HSV polymerase chain reaction were negative for fungal organisms, spirochetes, and HSV, respectively. The differential diagnosis included trauma, aphthous ulceration, and Behçet disease. Behçet disease was suspected by the referring dermatologist, and the patient was treated with colchicine, prednisone, pimecrolimus cream, and topical lidocaine; however, the lesions persisted, and he was subsequently referred to our Grand Rounds for further evaluation.
At the current presentation, physical examination revealed several small papules with white atrophic centers and erythematous rims on the trunk and extremities (Figure 2A). An ulceration was noted on the penile shaft (Figure 2B). Further evaluation for Behçet disease, including testing for pathergy and HLA-B51, was negative. Degos disease was strongly suspected clinically, and a repeat biopsy was performed of a lesion on the abdomen, which revealed central epidermal necrosis, atrophy, and parakeratosis with an underlying wedge-shaped dermal infarct surrounded by multiple small occluded dermal vessels, perivascular inflammation, and dermal edema (Figure 3). Direct immunofluorescence was performed using antibodies against IgG, IgA, IgM, fibrinogen, albumin, and C3, which was negative. These findings from direct immunofluorescence and histopathology as well as the clinical presentation were considered compatible with Degos disease. The patient was started on aspirin and pentoxifylline. Pentoxifylline 400 mg twice daily appeared to lessen some of the pain. Pain management specialists started the patient on gabapentin.
Approximately 4 months after the Grand Rounds evaluation, during which time he continued treatment with pentoxifylline, he was admitted to the hospital for intractable nausea and vomiting. His condition acutely declined due to bowel perforation, and he was started on eculizumab 1200 mg every 14 days. Because of an increased risk for meningococcal meningitis while on this medication, he also was given erythromycin 500 mg twice daily prophylactically. He was being followed by hematology for the vasculopathy, and they were planning to monitor for any disease changes with computed tomography of the chest, abdomen, and pelvis every 3 months, as well as echocardiogram every 6 months for any development of pericardial or pleural fibrosis. Approximately 1 month later, the patient was admitted to the hospital again but died after 1 week from gastrointestinal complications (approximately 22 months after the onset of the rash).
Degos disease (atrophic papulosis) is a rare small vessel vasculopathy of unknown etiology, but complement-mediated endothelial injury plays a role.1,2 It typically occurs in the fourth decade of life, with a slight female predominance.3,4 The skin lesions are characteristic and described as 5- to 10-mm papules with atrophic white centers and erythematous telangiectatic rims, most commonly on the upper body and typically sparing the head, palms, and soles.1 Penile ulceration is an uncommon cutaneous feature, with only a few cases reported in the literature.5,6 Approximately one-third of patients will have only skin lesions, but two-thirds will develop systemic involvement 1 to 2 years after onset, with the gastrointestinal tract and central nervous system most commonly involved. For those with systemic involvement, the 5-year survival rate is approximately 55%, and the most common causes of death are bowel perforation, peritonitis, and stroke.3,4 Because some patients appear to never develop systemic complications, Theodoridis et al4 proposed that the disease be classified as either malignant atrophic papulosis or benign atrophic papulosis to indicate the malignant systemic form and the benign cutaneous form, respectively.
The histopathology of Degos disease changes as the lesions evolve.7 Early lesions show a superficial and deep perivascular and periadnexal lymphocytic infiltrate, possible interface dermatitis, and dermal mucin resembling lupus. The more fully developed lesions show a greater degree of inflammation and interface change as well as lymphocytic vasculitis. This stage also may have epidermal atrophy and early papillary dermal sclerosis resembling lichen sclerosus. The late-stage lesions, clinically observed as papules with atrophic white centers and surrounding erythema, show the classic pathology of wedge-shaped dermal sclerosis and central epidermal atrophy with surrounding hyperkeratosis. Interface dermatitis and dermal mucin can be seen in all stages, though mucin is diminished in the later stage.
Effective treatment options are limited; however, antithrombotics or compounds that facilitate blood perfusion, such as aspirin or pentoxifylline, initially can be used.1 Eculizumab, a humanized monoclonal antibody that prevents the cleavage of C5, has been used for salvage therapy,8 as in our case. Treprostinil, a prostacyclin analog that causes arterial vasodilation and inhibition of platelet aggregation, has been reported to improve bowel and cutaneous lesions, functional status, and neurologic symptoms.9
Our case highlights important features of Degos disease. First, it is important for both the clinician and the pathologist to recognize that the histopathology of Degos disease changes as the lesions evolve. In our case, although the lesions were characteristic of Degos disease clinically, the initial biopsy was suspicious for connective tissue disease, which led to an autoimmune evaluation that ultimately was unremarkable. Recognizing that early lesions of Degos disease can resemble connective tissue disease histologically could have prevented this delay in diagnosis. However, Degos disease has been reported in association with autoimmune diseases.10 Second, although penile ulceration is uncommon, it can be a prominent cutaneous manifestation of the disease. Finally, eculizumab and treprostinil are therapeutic options that have shown some efficacy in improving symptoms and cutaneous lesions.8,9
- Theodoridis A, Makrantonaki E, Zouboulis CC. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10. doi:10.1186/1750-1172-8-10
- Magro CM, Poe JC, Kim C, et al. Degos disease: a C5b-9/interferon-α-mediated endotheliopathy syndrome. Am J Clin Pathol. 2011;135:599-610. doi:10.1309/AJCP66QIMFARLZKI
- Hu P, Mao Z, Liu C, et al. Malignant atrophic papulosis with motor aphasia and intestinal perforation: a case report and review of published works. J Dermatol. 2018;45:723-726. doi:10.1111/1346-8138.14280
- Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115. doi:10.1111/bjd.12642
- Thomson KF, Highet AS. Penile ulceration in fatal malignant atrophic papulosis (Degos’ disease). Br J Dermatol. 2000;143:1320-1322. doi:10.1046/j.1365-2133.2000.03911.x
- Aydogan K, Alkan G, Karadogan Koran S, et al. Painful penile ulceration in a patient with malignant atrophic papulosis. J Eur Acad Dermatol Venereol. 2005;19:612-616. doi:10.1111/j.1468-3083.2005.01227.x
- Harvell JD, Williford PL, White WL. Benign cutaneous Degos’ disease: a case report with emphasis on histopathology as papules chronologically evolve. Am J Dermatopathol. 2001;23:116-123. doi:10.1097/00000372-200104000-00006
- Oliver B, Boehm M, Rosing DR, et al. Diffuse atrophic papules and plaques, intermittent abdominal pain, paresthesias, and cardiac abnormalities in a 55-year-old woman. J Am Acad Dermatol. 2016;75:1274-1277. doi:10.1016/j.jaad.2016.09.015
- Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52. doi:10.1186/1750-1172-8-52
- Burgin S, Stone JH, Shenoy-Bhangle AS, et al. Case records of the Massachusetts General Hospital. Case 18-2014. A 32-year-old man with a rash, myalgia, and weakness. N Engl J Med. 2014;370:2327-2337. doi:10.1056/NEJMcpc1304161
To the Editor:
A 56-year-old man was referred to our Grand Rounds by another dermatologist in our health system for evaluation of a red scaly rash on the trunk that had been present for more than a year. More recently, over the course of approximately 9 months he experienced recurrent painful penile ulcers that lasted for approximately 4 weeks and then self-resolved. He had a medical history of central retinal vein occlusion, primary hyperparathyroidism, and nonspecific colitis. A family history was notable for lung cancer in the patient’s father and myelodysplastic syndrome and breast cancer in his mother; however, there was no family history of a similar rash. A bacterial culture of the penile ulcer was negative. Testing for antibodies against HIV and herpes simplex virus (HSV) types 1 and 2 was negative. Results of a serum VDRL test were nonreactive, which ruled out syphilis. The patient was treated by the referring dermatologist with azithromycin for possible chancroid without relief.
The patient was being followed by the referring dermatologist who initially was concerned for Degos disease based on clinical examination findings, prompting biopsy of a lesion on the back, which revealed vacuolar interface dermatitis, a sparse superficial perivascular lymphocytic infiltrate, and increased mucin—all highly suspicious for connective tissue disease (Figure 1). An antinuclear antibody test was positive, with a titer of 1:640. The patient was started on prednisone and referred to rheumatology; however, further evaluation by rheumatology for an autoimmune process—including anticardiolipin antibodies—was unremarkable. A few months prior to the current presentation, he also had mildly elevated liver function test results. A colonoscopy was performed, and a biopsy revealed nonspecific colitis. A biopsy of the penile ulcer also was nonspecific, showing only ulceration and acute and chronic inflammation. No epidermal interface change was seen. Results from a Grocott-Gomori methenamine-silver stain, Treponema pallidum immunostain, and HSV polymerase chain reaction were negative for fungal organisms, spirochetes, and HSV, respectively. The differential diagnosis included trauma, aphthous ulceration, and Behçet disease. Behçet disease was suspected by the referring dermatologist, and the patient was treated with colchicine, prednisone, pimecrolimus cream, and topical lidocaine; however, the lesions persisted, and he was subsequently referred to our Grand Rounds for further evaluation.
At the current presentation, physical examination revealed several small papules with white atrophic centers and erythematous rims on the trunk and extremities (Figure 2A). An ulceration was noted on the penile shaft (Figure 2B). Further evaluation for Behçet disease, including testing for pathergy and HLA-B51, was negative. Degos disease was strongly suspected clinically, and a repeat biopsy was performed of a lesion on the abdomen, which revealed central epidermal necrosis, atrophy, and parakeratosis with an underlying wedge-shaped dermal infarct surrounded by multiple small occluded dermal vessels, perivascular inflammation, and dermal edema (Figure 3). Direct immunofluorescence was performed using antibodies against IgG, IgA, IgM, fibrinogen, albumin, and C3, which was negative. These findings from direct immunofluorescence and histopathology as well as the clinical presentation were considered compatible with Degos disease. The patient was started on aspirin and pentoxifylline. Pentoxifylline 400 mg twice daily appeared to lessen some of the pain. Pain management specialists started the patient on gabapentin.
Approximately 4 months after the Grand Rounds evaluation, during which time he continued treatment with pentoxifylline, he was admitted to the hospital for intractable nausea and vomiting. His condition acutely declined due to bowel perforation, and he was started on eculizumab 1200 mg every 14 days. Because of an increased risk for meningococcal meningitis while on this medication, he also was given erythromycin 500 mg twice daily prophylactically. He was being followed by hematology for the vasculopathy, and they were planning to monitor for any disease changes with computed tomography of the chest, abdomen, and pelvis every 3 months, as well as echocardiogram every 6 months for any development of pericardial or pleural fibrosis. Approximately 1 month later, the patient was admitted to the hospital again but died after 1 week from gastrointestinal complications (approximately 22 months after the onset of the rash).
Degos disease (atrophic papulosis) is a rare small vessel vasculopathy of unknown etiology, but complement-mediated endothelial injury plays a role.1,2 It typically occurs in the fourth decade of life, with a slight female predominance.3,4 The skin lesions are characteristic and described as 5- to 10-mm papules with atrophic white centers and erythematous telangiectatic rims, most commonly on the upper body and typically sparing the head, palms, and soles.1 Penile ulceration is an uncommon cutaneous feature, with only a few cases reported in the literature.5,6 Approximately one-third of patients will have only skin lesions, but two-thirds will develop systemic involvement 1 to 2 years after onset, with the gastrointestinal tract and central nervous system most commonly involved. For those with systemic involvement, the 5-year survival rate is approximately 55%, and the most common causes of death are bowel perforation, peritonitis, and stroke.3,4 Because some patients appear to never develop systemic complications, Theodoridis et al4 proposed that the disease be classified as either malignant atrophic papulosis or benign atrophic papulosis to indicate the malignant systemic form and the benign cutaneous form, respectively.
The histopathology of Degos disease changes as the lesions evolve.7 Early lesions show a superficial and deep perivascular and periadnexal lymphocytic infiltrate, possible interface dermatitis, and dermal mucin resembling lupus. The more fully developed lesions show a greater degree of inflammation and interface change as well as lymphocytic vasculitis. This stage also may have epidermal atrophy and early papillary dermal sclerosis resembling lichen sclerosus. The late-stage lesions, clinically observed as papules with atrophic white centers and surrounding erythema, show the classic pathology of wedge-shaped dermal sclerosis and central epidermal atrophy with surrounding hyperkeratosis. Interface dermatitis and dermal mucin can be seen in all stages, though mucin is diminished in the later stage.
