MDedge Dermatology

During the annual conference of the American Society for Laser Medicine and Surgery, H. Ray Jalian, MD, shared his “top 10” tips and tricks for everyday cosmetic practice, based