Effective treatment options are limited; however, antithrombotics or compounds that facilitate blood perfusion, such as aspirin or pentoxifylline, initially can be used.1 Eculizumab, a humanized monoclonal antibody that prevents the cleavage of C5, has been used for salvage therapy,8 as in our case. Treprostinil, a prostacyclin analog that causes arterial vasodilation and inhibition of platelet aggregation, has been reported to improve bowel and cutaneous lesions, functional status, and neurologic symptoms.9
Our case highlights important features of Degos disease. First, it is important for both the clinician and the pathologist to recognize that the histopathology of Degos disease changes as the lesions evolve. In our case, although the lesions were characteristic of Degos disease clinically, the initial biopsy was suspicious for connective tissue disease, which led to an autoimmune evaluation that ultimately was unremarkable. Recognizing that early lesions of Degos disease can resemble connective tissue disease histologically could have prevented this delay in diagnosis. However, Degos disease has been reported in association with autoimmune diseases.10 Second, although penile ulceration is uncommon, it can be a prominent cutaneous manifestation of the disease. Finally, eculizumab and treprostinil are therapeutic options that have shown some efficacy in improving symptoms and cutaneous lesions.8,9
To the Editor:
A 56-year-old man was referred to our Grand Rounds by another dermatologist in our health system for evaluation of a red scaly rash on the trunk that had been present for more than a year. More recently, over the course of approximately 9 months he experienced recurrent painful penile ulcers that lasted for approximately 4 weeks and then self-resolved. He had a medical history of central retinal vein occlusion, primary hyperparathyroidism, and nonspecific colitis. A family history was notable for lung cancer in the patient’s father and myelodysplastic syndrome and breast cancer in his mother; however, there was no family history of a similar rash. A bacterial culture of the penile ulcer was negative. Testing for antibodies against HIV and herpes simplex virus (HSV) types 1 and 2 was negative. Results of a serum VDRL test were nonreactive, which ruled out syphilis. The patient was treated by the referring dermatologist with azithromycin for possible chancroid without relief.
The patient was being followed by the referring dermatologist who initially was concerned for Degos disease based on clinical examination findings, prompting biopsy of a lesion on the back, which revealed vacuolar interface dermatitis, a sparse superficial perivascular lymphocytic infiltrate, and increased mucin—all highly suspicious for connective tissue disease (Figure 1). An antinuclear antibody test was positive, with a titer of 1:640. The patient was started on prednisone and referred to rheumatology; however, further evaluation by rheumatology for an autoimmune process—including anticardiolipin antibodies—was unremarkable. A few months prior to the current presentation, he also had mildly elevated liver function test results. A colonoscopy was performed, and a biopsy revealed nonspecific colitis. A biopsy of the penile ulcer also was nonspecific, showing only ulceration and acute and chronic inflammation. No epidermal interface change was seen. Results from a Grocott-Gomori methenamine-silver stain, Treponema pallidum immunostain, and HSV polymerase chain reaction were negative for fungal organisms, spirochetes, and HSV, respectively. The differential diagnosis included trauma, aphthous ulceration, and Behçet disease. Behçet disease was suspected by the referring dermatologist, and the patient was treated with colchicine, prednisone, pimecrolimus cream, and topical lidocaine; however, the lesions persisted, and he was subsequently referred to our Grand Rounds for further evaluation.
At the current presentation, physical examination revealed several small papules with white atrophic centers and erythematous rims on the trunk and extremities (Figure 2A). An ulceration was noted on the penile shaft (Figure 2B). Further evaluation for Behçet disease, including testing for pathergy and HLA-B51, was negative. Degos disease was strongly suspected clinically, and a repeat biopsy was performed of a lesion on the abdomen, which revealed central epidermal necrosis, atrophy, and parakeratosis with an underlying wedge-shaped dermal infarct surrounded by multiple small occluded dermal vessels, perivascular inflammation, and dermal edema (Figure 3). Direct immunofluorescence was performed using antibodies against IgG, IgA, IgM, fibrinogen, albumin, and C3, which was negative. These findings from direct immunofluorescence and histopathology as well as the clinical presentation were considered compatible with Degos disease. The patient was started on aspirin and pentoxifylline. Pentoxifylline 400 mg twice daily appeared to lessen some of the pain. Pain management specialists started the patient on gabapentin.
Approximately 4 months after the Grand Rounds evaluation, during which time he continued treatment with pentoxifylline, he was admitted to the hospital for intractable nausea and vomiting. His condition acutely declined due to bowel perforation, and he was started on eculizumab 1200 mg every 14 days. Because of an increased risk for meningococcal meningitis while on this medication, he also was given erythromycin 500 mg twice daily prophylactically. He was being followed by hematology for the vasculopathy, and they were planning to monitor for any disease changes with computed tomography of the chest, abdomen, and pelvis every 3 months, as well as echocardiogram every 6 months for any development of pericardial or pleural fibrosis. Approximately 1 month later, the patient was admitted to the hospital again but died after 1 week from gastrointestinal complications (approximately 22 months after the onset of the rash).
Degos disease (atrophic papulosis) is a rare small vessel vasculopathy of unknown etiology, but complement-mediated endothelial injury plays a role.1,2 It typically occurs in the fourth decade of life, with a slight female predominance.3,4 The skin lesions are characteristic and described as 5- to 10-mm papules with atrophic white centers and erythematous telangiectatic rims, most commonly on the upper body and typically sparing the head, palms, and soles.1 Penile ulceration is an uncommon cutaneous feature, with only a few cases reported in the literature.5,6 Approximately one-third of patients will have only skin lesions, but two-thirds will develop systemic involvement 1 to 2 years after onset, with the gastrointestinal tract and central nervous system most commonly involved. For those with systemic involvement, the 5-year survival rate is approximately 55%, and the most common causes of death are bowel perforation, peritonitis, and stroke.3,4 Because some patients appear to never develop systemic complications, Theodoridis et al4 proposed that the disease be classified as either malignant atrophic papulosis or benign atrophic papulosis to indicate the malignant systemic form and the benign cutaneous form, respectively.
The histopathology of Degos disease changes as the lesions evolve.7 Early lesions show a superficial and deep perivascular and periadnexal lymphocytic infiltrate, possible interface dermatitis, and dermal mucin resembling lupus. The more fully developed lesions show a greater degree of inflammation and interface change as well as lymphocytic vasculitis. This stage also may have epidermal atrophy and early papillary dermal sclerosis resembling lichen sclerosus. The late-stage lesions, clinically observed as papules with atrophic white centers and surrounding erythema, show the classic pathology of wedge-shaped dermal sclerosis and central epidermal atrophy with surrounding hyperkeratosis. Interface dermatitis and dermal mucin can be seen in all stages, though mucin is diminished in the later stage.
Effective treatment options are limited; however, antithrombotics or compounds that facilitate blood perfusion, such as aspirin or pentoxifylline, initially can be used.1 Eculizumab, a humanized monoclonal antibody that prevents the cleavage of C5, has been used for salvage therapy,8 as in our case. Treprostinil, a prostacyclin analog that causes arterial vasodilation and inhibition of platelet aggregation, has been reported to improve bowel and cutaneous lesions, functional status, and neurologic symptoms.9
Our case highlights important features of Degos disease. First, it is important for both the clinician and the pathologist to recognize that the histopathology of Degos disease changes as the lesions evolve. In our case, although the lesions were characteristic of Degos disease clinically, the initial biopsy was suspicious for connective tissue disease, which led to an autoimmune evaluation that ultimately was unremarkable. Recognizing that early lesions of Degos disease can resemble connective tissue disease histologically could have prevented this delay in diagnosis. However, Degos disease has been reported in association with autoimmune diseases.10 Second, although penile ulceration is uncommon, it can be a prominent cutaneous manifestation of the disease. Finally, eculizumab and treprostinil are therapeutic options that have shown some efficacy in improving symptoms and cutaneous lesions.8,9
- Theodoridis A, Makrantonaki E, Zouboulis CC. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10. doi:10.1186/1750-1172-8-10
- Magro CM, Poe JC, Kim C, et al. Degos disease: a C5b-9/interferon-α-mediated endotheliopathy syndrome. Am J Clin Pathol. 2011;135:599-610. doi:10.1309/AJCP66QIMFARLZKI
- Hu P, Mao Z, Liu C, et al. Malignant atrophic papulosis with motor aphasia and intestinal perforation: a case report and review of published works. J Dermatol. 2018;45:723-726. doi:10.1111/1346-8138.14280
- Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115. doi:10.1111/bjd.12642
- Thomson KF, Highet AS. Penile ulceration in fatal malignant atrophic papulosis (Degos’ disease). Br J Dermatol. 2000;143:1320-1322. doi:10.1046/j.1365-2133.2000.03911.x
- Aydogan K, Alkan G, Karadogan Koran S, et al. Painful penile ulceration in a patient with malignant atrophic papulosis. J Eur Acad Dermatol Venereol. 2005;19:612-616. doi:10.1111/j.1468-3083.2005.01227.x
- Harvell JD, Williford PL, White WL. Benign cutaneous Degos’ disease: a case report with emphasis on histopathology as papules chronologically evolve. Am J Dermatopathol. 2001;23:116-123. doi:10.1097/00000372-200104000-00006
- Oliver B, Boehm M, Rosing DR, et al. Diffuse atrophic papules and plaques, intermittent abdominal pain, paresthesias, and cardiac abnormalities in a 55-year-old woman. J Am Acad Dermatol. 2016;75:1274-1277. doi:10.1016/j.jaad.2016.09.015
- Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52. doi:10.1186/1750-1172-8-52
- Burgin S, Stone JH, Shenoy-Bhangle AS, et al. Case records of the Massachusetts General Hospital. Case 18-2014. A 32-year-old man with a rash, myalgia, and weakness. N Engl J Med. 2014;370:2327-2337. doi:10.1056/NEJMcpc1304161
- Theodoridis A, Makrantonaki E, Zouboulis CC. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10. doi:10.1186/1750-1172-8-10
- Magro CM, Poe JC, Kim C, et al. Degos disease: a C5b-9/interferon-α-mediated endotheliopathy syndrome. Am J Clin Pathol. 2011;135:599-610. doi:10.1309/AJCP66QIMFARLZKI
- Hu P, Mao Z, Liu C, et al. Malignant atrophic papulosis with motor aphasia and intestinal perforation: a case report and review of published works. J Dermatol. 2018;45:723-726. doi:10.1111/1346-8138.14280
- Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115. doi:10.1111/bjd.12642
- Thomson KF, Highet AS. Penile ulceration in fatal malignant atrophic papulosis (Degos’ disease). Br J Dermatol. 2000;143:1320-1322. doi:10.1046/j.1365-2133.2000.03911.x
- Aydogan K, Alkan G, Karadogan Koran S, et al. Painful penile ulceration in a patient with malignant atrophic papulosis. J Eur Acad Dermatol Venereol. 2005;19:612-616. doi:10.1111/j.1468-3083.2005.01227.x
- Harvell JD, Williford PL, White WL. Benign cutaneous Degos’ disease: a case report with emphasis on histopathology as papules chronologically evolve. Am J Dermatopathol. 2001;23:116-123. doi:10.1097/00000372-200104000-00006
- Oliver B, Boehm M, Rosing DR, et al. Diffuse atrophic papules and plaques, intermittent abdominal pain, paresthesias, and cardiac abnormalities in a 55-year-old woman. J Am Acad Dermatol. 2016;75:1274-1277. doi:10.1016/j.jaad.2016.09.015
- Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52. doi:10.1186/1750-1172-8-52
- Burgin S, Stone JH, Shenoy-Bhangle AS, et al. Case records of the Massachusetts General Hospital. Case 18-2014. A 32-year-old man with a rash, myalgia, and weakness. N Engl J Med. 2014;370:2327-2337. doi:10.1056/NEJMcpc1304161
PRACTICE POINTS
- Papules with atrophic white centers and erythematous telangiectatic rims are the characteristic skin lesions found in Degos disease.
- A painful penile ulceration also may occur in Degos disease, though it is uncommon.
- The histopathology of skin lesions changes as the lesions evolve. Early lesions may resemble connective tissue disease. Late lesions show the classic pathology of wedge-shaped dermal sclerosis.
Chronic Cribriform Ulcerated Plaque on the Left Calf
The Diagnosis: Nodular Basal Cell Carcinoma
Histopathology of the lesion showed a large basaloid lobule with focal epidermal attachment, peripheral nuclear palisading with cleft formation between the tumor and surrounding stroma, fibromyxoid stroma and mild pleomorphism, and variable mitotic activity and apoptosis (Figure). Based on the clinical presentation and histopathology, the patient was diagnosed with nodular basal cell carcinoma (BCC). He underwent a wide local excision of the affected area that was repaired with a splitthickness skin graft.
Basal cell carcinoma is the most common skin cancer worldwide and typically occurs due to years of UV radiation damage on sun-exposed skin, which accounts for a higher frequency of BCC occurring in patients residing in geographic locations with greater UV exposure (eg, higher and lower latitudes). In addition to cumulative UV dose, the duration of the exposure as well as its intensity also play a role in the development of BCC, particularly in early childhood and adolescence. Nevertheless, UV exposure is not the only risk factor, as 20% of BCCs arise in skin that is not exposed to the sun. Other risk factors include exposure to ionizing radiation and arsenic, immunosuppression, and genetic predisposition.1 Although these malignancies typically do not metastasize, growth can lead to local tissue destruction and major disfigurement if not treated in a timely fashion.2
In our patient, the differential diagnosis included pyoderma gangrenosum (PG) given the clinical appearance of the cribriform base and violaceous undermined rim of the ulcer. Pyoderma gangrenosum is a rare neutrophilic disorder that often results in ulcers that have been associated with various systemic autoimmune and inflammatory conditions, such as inflammatory bowel disease. There are 4 main subtypes of PG: the classic ulcerative type (our patient); the pustular type, which most often is seen in patients with inflammatory bowel disease; the bullous type, which can be seen in patients with an associated lymphoproliferative disorder; and the vegetative type. It frequently is thought of as both a clinical and histologic diagnosis of exclusion due to the nonspecific histopathologic features; most lesions demonstrate an infiltrate of neutrophils in the dermis. A biopsy was crucial in our patient, considering that diagnosis and treatment would have been further delayed had the patient been empirically treated with oral and topical steroids for presumed PG, which is precisely why PG is a diagnosis of exclusion. It is imperative for clinicians to rule out other pathologies, such as infection or malignancy, as demonstrated in our patient. The progressive onset and slow evolution of the lesion over years along with a lack of pain were more suggestive of BCC rather than PG. However, there is a report in the literature of PG mimicking BCC with both clinical and dermoscopic findings.3
Venous or stasis ulcers are painless, and although they rarely occur on the calf, they typically are seen lower on the leg such as on the medial ankles. Our patient endorsed occasional swelling of the affected leg and presented with edema, but overlying stasis change and other signs of venous insufficiency were absent.
Buruli ulcer is a painless chronic debilitating cutaneous disease resulting in indolent necrotizing skin as well as subcutaneous and bone lesions. It is caused by the environmental organism Mycobacterium ulcerans and typically is reported in Africa, Central/South America, the Western Pacific Region, and Australia.4 Histopathology usually demonstrates necrosis of subcutaneous tissue and dermal collagen accompanied by inflammation and acidfast bacilli highlighted by Ziehl-Neelsen stain.5 Smears of the lesions as well as culture and polymerase chain reaction for acid-fast bacilli also can be performed. Our patient reported no recent travel to any endemic areas and had no other risk factors or exposures to the pathogen responsible for this condition.
Traumatic ulcer also was included in the differential diagnosis, but the patient denied preceding trauma to the area, and the contralateral foot prosthesis did not rub on or impact the affected leg.
Basal cell carcinoma typically is treated surgically, but choice of treatment can depend on the subtype, size, tumor site, and/or patient preference.1 Other treatment modalities include electrodesiccation and curettage, cryosurgical destruction, photodynamic therapy, radiation, topical therapies, and systemic medications. Radiotherapy can be considered as a primary treatment option for BCC if surgery is contraindicated or declined by the patient, but it also is useful as an adjuvant therapy when there is perineural invasion of the tumor or positive margins. Hedgehog pathway inhibitors such as vismodegib currently are indicated for patients who are not candidates for surgery or radiation as well as for those with metastatic or locally advanced, recurrent BCC. There is no single treatment method ideal for every lesion or patient. Specific populations such as the elderly, the immunosuppressed, or those with poor baseline functional status may warrant a nonsurgical approach. The clinician must take into consideration all factors while at the same time thinking about how to best accomplish the goals of recurrencefree tumor removal, correction of any underlying functional impairment from the tumor, and maintenance of cosmesis.1
- McDaniel B, Badri T, Steele RB. Basal cell carcinoma. In: StatPearls. StatPearls; 2022.
- Marzuka AG, Book SE. Basal cell carcinoma: pathogenesis, epidemiology, clinical features, diagnosis, histopathology, and management. Yale J Biol Med. 2015;88:167-179.
- Rosina P, Papagrigoraki A, Colato C. A case of superficial granulomatous pyoderma mimicking a basal cell carcinoma. Acta Dermatovenerol Croat. 2014;22:48-51.
- Yotsu RR, Suzuki K, Simmonds RE, et al. Buruli ulcer: a review of the current knowledge. Curr Trop Med Rep. 2018;5:247-256.
- Guarner J, Bartlett J, Whitney EA, et al. Histopathologic features of Mycobacterium ulcerans infection. Emerg Infect Dis. 2003;9:651-656.
The Diagnosis: Nodular Basal Cell Carcinoma
Histopathology of the lesion showed a large basaloid lobule with focal epidermal attachment, peripheral nuclear palisading with cleft formation between the tumor and surrounding stroma, fibromyxoid stroma and mild pleomorphism, and variable mitotic activity and apoptosis (Figure). Based on the clinical presentation and histopathology, the patient was diagnosed with nodular basal cell carcinoma (BCC). He underwent a wide local excision of the affected area that was repaired with a splitthickness skin graft.
Basal cell carcinoma is the most common skin cancer worldwide and typically occurs due to years of UV radiation damage on sun-exposed skin, which accounts for a higher frequency of BCC occurring in patients residing in geographic locations with greater UV exposure (eg, higher and lower latitudes). In addition to cumulative UV dose, the duration of the exposure as well as its intensity also play a role in the development of BCC, particularly in early childhood and adolescence. Nevertheless, UV exposure is not the only risk factor, as 20% of BCCs arise in skin that is not exposed to the sun. Other risk factors include exposure to ionizing radiation and arsenic, immunosuppression, and genetic predisposition.1 Although these malignancies typically do not metastasize, growth can lead to local tissue destruction and major disfigurement if not treated in a timely fashion.2
In our patient, the differential diagnosis included pyoderma gangrenosum (PG) given the clinical appearance of the cribriform base and violaceous undermined rim of the ulcer. Pyoderma gangrenosum is a rare neutrophilic disorder that often results in ulcers that have been associated with various systemic autoimmune and inflammatory conditions, such as inflammatory bowel disease. There are 4 main subtypes of PG: the classic ulcerative type (our patient); the pustular type, which most often is seen in patients with inflammatory bowel disease; the bullous type, which can be seen in patients with an associated lymphoproliferative disorder; and the vegetative type. It frequently is thought of as both a clinical and histologic diagnosis of exclusion due to the nonspecific histopathologic features; most lesions demonstrate an infiltrate of neutrophils in the dermis. A biopsy was crucial in our patient, considering that diagnosis and treatment would have been further delayed had the patient been empirically treated with oral and topical steroids for presumed PG, which is precisely why PG is a diagnosis of exclusion. It is imperative for clinicians to rule out other pathologies, such as infection or malignancy, as demonstrated in our patient. The progressive onset and slow evolution of the lesion over years along with a lack of pain were more suggestive of BCC rather than PG. However, there is a report in the literature of PG mimicking BCC with both clinical and dermoscopic findings.3
Venous or stasis ulcers are painless, and although they rarely occur on the calf, they typically are seen lower on the leg such as on the medial ankles. Our patient endorsed occasional swelling of the affected leg and presented with edema, but overlying stasis change and other signs of venous insufficiency were absent.
Buruli ulcer is a painless chronic debilitating cutaneous disease resulting in indolent necrotizing skin as well as subcutaneous and bone lesions. It is caused by the environmental organism Mycobacterium ulcerans and typically is reported in Africa, Central/South America, the Western Pacific Region, and Australia.4 Histopathology usually demonstrates necrosis of subcutaneous tissue and dermal collagen accompanied by inflammation and acidfast bacilli highlighted by Ziehl-Neelsen stain.5 Smears of the lesions as well as culture and polymerase chain reaction for acid-fast bacilli also can be performed. Our patient reported no recent travel to any endemic areas and had no other risk factors or exposures to the pathogen responsible for this condition.
Traumatic ulcer also was included in the differential diagnosis, but the patient denied preceding trauma to the area, and the contralateral foot prosthesis did not rub on or impact the affected leg.
Basal cell carcinoma typically is treated surgically, but choice of treatment can depend on the subtype, size, tumor site, and/or patient preference.1 Other treatment modalities include electrodesiccation and curettage, cryosurgical destruction, photodynamic therapy, radiation, topical therapies, and systemic medications. Radiotherapy can be considered as a primary treatment option for BCC if surgery is contraindicated or declined by the patient, but it also is useful as an adjuvant therapy when there is perineural invasion of the tumor or positive margins. Hedgehog pathway inhibitors such as vismodegib currently are indicated for patients who are not candidates for surgery or radiation as well as for those with metastatic or locally advanced, recurrent BCC. There is no single treatment method ideal for every lesion or patient. Specific populations such as the elderly, the immunosuppressed, or those with poor baseline functional status may warrant a nonsurgical approach. The clinician must take into consideration all factors while at the same time thinking about how to best accomplish the goals of recurrencefree tumor removal, correction of any underlying functional impairment from the tumor, and maintenance of cosmesis.1
The Diagnosis: Nodular Basal Cell Carcinoma
Histopathology of the lesion showed a large basaloid lobule with focal epidermal attachment, peripheral nuclear palisading with cleft formation between the tumor and surrounding stroma, fibromyxoid stroma and mild pleomorphism, and variable mitotic activity and apoptosis (Figure). Based on the clinical presentation and histopathology, the patient was diagnosed with nodular basal cell carcinoma (BCC). He underwent a wide local excision of the affected area that was repaired with a splitthickness skin graft.
Basal cell carcinoma is the most common skin cancer worldwide and typically occurs due to years of UV radiation damage on sun-exposed skin, which accounts for a higher frequency of BCC occurring in patients residing in geographic locations with greater UV exposure (eg, higher and lower latitudes). In addition to cumulative UV dose, the duration of the exposure as well as its intensity also play a role in the development of BCC, particularly in early childhood and adolescence. Nevertheless, UV exposure is not the only risk factor, as 20% of BCCs arise in skin that is not exposed to the sun. Other risk factors include exposure to ionizing radiation and arsenic, immunosuppression, and genetic predisposition.1 Although these malignancies typically do not metastasize, growth can lead to local tissue destruction and major disfigurement if not treated in a timely fashion.2
In our patient, the differential diagnosis included pyoderma gangrenosum (PG) given the clinical appearance of the cribriform base and violaceous undermined rim of the ulcer. Pyoderma gangrenosum is a rare neutrophilic disorder that often results in ulcers that have been associated with various systemic autoimmune and inflammatory conditions, such as inflammatory bowel disease. There are 4 main subtypes of PG: the classic ulcerative type (our patient); the pustular type, which most often is seen in patients with inflammatory bowel disease; the bullous type, which can be seen in patients with an associated lymphoproliferative disorder; and the vegetative type. It frequently is thought of as both a clinical and histologic diagnosis of exclusion due to the nonspecific histopathologic features; most lesions demonstrate an infiltrate of neutrophils in the dermis. A biopsy was crucial in our patient, considering that diagnosis and treatment would have been further delayed had the patient been empirically treated with oral and topical steroids for presumed PG, which is precisely why PG is a diagnosis of exclusion. It is imperative for clinicians to rule out other pathologies, such as infection or malignancy, as demonstrated in our patient. The progressive onset and slow evolution of the lesion over years along with a lack of pain were more suggestive of BCC rather than PG. However, there is a report in the literature of PG mimicking BCC with both clinical and dermoscopic findings.3
Venous or stasis ulcers are painless, and although they rarely occur on the calf, they typically are seen lower on the leg such as on the medial ankles. Our patient endorsed occasional swelling of the affected leg and presented with edema, but overlying stasis change and other signs of venous insufficiency were absent.
Buruli ulcer is a painless chronic debilitating cutaneous disease resulting in indolent necrotizing skin as well as subcutaneous and bone lesions. It is caused by the environmental organism Mycobacterium ulcerans and typically is reported in Africa, Central/South America, the Western Pacific Region, and Australia.4 Histopathology usually demonstrates necrosis of subcutaneous tissue and dermal collagen accompanied by inflammation and acidfast bacilli highlighted by Ziehl-Neelsen stain.5 Smears of the lesions as well as culture and polymerase chain reaction for acid-fast bacilli also can be performed. Our patient reported no recent travel to any endemic areas and had no other risk factors or exposures to the pathogen responsible for this condition.
Traumatic ulcer also was included in the differential diagnosis, but the patient denied preceding trauma to the area, and the contralateral foot prosthesis did not rub on or impact the affected leg.
Basal cell carcinoma typically is treated surgically, but choice of treatment can depend on the subtype, size, tumor site, and/or patient preference.1 Other treatment modalities include electrodesiccation and curettage, cryosurgical destruction, photodynamic therapy, radiation, topical therapies, and systemic medications. Radiotherapy can be considered as a primary treatment option for BCC if surgery is contraindicated or declined by the patient, but it also is useful as an adjuvant therapy when there is perineural invasion of the tumor or positive margins. Hedgehog pathway inhibitors such as vismodegib currently are indicated for patients who are not candidates for surgery or radiation as well as for those with metastatic or locally advanced, recurrent BCC. There is no single treatment method ideal for every lesion or patient. Specific populations such as the elderly, the immunosuppressed, or those with poor baseline functional status may warrant a nonsurgical approach. The clinician must take into consideration all factors while at the same time thinking about how to best accomplish the goals of recurrencefree tumor removal, correction of any underlying functional impairment from the tumor, and maintenance of cosmesis.1
- McDaniel B, Badri T, Steele RB. Basal cell carcinoma. In: StatPearls. StatPearls; 2022.
- Marzuka AG, Book SE. Basal cell carcinoma: pathogenesis, epidemiology, clinical features, diagnosis, histopathology, and management. Yale J Biol Med. 2015;88:167-179.
- Rosina P, Papagrigoraki A, Colato C. A case of superficial granulomatous pyoderma mimicking a basal cell carcinoma. Acta Dermatovenerol Croat. 2014;22:48-51.
- Yotsu RR, Suzuki K, Simmonds RE, et al. Buruli ulcer: a review of the current knowledge. Curr Trop Med Rep. 2018;5:247-256.
- Guarner J, Bartlett J, Whitney EA, et al. Histopathologic features of Mycobacterium ulcerans infection. Emerg Infect Dis. 2003;9:651-656.
- McDaniel B, Badri T, Steele RB. Basal cell carcinoma. In: StatPearls. StatPearls; 2022.
- Marzuka AG, Book SE. Basal cell carcinoma: pathogenesis, epidemiology, clinical features, diagnosis, histopathology, and management. Yale J Biol Med. 2015;88:167-179.
- Rosina P, Papagrigoraki A, Colato C. A case of superficial granulomatous pyoderma mimicking a basal cell carcinoma. Acta Dermatovenerol Croat. 2014;22:48-51.
- Yotsu RR, Suzuki K, Simmonds RE, et al. Buruli ulcer: a review of the current knowledge. Curr Trop Med Rep. 2018;5:247-256.
- Guarner J, Bartlett J, Whitney EA, et al. Histopathologic features of Mycobacterium ulcerans infection. Emerg Infect Dis. 2003;9:651-656.
A 61-year-old man presented to the dermatology clinic for evaluation of a painless nonhealing wound on the left calf of 4 years’ duration. The patient had a history of amputation of the right foot as an infant, for which he wore an orthopedic prosthesis. He also had chronic lymphedema of the left leg, hyperlipidemia, and osteoarthritis of the right hip. There was no history of gastrointestinal tract issues. The lesion initially was small, then grew and began to ulcerate and bleed. His presentation to dermatology was delayed due to office closures during the COVID-19 pandemic. Physical examination revealed a 5-cm, erythematous, cribriform ulcer with a violaceous undermined rim. A punch biopsy was performed on the edge of the ulcer.
Working Hard or Work Addiction — Have You Crossed the Line?
When child psychiatrist Javeed Sukhera, MD, PhD, was a few years into his career, he found himself doing it all. “I was in a leadership role academically at the medical school, I had a leadership role at the hospital, and I was seeing as many patients as I could. I could work all day every day.”
“It still wouldn’t have been enough,” he said.
Whenever there was a shift available, Dr. Sukhera would take it. His job was stressful, but as a new physician with a young family, he saw this obsession with work as necessary. “I began to cope with the stress from work by doing extra work and feeling like I needed to be everywhere. It was like I became a hamster on a spinning wheel. I was just running, running, running.”
Things shifted for Dr. Sukhera when he realized that while he was emotionally available for the children who were his patients, at home, his own children weren’t getting the best of him. “There was a specific moment when I thought my son was afraid of me,” he said. “I just stopped and realized that there was something happening that I needed to break. I needed to make a change.”
Dr. Sukhera, now chair of psychiatry at the Institute of Living and chief of the Department of Psychiatry at Hartford Hospital, Hartford, Connecticut, believes what he experienced was a steep fall into work addiction.
What Does Work Addiction Look Like for Doctors?
Behavioral addictions are fairly new in the addiction space. When gambling disorder, the first and only behavioral addiction in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, was added in 2013, it was seen as a “breakthrough addiction,” said Mark D. Griffiths, PhD, a leading behavioral addiction researcher and a distinguished professor at Nottingham Trent University.
Because there is not enough evidence yet to classify work addiction as a formal diagnosis, there is no clear consensus on how to define it. To further complicate things, the terms “workaholism” and “work addiction” can be used interchangeably, and some experts say the two are not the same, though they can overlap.
That said, a 2018 review of literature from several countries found that work addiction “fits very well into recently postulated criteria for conceptualization of a behavioral addiction.
“If you accept that gambling can be genuinely addictive, then there’s no reason to think that something like work, exercise, or video game playing couldn’t be an addiction as well,” said Dr. Griffiths.
“The neurobiology of addiction is that we get drawn to something that gives us a dopamine hit,” Dr. Sukhera added. “But to do that all day, every day, has consequences. It drains our emotional reserves, and it can greatly impact our relationships.”
On top of that, work addiction has been linked with poor sleep, poor cardiovascular health, high blood pressure, burnout, the development of autoimmune disorders, and other health issues.
Physicians are particularly susceptible. Doctors, after all, are expected to work long hours and put their patients’ needs first, even at the expense of their own health and well-being.
“Workaholism is not just socially acceptable in medicine,” said Dr. Sukhera. “It’s baked into the system and built into the structures. The healthcare system has largely functioned on the emotional labor of health workers, whose tendency to show up and work harder can, at times, in certain organizations, be exploited.”
Dr. Griffiths agreed that with the limited amount of data available, work addiction does appear to exist at higher rates in medicine than in other fields. As early as the 1970s, medical literature describes work as a “socially acceptable” addiction among doctors. A 2014 study published in Occupational Medicine reported that of 445 physicians who took part in the research, nearly half exhibited some level of work addiction with 13% “highly work addicted.”
Of course, working hard or even meeting unreasonable demands from work is not the same as work addiction, as Dr. Griffiths clarified in a 2023 editorial in BMJ Quality & Safety. The difference, as with other behavioral addictions, is when people obsess about work and use it to cope with stress. It can be easier to stay distracted and busy to gain a sense of control rather than learning to deal with complex emotions.
A 2021 study that Dr. Sukhera conducted with resident physicians found that working harder was one of the main ways they dealt with stress during the COVID-19 pandemic. “This idea that we deal with the stress of being burnt out by doing more and more of what burns us out is fairly ubiquitous at all stages of medical professionals’ careers,” he said.
Financial incentives also can fuel work addiction, said Dr. Sukhera. In residency, there are some safeguards around overwork and duty hours. When you become an attending, those limits no longer exist. As a young physician, Dr. Sukhera had student debt to pay off and a family to support. When he found opportunities to earn more by working more, his answer was always “yes.”
Pressure to produce medical research also can pose issues. Some physicians can become addicted to publishing studies, fearing that they might lose their professional status or position if they stop. It’s a cycle that can force a doctor to not only work long hours doing their job but also practically take on a second one.
How Physicians Can Recognize Work Addiction in Themselves
Work addiction can look and feel different for every person, said Malissa Clark, PhD, associate professor at the University of Georgia and author of the recent book Never Not Working: Why the Always-On Culture Is Bad for Business—and How to Fix It.
Dr. Clark noted that people who are highly engaged in their work tend to be driven by intrinsic motivation: “You work because you love it.” With work addiction, “you work because you feel like you ought to be working all the time.”
Of course, it’s not always so cut and dried; you can experience both forms of motivation and not necessarily become addicted to work. But if you are solely driven by the feeling that you ought to be working all the time, that can be a red flag.
Dr. Griffiths said that while many people may have problematic work habits or work too much, true work addicts must meet six criteria that apply to all addictions:
1. Salience: Work is the single most important thing in your life, to the point of neglecting everything else. Even if you’re on vacation, your mind might be flooded with work thoughts.
2. Mood modification: You use work to modify your mood, either to get a “high” or to cope with stress.
3. Tolerance: Over time, you’ve gone from working 8 or 10 hours a day to 12 hours a day, to a point where you’re working all the time.
4. Withdrawal: On a physiological level, you will have symptoms such as anxiety, nausea, or headaches when unable to work.
5. Conflict: You feel conflicted with yourself (you know you’re working too much) or with others (partners, friends, and children) about work, but you can’t stop.
6. Relapse: If you manage to cut down your hours but can’t resist overworking 1 day, you wind up right back where you were.
When It’s Time to Address Work Addiction
The lack of a formal diagnosis for work addiction makes getting treatment difficult. But there are ways to seek help. Unlike the drug and alcohol literature, abstinence is not the goal. “The therapeutic goal is getting a behavior under control and looking for the triggers of why you’re compulsively working,” said Dr. Griffiths.
Practice self-compassion
Dr. Sukhera eventually realized that his work addiction stemmed from the fear of being somehow excluded or unworthy. He actively corrected much of this through self-compassion and self-kindness, which helped him set boundaries. “Self-compassion is the root of everything,” he said. “Reminding ourselves that we’re doing our best is an important ingredient in breaking the cycle.”
Slowly expose yourself to relaxation
Many workaholics find rest very difficult. “When I conducted interviews with people [who considered themselves workaholics], a very common thing I heard was, ‘I have a very hard time being idle,’ ” said Dr. Clark. If rest feels hard, Dr. Sukhera suggests practicing relaxation for 2 minutes to start. Even small periods of downtime can challenge the belief that you must be constantly productive.
Reframe your to-do list
For work addicts, to-do lists can seem like they must be finished, which prolongs work hours. Instead, use to-do lists to help prioritize what is urgent, identify what can wait, and delegate out tasks to others, Dr. Clark recommends.
Pick up a mastery experience
Research from professor Sabine Sonnentag, Dr. rer. nat., at the University of Mannheim, Mannheim, Germany, suggests that mastery experiences — leisure activities that require thought and focus like learning a new language or taking a woodworking class — can help you actively disengage from work.
Try cognitive behavioral therapy
Widely used for other forms of addiction, cognitive behavioral therapy centers around recognizing emotions, challenging thought patterns, and changing behaviors. However, Dr. Clark admits the research on its impact on work addiction, in particular, is “pretty nascent.”
Shift your mindset
It seems logical to think that detaching from your feelings will allow you to “do more,” but experts say that idea is both untrue and dangerous. “The safest hospitals are the hospitals where people are attuned to their humanness,” said Dr. Sukhera. “It’s normal to overwork in medicine, and if you’re challenging a norm, you really have to be thoughtful about how you frame that for yourself.”
Most importantly: Seek support
Today, there is increased awareness about work addiction and more resources for physicians who are struggling, including programs such as Workaholics Anonymous or Physicians Anonymous and workplace wellness initiatives. But try not to overwhelm yourself with choosing whom to talk to or what specific resource to utilize, Dr. Sukhera advised. “Just talk to someone about it. You don’t have to carry this on your own.”
A version of this article appeared on Medscape.com.
When child psychiatrist Javeed Sukhera, MD, PhD, was a few years into his career, he found himself doing it all. “I was in a leadership role academically at the medical school, I had a leadership role at the hospital, and I was seeing as many patients as I could. I could work all day every day.”
“It still wouldn’t have been enough,” he said.
Whenever there was a shift available, Dr. Sukhera would take it. His job was stressful, but as a new physician with a young family, he saw this obsession with work as necessary. “I began to cope with the stress from work by doing extra work and feeling like I needed to be everywhere. It was like I became a hamster on a spinning wheel. I was just running, running, running.”
Things shifted for Dr. Sukhera when he realized that while he was emotionally available for the children who were his patients, at home, his own children weren’t getting the best of him. “There was a specific moment when I thought my son was afraid of me,” he said. “I just stopped and realized that there was something happening that I needed to break. I needed to make a change.”
Dr. Sukhera, now chair of psychiatry at the Institute of Living and chief of the Department of Psychiatry at Hartford Hospital, Hartford, Connecticut, believes what he experienced was a steep fall into work addiction.
What Does Work Addiction Look Like for Doctors?
Behavioral addictions are fairly new in the addiction space. When gambling disorder, the first and only behavioral addiction in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, was added in 2013, it was seen as a “breakthrough addiction,” said Mark D. Griffiths, PhD, a leading behavioral addiction researcher and a distinguished professor at Nottingham Trent University.
Because there is not enough evidence yet to classify work addiction as a formal diagnosis, there is no clear consensus on how to define it. To further complicate things, the terms “workaholism” and “work addiction” can be used interchangeably, and some experts say the two are not the same, though they can overlap.
That said, a 2018 review of literature from several countries found that work addiction “fits very well into recently postulated criteria for conceptualization of a behavioral addiction.
“If you accept that gambling can be genuinely addictive, then there’s no reason to think that something like work, exercise, or video game playing couldn’t be an addiction as well,” said Dr. Griffiths.
“The neurobiology of addiction is that we get drawn to something that gives us a dopamine hit,” Dr. Sukhera added. “But to do that all day, every day, has consequences. It drains our emotional reserves, and it can greatly impact our relationships.”
On top of that, work addiction has been linked with poor sleep, poor cardiovascular health, high blood pressure, burnout, the development of autoimmune disorders, and other health issues.
Physicians are particularly susceptible. Doctors, after all, are expected to work long hours and put their patients’ needs first, even at the expense of their own health and well-being.
“Workaholism is not just socially acceptable in medicine,” said Dr. Sukhera. “It’s baked into the system and built into the structures. The healthcare system has largely functioned on the emotional labor of health workers, whose tendency to show up and work harder can, at times, in certain organizations, be exploited.”
Dr. Griffiths agreed that with the limited amount of data available, work addiction does appear to exist at higher rates in medicine than in other fields. As early as the 1970s, medical literature describes work as a “socially acceptable” addiction among doctors. A 2014 study published in Occupational Medicine reported that of 445 physicians who took part in the research, nearly half exhibited some level of work addiction with 13% “highly work addicted.”
Of course, working hard or even meeting unreasonable demands from work is not the same as work addiction, as Dr. Griffiths clarified in a 2023 editorial in BMJ Quality & Safety. The difference, as with other behavioral addictions, is when people obsess about work and use it to cope with stress. It can be easier to stay distracted and busy to gain a sense of control rather than learning to deal with complex emotions.
A 2021 study that Dr. Sukhera conducted with resident physicians found that working harder was one of the main ways they dealt with stress during the COVID-19 pandemic. “This idea that we deal with the stress of being burnt out by doing more and more of what burns us out is fairly ubiquitous at all stages of medical professionals’ careers,” he said.
Financial incentives also can fuel work addiction, said Dr. Sukhera. In residency, there are some safeguards around overwork and duty hours. When you become an attending, those limits no longer exist. As a young physician, Dr. Sukhera had student debt to pay off and a family to support. When he found opportunities to earn more by working more, his answer was always “yes.”
Pressure to produce medical research also can pose issues. Some physicians can become addicted to publishing studies, fearing that they might lose their professional status or position if they stop. It’s a cycle that can force a doctor to not only work long hours doing their job but also practically take on a second one.
How Physicians Can Recognize Work Addiction in Themselves
Work addiction can look and feel different for every person, said Malissa Clark, PhD, associate professor at the University of Georgia and author of the recent book Never Not Working: Why the Always-On Culture Is Bad for Business—and How to Fix It.
Dr. Clark noted that people who are highly engaged in their work tend to be driven by intrinsic motivation: “You work because you love it.” With work addiction, “you work because you feel like you ought to be working all the time.”
Of course, it’s not always so cut and dried; you can experience both forms of motivation and not necessarily become addicted to work. But if you are solely driven by the feeling that you ought to be working all the time, that can be a red flag.
Dr. Griffiths said that while many people may have problematic work habits or work too much, true work addicts must meet six criteria that apply to all addictions:
1. Salience: Work is the single most important thing in your life, to the point of neglecting everything else. Even if you’re on vacation, your mind might be flooded with work thoughts.
2. Mood modification: You use work to modify your mood, either to get a “high” or to cope with stress.
3. Tolerance: Over time, you’ve gone from working 8 or 10 hours a day to 12 hours a day, to a point where you’re working all the time.
4. Withdrawal: On a physiological level, you will have symptoms such as anxiety, nausea, or headaches when unable to work.
5. Conflict: You feel conflicted with yourself (you know you’re working too much) or with others (partners, friends, and children) about work, but you can’t stop.
6. Relapse: If you manage to cut down your hours but can’t resist overworking 1 day, you wind up right back where you were.
When It’s Time to Address Work Addiction
The lack of a formal diagnosis for work addiction makes getting treatment difficult. But there are ways to seek help. Unlike the drug and alcohol literature, abstinence is not the goal. “The therapeutic goal is getting a behavior under control and looking for the triggers of why you’re compulsively working,” said Dr. Griffiths.
Practice self-compassion
Dr. Sukhera eventually realized that his work addiction stemmed from the fear of being somehow excluded or unworthy. He actively corrected much of this through self-compassion and self-kindness, which helped him set boundaries. “Self-compassion is the root of everything,” he said. “Reminding ourselves that we’re doing our best is an important ingredient in breaking the cycle.”
Slowly expose yourself to relaxation
Many workaholics find rest very difficult. “When I conducted interviews with people [who considered themselves workaholics], a very common thing I heard was, ‘I have a very hard time being idle,’ ” said Dr. Clark. If rest feels hard, Dr. Sukhera suggests practicing relaxation for 2 minutes to start. Even small periods of downtime can challenge the belief that you must be constantly productive.
Reframe your to-do list
For work addicts, to-do lists can seem like they must be finished, which prolongs work hours. Instead, use to-do lists to help prioritize what is urgent, identify what can wait, and delegate out tasks to others, Dr. Clark recommends.
Pick up a mastery experience
Research from professor Sabine Sonnentag, Dr. rer. nat., at the University of Mannheim, Mannheim, Germany, suggests that mastery experiences — leisure activities that require thought and focus like learning a new language or taking a woodworking class — can help you actively disengage from work.
Try cognitive behavioral therapy
Widely used for other forms of addiction, cognitive behavioral therapy centers around recognizing emotions, challenging thought patterns, and changing behaviors. However, Dr. Clark admits the research on its impact on work addiction, in particular, is “pretty nascent.”
Shift your mindset
It seems logical to think that detaching from your feelings will allow you to “do more,” but experts say that idea is both untrue and dangerous. “The safest hospitals are the hospitals where people are attuned to their humanness,” said Dr. Sukhera. “It’s normal to overwork in medicine, and if you’re challenging a norm, you really have to be thoughtful about how you frame that for yourself.”
Most importantly: Seek support
Today, there is increased awareness about work addiction and more resources for physicians who are struggling, including programs such as Workaholics Anonymous or Physicians Anonymous and workplace wellness initiatives. But try not to overwhelm yourself with choosing whom to talk to or what specific resource to utilize, Dr. Sukhera advised. “Just talk to someone about it. You don’t have to carry this on your own.”
A version of this article appeared on Medscape.com.
When child psychiatrist Javeed Sukhera, MD, PhD, was a few years into his career, he found himself doing it all. “I was in a leadership role academically at the medical school, I had a leadership role at the hospital, and I was seeing as many patients as I could. I could work all day every day.”
“It still wouldn’t have been enough,” he said.
Whenever there was a shift available, Dr. Sukhera would take it. His job was stressful, but as a new physician with a young family, he saw this obsession with work as necessary. “I began to cope with the stress from work by doing extra work and feeling like I needed to be everywhere. It was like I became a hamster on a spinning wheel. I was just running, running, running.”
Things shifted for Dr. Sukhera when he realized that while he was emotionally available for the children who were his patients, at home, his own children weren’t getting the best of him. “There was a specific moment when I thought my son was afraid of me,” he said. “I just stopped and realized that there was something happening that I needed to break. I needed to make a change.”
Dr. Sukhera, now chair of psychiatry at the Institute of Living and chief of the Department of Psychiatry at Hartford Hospital, Hartford, Connecticut, believes what he experienced was a steep fall into work addiction.
What Does Work Addiction Look Like for Doctors?
Behavioral addictions are fairly new in the addiction space. When gambling disorder, the first and only behavioral addiction in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, was added in 2013, it was seen as a “breakthrough addiction,” said Mark D. Griffiths, PhD, a leading behavioral addiction researcher and a distinguished professor at Nottingham Trent University.
Because there is not enough evidence yet to classify work addiction as a formal diagnosis, there is no clear consensus on how to define it. To further complicate things, the terms “workaholism” and “work addiction” can be used interchangeably, and some experts say the two are not the same, though they can overlap.
That said, a 2018 review of literature from several countries found that work addiction “fits very well into recently postulated criteria for conceptualization of a behavioral addiction.
“If you accept that gambling can be genuinely addictive, then there’s no reason to think that something like work, exercise, or video game playing couldn’t be an addiction as well,” said Dr. Griffiths.
“The neurobiology of addiction is that we get drawn to something that gives us a dopamine hit,” Dr. Sukhera added. “But to do that all day, every day, has consequences. It drains our emotional reserves, and it can greatly impact our relationships.”
On top of that, work addiction has been linked with poor sleep, poor cardiovascular health, high blood pressure, burnout, the development of autoimmune disorders, and other health issues.
Physicians are particularly susceptible. Doctors, after all, are expected to work long hours and put their patients’ needs first, even at the expense of their own health and well-being.
“Workaholism is not just socially acceptable in medicine,” said Dr. Sukhera. “It’s baked into the system and built into the structures. The healthcare system has largely functioned on the emotional labor of health workers, whose tendency to show up and work harder can, at times, in certain organizations, be exploited.”
Dr. Griffiths agreed that with the limited amount of data available, work addiction does appear to exist at higher rates in medicine than in other fields. As early as the 1970s, medical literature describes work as a “socially acceptable” addiction among doctors. A 2014 study published in Occupational Medicine reported that of 445 physicians who took part in the research, nearly half exhibited some level of work addiction with 13% “highly work addicted.”
Of course, working hard or even meeting unreasonable demands from work is not the same as work addiction, as Dr. Griffiths clarified in a 2023 editorial in BMJ Quality & Safety. The difference, as with other behavioral addictions, is when people obsess about work and use it to cope with stress. It can be easier to stay distracted and busy to gain a sense of control rather than learning to deal with complex emotions.
A 2021 study that Dr. Sukhera conducted with resident physicians found that working harder was one of the main ways they dealt with stress during the COVID-19 pandemic. “This idea that we deal with the stress of being burnt out by doing more and more of what burns us out is fairly ubiquitous at all stages of medical professionals’ careers,” he said.
Financial incentives also can fuel work addiction, said Dr. Sukhera. In residency, there are some safeguards around overwork and duty hours. When you become an attending, those limits no longer exist. As a young physician, Dr. Sukhera had student debt to pay off and a family to support. When he found opportunities to earn more by working more, his answer was always “yes.”
Pressure to produce medical research also can pose issues. Some physicians can become addicted to publishing studies, fearing that they might lose their professional status or position if they stop. It’s a cycle that can force a doctor to not only work long hours doing their job but also practically take on a second one.
How Physicians Can Recognize Work Addiction in Themselves
Work addiction can look and feel different for every person, said Malissa Clark, PhD, associate professor at the University of Georgia and author of the recent book Never Not Working: Why the Always-On Culture Is Bad for Business—and How to Fix It.
Dr. Clark noted that people who are highly engaged in their work tend to be driven by intrinsic motivation: “You work because you love it.” With work addiction, “you work because you feel like you ought to be working all the time.”
Of course, it’s not always so cut and dried; you can experience both forms of motivation and not necessarily become addicted to work. But if you are solely driven by the feeling that you ought to be working all the time, that can be a red flag.
Dr. Griffiths said that while many people may have problematic work habits or work too much, true work addicts must meet six criteria that apply to all addictions:
1. Salience: Work is the single most important thing in your life, to the point of neglecting everything else. Even if you’re on vacation, your mind might be flooded with work thoughts.
2. Mood modification: You use work to modify your mood, either to get a “high” or to cope with stress.
3. Tolerance: Over time, you’ve gone from working 8 or 10 hours a day to 12 hours a day, to a point where you’re working all the time.
4. Withdrawal: On a physiological level, you will have symptoms such as anxiety, nausea, or headaches when unable to work.
5. Conflict: You feel conflicted with yourself (you know you’re working too much) or with others (partners, friends, and children) about work, but you can’t stop.
6. Relapse: If you manage to cut down your hours but can’t resist overworking 1 day, you wind up right back where you were.
When It’s Time to Address Work Addiction
The lack of a formal diagnosis for work addiction makes getting treatment difficult. But there are ways to seek help. Unlike the drug and alcohol literature, abstinence is not the goal. “The therapeutic goal is getting a behavior under control and looking for the triggers of why you’re compulsively working,” said Dr. Griffiths.
Practice self-compassion
Dr. Sukhera eventually realized that his work addiction stemmed from the fear of being somehow excluded or unworthy. He actively corrected much of this through self-compassion and self-kindness, which helped him set boundaries. “Self-compassion is the root of everything,” he said. “Reminding ourselves that we’re doing our best is an important ingredient in breaking the cycle.”
Slowly expose yourself to relaxation
Many workaholics find rest very difficult. “When I conducted interviews with people [who considered themselves workaholics], a very common thing I heard was, ‘I have a very hard time being idle,’ ” said Dr. Clark. If rest feels hard, Dr. Sukhera suggests practicing relaxation for 2 minutes to start. Even small periods of downtime can challenge the belief that you must be constantly productive.
Reframe your to-do list
For work addicts, to-do lists can seem like they must be finished, which prolongs work hours. Instead, use to-do lists to help prioritize what is urgent, identify what can wait, and delegate out tasks to others, Dr. Clark recommends.
Pick up a mastery experience
Research from professor Sabine Sonnentag, Dr. rer. nat., at the University of Mannheim, Mannheim, Germany, suggests that mastery experiences — leisure activities that require thought and focus like learning a new language or taking a woodworking class — can help you actively disengage from work.
Try cognitive behavioral therapy
Widely used for other forms of addiction, cognitive behavioral therapy centers around recognizing emotions, challenging thought patterns, and changing behaviors. However, Dr. Clark admits the research on its impact on work addiction, in particular, is “pretty nascent.”
Shift your mindset
It seems logical to think that detaching from your feelings will allow you to “do more,” but experts say that idea is both untrue and dangerous. “The safest hospitals are the hospitals where people are attuned to their humanness,” said Dr. Sukhera. “It’s normal to overwork in medicine, and if you’re challenging a norm, you really have to be thoughtful about how you frame that for yourself.”
Most importantly: Seek support
Today, there is increased awareness about work addiction and more resources for physicians who are struggling, including programs such as Workaholics Anonymous or Physicians Anonymous and workplace wellness initiatives. But try not to overwhelm yourself with choosing whom to talk to or what specific resource to utilize, Dr. Sukhera advised. “Just talk to someone about it. You don’t have to carry this on your own.”
A version of this article appeared on Medscape.com.
Periorbital Changes Induced by Prostaglandin Eye Drops
To the Editor:
A 42-year man presented with hollowing of the upper eyelid and skin discoloration of the left periorbital area of 10 years’ duration. He was a professional mixed martial arts fighter with a history of 2 surgeries for retinal detachment of the left eye 13 years prior to the current presentation. The patient also has macular scarring in the left eye. He denied a history of facial fracture, reconstructive surgery, or other medical conditions. His visual acuity was unknown; however, he did not require corrective glasses. He used 3 prescription ophthalmic eye drops—dorzolamide hydrochloride plus timolol maleate, 10 mL; brimonidine tartrate ophthalmic solution 0.15%, 5 mL; and latanoprost ophthalmic solution 0.005%, 125 μg/2.5 mL—in the left eye to lower intraocular pressure, as therapy for glaucoma. If left untreated, glaucoma can lead to vision loss.
Physical examination revealed periorbital hyperpigmentation on the left side; hypertrichosis and eyelash trichomegaly compared to the right side; and a deep left upper orbital sulcus compared to the right side (Figure). The patient was alert and oriented to person, place, and time. Extraocular movement was intact bilaterally, and his pupillary reflex was symmetric. No tenderness was noted over the affected area on palpation; no subcutaneous masses or lesions were observed or palpated. There was no ocular discharge, the conjunctiva was pink, and the sclera was white bilaterally.
The differential diagnosis included professional trauma-induced orbital changes, nevus of Ota (oculomucodermal melanocytosis), prostaglandin-associated periorbitopathy (PAP), and melasma. Although the patient sustained an injury that caused retinal detachment, he never experienced an orbital bone fracture; additionally, a fracture would not explain the skin discoloration or longer eyelashes. Periorbital nevus of Ota most commonly manifests as a unilateral scleral and brown-bluish skin discoloration but does not cause hollowing of the orbital sulcus or affect the length and thickness of eyelashes. Melasma—bilateral skin hyperpigmentation that most commonly affects women—can be induced by oral contraceptives, antibiotics, heat, sun exposure, and pregnancy. It does not affect the color of the iris or the depth of the scleral sulcus, and it does not increase the length and thickness of eyelashes. Based on the clinical presentation and a review of the eye drops used, he was diagnosed with PAP due to prolonged use of latanoprost ophthalmic solution. The patient was referred to an ophthalmologist for consideration of a switch to a different class of medication.
Of the 3 eye drops used by this patient, latanoprost, a prostaglandin analog, decreases intraocular pressure and is known to cause PAP. This condition comprises a constellation of changes, including upper eyelid ptosis, deepening of the upper eyelid sulcus, involution of dermatochalasis, periorbital fat atrophy, mild enophthalmos (sunken eye), inferior scleral show, increased prominence of eyelid vessels, and tight eyelids.1 Latanoprost most often produces these findings, but all prostaglandin ophthalmic medications can, including the dual-indication bimatoprost, which was approved by the US Food and Drug Administration to reduce elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension but also is used to grow darker, thicker, and longer eyelashes. Clinicians who prescribe bimatoprost for this cosmetic indication should be mindful of the potential for PAP and discuss it with patients.
The prescribing information (PI) for bimatoprost (Latisse; Allergan) does not list PAP as an adverse reaction observed in the 4-month multicenter, double-blind, randomized, vehicle-controlled study of bimatoprost (as Latisse) in 278 adults.2 The PI does list “periorbital and lid changes associated with periorbital fat atrophy and skin tightness resulting in deepening of eyelid sulcus and eyelid ptosis” as an adverse reaction in postmarketing experience. However, according to the PI, the frequency of these adverse reactions cannot be established, as the reporting of such incidents was voluntary and the size of the treated population was uncertain.2
Prostaglandins can cause periorbitopathy by several mechanisms; one speculated cause is that this group of medications might provoke smooth muscle contraction. Prostaglandin medications also have an affinity for fat cells1; atrophy of fat cells can lead to enophthalmos and deepening upper eyelid sulcus. In an observational study of 105 participants who were using a prostaglandin in 1 eye for longer than 1 month (the other eye was used as a control), the overall frequency of prostaglandin-associated periorbitopathy was 93.3% in the bimatoprost group, 41.4% in the latanoprost group, and 70% in the travoprost group, while the frequency of deepening of the upper eyelid sulcus was 80% in the bimatoprost group, 15.7% in the latanoprost group, and 45% in the travoprost group.3 These changes may not be as striking when a patient is using a prostaglandin ophthalmic medication in both eyes and may not be noticed even by the patient. It is prudent for the clinician to take a baseline photograph of the patient when these medications are prescribed to observe for early signs of periorbitopathy. These adverse effects may not be reversible when the medication is discontinued4 and have been observed as early as 4 to 6 weeks after the start of treatment.5
Our patient was counseled that his constellation of PAP findings potentially could be partially reversed over months or even a year or longer if the offending agent was discontinued. However, he was cautioned that cessation of latanoprost first needed to be discussed with his ophthalmologist, who would determine if there was a suitable alternative to a prostaglandin analog for him. The patient’s only concern was the aesthetic appearance of the left periorbital area. A hyaluronic acid filler or fat grafting can be considered for correction of orbital sulcus hollowing; however, we could not locate any long-term studies in which such corrective treatments were applied for PAP. Our patient continues to use latanoprost with no change in the frequency of use. There have been no further changes or progression in the physical appearance of the left eye or periorbital area. The patient has not undergone any corrective treatments.
- Berke SJ. PAP: new concerns for prostaglandin use. Rev Ophthalmol. 2012;19:70.
- Latisse (bimatoprost ophthalmic solution 0.03%). Package insert. Allergan; 2021. Accessed April 11, 2024. https://www.rxabbvie.com/pdf/latisse_pi.pdf
- Kucukevcilioglu M, Bayer A, Uysal Y, et al. Prostaglandin associated periorbitopathy in patients using bimatoprost, latanoprost and travoprost. Clin Exp Ophthalmol. 2014;42:126-131. doi:10.1111/ceo.12163
- Filippopoulos T, Paula JS, Torun N, et al. Periorbital changes associated with topical bimatoprost. Ophthalmic Plast Reconstr Surg. 2008;24:302-307. doi:10.1097/IOP.0b013e31817d81df
- Peplinski LS, Smith KA. Deepening of lid sulcus from topical bimatoprost therapy. Optom Vis Sci. 2004;81:574-577. doi:10.1097/01.opx.0000141791.16683.4a
To the Editor:
A 42-year man presented with hollowing of the upper eyelid and skin discoloration of the left periorbital area of 10 years’ duration. He was a professional mixed martial arts fighter with a history of 2 surgeries for retinal detachment of the left eye 13 years prior to the current presentation. The patient also has macular scarring in the left eye. He denied a history of facial fracture, reconstructive surgery, or other medical conditions. His visual acuity was unknown; however, he did not require corrective glasses. He used 3 prescription ophthalmic eye drops—dorzolamide hydrochloride plus timolol maleate, 10 mL; brimonidine tartrate ophthalmic solution 0.15%, 5 mL; and latanoprost ophthalmic solution 0.005%, 125 μg/2.5 mL—in the left eye to lower intraocular pressure, as therapy for glaucoma. If left untreated, glaucoma can lead to vision loss.
Physical examination revealed periorbital hyperpigmentation on the left side; hypertrichosis and eyelash trichomegaly compared to the right side; and a deep left upper orbital sulcus compared to the right side (Figure). The patient was alert and oriented to person, place, and time. Extraocular movement was intact bilaterally, and his pupillary reflex was symmetric. No tenderness was noted over the affected area on palpation; no subcutaneous masses or lesions were observed or palpated. There was no ocular discharge, the conjunctiva was pink, and the sclera was white bilaterally.
The differential diagnosis included professional trauma-induced orbital changes, nevus of Ota (oculomucodermal melanocytosis), prostaglandin-associated periorbitopathy (PAP), and melasma. Although the patient sustained an injury that caused retinal detachment, he never experienced an orbital bone fracture; additionally, a fracture would not explain the skin discoloration or longer eyelashes. Periorbital nevus of Ota most commonly manifests as a unilateral scleral and brown-bluish skin discoloration but does not cause hollowing of the orbital sulcus or affect the length and thickness of eyelashes. Melasma—bilateral skin hyperpigmentation that most commonly affects women—can be induced by oral contraceptives, antibiotics, heat, sun exposure, and pregnancy. It does not affect the color of the iris or the depth of the scleral sulcus, and it does not increase the length and thickness of eyelashes. Based on the clinical presentation and a review of the eye drops used, he was diagnosed with PAP due to prolonged use of latanoprost ophthalmic solution. The patient was referred to an ophthalmologist for consideration of a switch to a different class of medication.
Of the 3 eye drops used by this patient, latanoprost, a prostaglandin analog, decreases intraocular pressure and is known to cause PAP. This condition comprises a constellation of changes, including upper eyelid ptosis, deepening of the upper eyelid sulcus, involution of dermatochalasis, periorbital fat atrophy, mild enophthalmos (sunken eye), inferior scleral show, increased prominence of eyelid vessels, and tight eyelids.1 Latanoprost most often produces these findings, but all prostaglandin ophthalmic medications can, including the dual-indication bimatoprost, which was approved by the US Food and Drug Administration to reduce elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension but also is used to grow darker, thicker, and longer eyelashes. Clinicians who prescribe bimatoprost for this cosmetic indication should be mindful of the potential for PAP and discuss it with patients.
The prescribing information (PI) for bimatoprost (Latisse; Allergan) does not list PAP as an adverse reaction observed in the 4-month multicenter, double-blind, randomized, vehicle-controlled study of bimatoprost (as Latisse) in 278 adults.2 The PI does list “periorbital and lid changes associated with periorbital fat atrophy and skin tightness resulting in deepening of eyelid sulcus and eyelid ptosis” as an adverse reaction in postmarketing experience. However, according to the PI, the frequency of these adverse reactions cannot be established, as the reporting of such incidents was voluntary and the size of the treated population was uncertain.2
Prostaglandins can cause periorbitopathy by several mechanisms; one speculated cause is that this group of medications might provoke smooth muscle contraction. Prostaglandin medications also have an affinity for fat cells1; atrophy of fat cells can lead to enophthalmos and deepening upper eyelid sulcus. In an observational study of 105 participants who were using a prostaglandin in 1 eye for longer than 1 month (the other eye was used as a control), the overall frequency of prostaglandin-associated periorbitopathy was 93.3% in the bimatoprost group, 41.4% in the latanoprost group, and 70% in the travoprost group, while the frequency of deepening of the upper eyelid sulcus was 80% in the bimatoprost group, 15.7% in the latanoprost group, and 45% in the travoprost group.3 These changes may not be as striking when a patient is using a prostaglandin ophthalmic medication in both eyes and may not be noticed even by the patient. It is prudent for the clinician to take a baseline photograph of the patient when these medications are prescribed to observe for early signs of periorbitopathy. These adverse effects may not be reversible when the medication is discontinued4 and have been observed as early as 4 to 6 weeks after the start of treatment.5
Our patient was counseled that his constellation of PAP findings potentially could be partially reversed over months or even a year or longer if the offending agent was discontinued. However, he was cautioned that cessation of latanoprost first needed to be discussed with his ophthalmologist, who would determine if there was a suitable alternative to a prostaglandin analog for him. The patient’s only concern was the aesthetic appearance of the left periorbital area. A hyaluronic acid filler or fat grafting can be considered for correction of orbital sulcus hollowing; however, we could not locate any long-term studies in which such corrective treatments were applied for PAP. Our patient continues to use latanoprost with no change in the frequency of use. There have been no further changes or progression in the physical appearance of the left eye or periorbital area. The patient has not undergone any corrective treatments.
To the Editor:
A 42-year man presented with hollowing of the upper eyelid and skin discoloration of the left periorbital area of 10 years’ duration. He was a professional mixed martial arts fighter with a history of 2 surgeries for retinal detachment of the left eye 13 years prior to the current presentation. The patient also has macular scarring in the left eye. He denied a history of facial fracture, reconstructive surgery, or other medical conditions. His visual acuity was unknown; however, he did not require corrective glasses. He used 3 prescription ophthalmic eye drops—dorzolamide hydrochloride plus timolol maleate, 10 mL; brimonidine tartrate ophthalmic solution 0.15%, 5 mL; and latanoprost ophthalmic solution 0.005%, 125 μg/2.5 mL—in the left eye to lower intraocular pressure, as therapy for glaucoma. If left untreated, glaucoma can lead to vision loss.
Physical examination revealed periorbital hyperpigmentation on the left side; hypertrichosis and eyelash trichomegaly compared to the right side; and a deep left upper orbital sulcus compared to the right side (Figure). The patient was alert and oriented to person, place, and time. Extraocular movement was intact bilaterally, and his pupillary reflex was symmetric. No tenderness was noted over the affected area on palpation; no subcutaneous masses or lesions were observed or palpated. There was no ocular discharge, the conjunctiva was pink, and the sclera was white bilaterally.
The differential diagnosis included professional trauma-induced orbital changes, nevus of Ota (oculomucodermal melanocytosis), prostaglandin-associated periorbitopathy (PAP), and melasma. Although the patient sustained an injury that caused retinal detachment, he never experienced an orbital bone fracture; additionally, a fracture would not explain the skin discoloration or longer eyelashes. Periorbital nevus of Ota most commonly manifests as a unilateral scleral and brown-bluish skin discoloration but does not cause hollowing of the orbital sulcus or affect the length and thickness of eyelashes. Melasma—bilateral skin hyperpigmentation that most commonly affects women—can be induced by oral contraceptives, antibiotics, heat, sun exposure, and pregnancy. It does not affect the color of the iris or the depth of the scleral sulcus, and it does not increase the length and thickness of eyelashes. Based on the clinical presentation and a review of the eye drops used, he was diagnosed with PAP due to prolonged use of latanoprost ophthalmic solution. The patient was referred to an ophthalmologist for consideration of a switch to a different class of medication.
Of the 3 eye drops used by this patient, latanoprost, a prostaglandin analog, decreases intraocular pressure and is known to cause PAP. This condition comprises a constellation of changes, including upper eyelid ptosis, deepening of the upper eyelid sulcus, involution of dermatochalasis, periorbital fat atrophy, mild enophthalmos (sunken eye), inferior scleral show, increased prominence of eyelid vessels, and tight eyelids.1 Latanoprost most often produces these findings, but all prostaglandin ophthalmic medications can, including the dual-indication bimatoprost, which was approved by the US Food and Drug Administration to reduce elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension but also is used to grow darker, thicker, and longer eyelashes. Clinicians who prescribe bimatoprost for this cosmetic indication should be mindful of the potential for PAP and discuss it with patients.
The prescribing information (PI) for bimatoprost (Latisse; Allergan) does not list PAP as an adverse reaction observed in the 4-month multicenter, double-blind, randomized, vehicle-controlled study of bimatoprost (as Latisse) in 278 adults.2 The PI does list “periorbital and lid changes associated with periorbital fat atrophy and skin tightness resulting in deepening of eyelid sulcus and eyelid ptosis” as an adverse reaction in postmarketing experience. However, according to the PI, the frequency of these adverse reactions cannot be established, as the reporting of such incidents was voluntary and the size of the treated population was uncertain.2
Prostaglandins can cause periorbitopathy by several mechanisms; one speculated cause is that this group of medications might provoke smooth muscle contraction. Prostaglandin medications also have an affinity for fat cells1; atrophy of fat cells can lead to enophthalmos and deepening upper eyelid sulcus. In an observational study of 105 participants who were using a prostaglandin in 1 eye for longer than 1 month (the other eye was used as a control), the overall frequency of prostaglandin-associated periorbitopathy was 93.3% in the bimatoprost group, 41.4% in the latanoprost group, and 70% in the travoprost group, while the frequency of deepening of the upper eyelid sulcus was 80% in the bimatoprost group, 15.7% in the latanoprost group, and 45% in the travoprost group.3 These changes may not be as striking when a patient is using a prostaglandin ophthalmic medication in both eyes and may not be noticed even by the patient. It is prudent for the clinician to take a baseline photograph of the patient when these medications are prescribed to observe for early signs of periorbitopathy. These adverse effects may not be reversible when the medication is discontinued4 and have been observed as early as 4 to 6 weeks after the start of treatment.5
Our patient was counseled that his constellation of PAP findings potentially could be partially reversed over months or even a year or longer if the offending agent was discontinued. However, he was cautioned that cessation of latanoprost first needed to be discussed with his ophthalmologist, who would determine if there was a suitable alternative to a prostaglandin analog for him. The patient’s only concern was the aesthetic appearance of the left periorbital area. A hyaluronic acid filler or fat grafting can be considered for correction of orbital sulcus hollowing; however, we could not locate any long-term studies in which such corrective treatments were applied for PAP. Our patient continues to use latanoprost with no change in the frequency of use. There have been no further changes or progression in the physical appearance of the left eye or periorbital area. The patient has not undergone any corrective treatments.
- Berke SJ. PAP: new concerns for prostaglandin use. Rev Ophthalmol. 2012;19:70.
- Latisse (bimatoprost ophthalmic solution 0.03%). Package insert. Allergan; 2021. Accessed April 11, 2024. https://www.rxabbvie.com/pdf/latisse_pi.pdf
- Kucukevcilioglu M, Bayer A, Uysal Y, et al. Prostaglandin associated periorbitopathy in patients using bimatoprost, latanoprost and travoprost. Clin Exp Ophthalmol. 2014;42:126-131. doi:10.1111/ceo.12163
- Filippopoulos T, Paula JS, Torun N, et al. Periorbital changes associated with topical bimatoprost. Ophthalmic Plast Reconstr Surg. 2008;24:302-307. doi:10.1097/IOP.0b013e31817d81df
- Peplinski LS, Smith KA. Deepening of lid sulcus from topical bimatoprost therapy. Optom Vis Sci. 2004;81:574-577. doi:10.1097/01.opx.0000141791.16683.4a
- Berke SJ. PAP: new concerns for prostaglandin use. Rev Ophthalmol. 2012;19:70.
- Latisse (bimatoprost ophthalmic solution 0.03%). Package insert. Allergan; 2021. Accessed April 11, 2024. https://www.rxabbvie.com/pdf/latisse_pi.pdf
- Kucukevcilioglu M, Bayer A, Uysal Y, et al. Prostaglandin associated periorbitopathy in patients using bimatoprost, latanoprost and travoprost. Clin Exp Ophthalmol. 2014;42:126-131. doi:10.1111/ceo.12163
- Filippopoulos T, Paula JS, Torun N, et al. Periorbital changes associated with topical bimatoprost. Ophthalmic Plast Reconstr Surg. 2008;24:302-307. doi:10.1097/IOP.0b013e31817d81df
- Peplinski LS, Smith KA. Deepening of lid sulcus from topical bimatoprost therapy. Optom Vis Sci. 2004;81:574-577. doi:10.1097/01.opx.0000141791.16683.4a
PRACTICE POINTS
- Ask patients to provide photographs taken prior to noticed changes to assess progression if they are new to your practice.
- Take photographs of patients in good light against a solid-colored background to have a baseline. It may be helpful to update patient images annually.
- Discuss with patients the aesthetic changes that may occur with the use of prescription medications. Provide pamphlets with images to educate them on what to expect.
Risk for COVID-19 Infection in Patients With Vitiligo
To the Editor:
Vitiligo is a depigmentation disorder that results from the loss of melanocytes in the epidermis.1 The most widely accepted pathophysiology for melanocyte destruction in vitiligo is an autoimmune process involving dysregulated cytokine production and autoreactive T-cell activation.1 Individuals with cutaneous autoinflammatory conditions currently are vital patient populations warranting research, as their susceptibility to COVID-19 infection may differ from the general population. We previously found a small increased risk for COVID-19 infection in patients with psoriasis,2 which suggests that other dermatologic conditions also may impact COVID-19 risk. The risk for COVID-19 infection in patients with vitiligo remains largely unknown. In this retrospective cohort study, we investigated the risk for COVID-19 infection in patients with vitiligo compared with those without vitiligo utilizing claims data from the COVID-19 Research Database (https://covid19researchdatabase.org/).
Claims were evaluated for patients aged 3 years and older with a vitiligo diagnosis (International Classification of Diseases, Tenth Revision [ICD-10] code L80) that was made between January 1, 2016, and January 1, 2020. Individuals without a vitiligo diagnosis during the same period were placed (4:1 ratio) in the control group and were matched with study group patients for age and sex. All comorbidity variables and vitiligo diagnoses were extracted from ICD-10 codes that were given prior to a diagnosis of COVID-19. We then constructed multivariable logistic regression models adjusting for measured confounders to evaluate if vitiligo was associated with higher risk for COVID-19 infection after January 1, 2020.
The vitiligo and nonvitiligo cohorts included 40,363 and 161,452 patients, respectively (Table 1). Logistic regression analysis with adjustment for confounding variables, including high comorbid risk factors (Table 2) revealed that patients with a diagnosis of vitiligo had significantly increased odds of COVID-19 infection compared with patients without vitiligo (adjusted odds ratio [AOR], 1.47; 95% CI, 1.37-1.57; P<.001)(Table 3). Additionally, subgroup logistic analyses for sex, age, and exclusion of patients who were HIV positive revealed that females with vitiligo had higher odds of contracting COVID-19 than males with vitiligo (Table 3).
Our results showed that patients with vitiligo had a higher relative risk for contracting COVID-19 than individuals without vitiligo. It has been reported that the prevalence of COVID-19 is higher among patients with autoimmune diseases compared to the general population.3 Additionally, a handful of vitiligo patients are managed with immunosuppressive agents that may further weaken their immune response.1 Moreover, survey results from dermatologists managing vitiligo patients revealed that physicians were fairly comfortable prescribing immunosuppressants and encouraging in-office phototherapy during the COVID-19 pandemic.4 As a result, more patients may have been attending in-office visits for their phototherapy, which may have increased their risk for COVID-19. Although these factors play a role in COVID-19 infection rates, the underlying immune dysregulation in vitiligo in relation to COVID-19 remains unknown and should be further explored.
Our findings are limited by the use of ICD-10 codes, the inability to control for all potential confounding variables, the lack of data regarding the stage of vitiligo, and the absence of data for undiagnosed COVID-19 infections. In addition, patients with vitiligo may be more likely to seek care, potentially increasing their rates of COVID-19 testing. The inability to identify the stage of vitiligo during enrollment in the database may have altered our results, as individuals with active disease have increased levels of IFN-γ. Increased secretion of IFN-γ also potentially helps in the clearance of COVID-19 infection.1 Future studies should investigate this relationship via planned COVID-19 testing, identification of vitiligo stage, and controlling for other associated comorbidities.
- Rashighi M, Harris JE. Vitiligo pathogenesis and emerging treatments. Dermatol Clin. 2017;35:257-265. doi:10.1016/j.det.2016.11.014
- Wu JJ, Liu J, Thatiparthi A, et al. The risk of COVID-19 in patients with psoriasis—a retrospective cohort study [published online September 20, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.040
- Zhong J, Shen G, Yang H, et al. COVID-19 in patients with rheumatic disease in Hubei province, China: a multicentre retrospective observational study. Lancet Rheumatol. 2020;2:E557-E564. doi:10.1016/S2665-9913(20)30227-7
- Chatterjee M, Das A. Management of vitiligo amidst the COVID-19 pandemic: a survey and resulting consensus. Indian J Dermatol. 2021;66:479-483. doi:10.4103/ijd.ijd_859_20
To the Editor:
Vitiligo is a depigmentation disorder that results from the loss of melanocytes in the epidermis.1 The most widely accepted pathophysiology for melanocyte destruction in vitiligo is an autoimmune process involving dysregulated cytokine production and autoreactive T-cell activation.1 Individuals with cutaneous autoinflammatory conditions currently are vital patient populations warranting research, as their susceptibility to COVID-19 infection may differ from the general population. We previously found a small increased risk for COVID-19 infection in patients with psoriasis,2 which suggests that other dermatologic conditions also may impact COVID-19 risk. The risk for COVID-19 infection in patients with vitiligo remains largely unknown. In this retrospective cohort study, we investigated the risk for COVID-19 infection in patients with vitiligo compared with those without vitiligo utilizing claims data from the COVID-19 Research Database (https://covid19researchdatabase.org/).
Claims were evaluated for patients aged 3 years and older with a vitiligo diagnosis (International Classification of Diseases, Tenth Revision [ICD-10] code L80) that was made between January 1, 2016, and January 1, 2020. Individuals without a vitiligo diagnosis during the same period were placed (4:1 ratio) in the control group and were matched with study group patients for age and sex. All comorbidity variables and vitiligo diagnoses were extracted from ICD-10 codes that were given prior to a diagnosis of COVID-19. We then constructed multivariable logistic regression models adjusting for measured confounders to evaluate if vitiligo was associated with higher risk for COVID-19 infection after January 1, 2020.
The vitiligo and nonvitiligo cohorts included 40,363 and 161,452 patients, respectively (Table 1). Logistic regression analysis with adjustment for confounding variables, including high comorbid risk factors (Table 2) revealed that patients with a diagnosis of vitiligo had significantly increased odds of COVID-19 infection compared with patients without vitiligo (adjusted odds ratio [AOR], 1.47; 95% CI, 1.37-1.57; P<.001)(Table 3). Additionally, subgroup logistic analyses for sex, age, and exclusion of patients who were HIV positive revealed that females with vitiligo had higher odds of contracting COVID-19 than males with vitiligo (Table 3).
Our results showed that patients with vitiligo had a higher relative risk for contracting COVID-19 than individuals without vitiligo. It has been reported that the prevalence of COVID-19 is higher among patients with autoimmune diseases compared to the general population.3 Additionally, a handful of vitiligo patients are managed with immunosuppressive agents that may further weaken their immune response.1 Moreover, survey results from dermatologists managing vitiligo patients revealed that physicians were fairly comfortable prescribing immunosuppressants and encouraging in-office phototherapy during the COVID-19 pandemic.4 As a result, more patients may have been attending in-office visits for their phototherapy, which may have increased their risk for COVID-19. Although these factors play a role in COVID-19 infection rates, the underlying immune dysregulation in vitiligo in relation to COVID-19 remains unknown and should be further explored.
Our findings are limited by the use of ICD-10 codes, the inability to control for all potential confounding variables, the lack of data regarding the stage of vitiligo, and the absence of data for undiagnosed COVID-19 infections. In addition, patients with vitiligo may be more likely to seek care, potentially increasing their rates of COVID-19 testing. The inability to identify the stage of vitiligo during enrollment in the database may have altered our results, as individuals with active disease have increased levels of IFN-γ. Increased secretion of IFN-γ also potentially helps in the clearance of COVID-19 infection.1 Future studies should investigate this relationship via planned COVID-19 testing, identification of vitiligo stage, and controlling for other associated comorbidities.
To the Editor:
Vitiligo is a depigmentation disorder that results from the loss of melanocytes in the epidermis.1 The most widely accepted pathophysiology for melanocyte destruction in vitiligo is an autoimmune process involving dysregulated cytokine production and autoreactive T-cell activation.1 Individuals with cutaneous autoinflammatory conditions currently are vital patient populations warranting research, as their susceptibility to COVID-19 infection may differ from the general population. We previously found a small increased risk for COVID-19 infection in patients with psoriasis,2 which suggests that other dermatologic conditions also may impact COVID-19 risk. The risk for COVID-19 infection in patients with vitiligo remains largely unknown. In this retrospective cohort study, we investigated the risk for COVID-19 infection in patients with vitiligo compared with those without vitiligo utilizing claims data from the COVID-19 Research Database (https://covid19researchdatabase.org/).
Claims were evaluated for patients aged 3 years and older with a vitiligo diagnosis (International Classification of Diseases, Tenth Revision [ICD-10] code L80) that was made between January 1, 2016, and January 1, 2020. Individuals without a vitiligo diagnosis during the same period were placed (4:1 ratio) in the control group and were matched with study group patients for age and sex. All comorbidity variables and vitiligo diagnoses were extracted from ICD-10 codes that were given prior to a diagnosis of COVID-19. We then constructed multivariable logistic regression models adjusting for measured confounders to evaluate if vitiligo was associated with higher risk for COVID-19 infection after January 1, 2020.
The vitiligo and nonvitiligo cohorts included 40,363 and 161,452 patients, respectively (Table 1). Logistic regression analysis with adjustment for confounding variables, including high comorbid risk factors (Table 2) revealed that patients with a diagnosis of vitiligo had significantly increased odds of COVID-19 infection compared with patients without vitiligo (adjusted odds ratio [AOR], 1.47; 95% CI, 1.37-1.57; P<.001)(Table 3). Additionally, subgroup logistic analyses for sex, age, and exclusion of patients who were HIV positive revealed that females with vitiligo had higher odds of contracting COVID-19 than males with vitiligo (Table 3).
Our results showed that patients with vitiligo had a higher relative risk for contracting COVID-19 than individuals without vitiligo. It has been reported that the prevalence of COVID-19 is higher among patients with autoimmune diseases compared to the general population.3 Additionally, a handful of vitiligo patients are managed with immunosuppressive agents that may further weaken their immune response.1 Moreover, survey results from dermatologists managing vitiligo patients revealed that physicians were fairly comfortable prescribing immunosuppressants and encouraging in-office phototherapy during the COVID-19 pandemic.4 As a result, more patients may have been attending in-office visits for their phototherapy, which may have increased their risk for COVID-19. Although these factors play a role in COVID-19 infection rates, the underlying immune dysregulation in vitiligo in relation to COVID-19 remains unknown and should be further explored.
Our findings are limited by the use of ICD-10 codes, the inability to control for all potential confounding variables, the lack of data regarding the stage of vitiligo, and the absence of data for undiagnosed COVID-19 infections. In addition, patients with vitiligo may be more likely to seek care, potentially increasing their rates of COVID-19 testing. The inability to identify the stage of vitiligo during enrollment in the database may have altered our results, as individuals with active disease have increased levels of IFN-γ. Increased secretion of IFN-γ also potentially helps in the clearance of COVID-19 infection.1 Future studies should investigate this relationship via planned COVID-19 testing, identification of vitiligo stage, and controlling for other associated comorbidities.
- Rashighi M, Harris JE. Vitiligo pathogenesis and emerging treatments. Dermatol Clin. 2017;35:257-265. doi:10.1016/j.det.2016.11.014
- Wu JJ, Liu J, Thatiparthi A, et al. The risk of COVID-19 in patients with psoriasis—a retrospective cohort study [published online September 20, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.040
- Zhong J, Shen G, Yang H, et al. COVID-19 in patients with rheumatic disease in Hubei province, China: a multicentre retrospective observational study. Lancet Rheumatol. 2020;2:E557-E564. doi:10.1016/S2665-9913(20)30227-7
- Chatterjee M, Das A. Management of vitiligo amidst the COVID-19 pandemic: a survey and resulting consensus. Indian J Dermatol. 2021;66:479-483. doi:10.4103/ijd.ijd_859_20
- Rashighi M, Harris JE. Vitiligo pathogenesis and emerging treatments. Dermatol Clin. 2017;35:257-265. doi:10.1016/j.det.2016.11.014
- Wu JJ, Liu J, Thatiparthi A, et al. The risk of COVID-19 in patients with psoriasis—a retrospective cohort study [published online September 20, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.040
- Zhong J, Shen G, Yang H, et al. COVID-19 in patients with rheumatic disease in Hubei province, China: a multicentre retrospective observational study. Lancet Rheumatol. 2020;2:E557-E564. doi:10.1016/S2665-9913(20)30227-7
- Chatterjee M, Das A. Management of vitiligo amidst the COVID-19 pandemic: a survey and resulting consensus. Indian J Dermatol. 2021;66:479-483. doi:10.4103/ijd.ijd_859_20
Practice Points
- The underlying autoimmune process in vitiligo can result in various changes to the immune system.
- A diagnosis of vitiligo may alter the body’s immune response to COVID-19 infection.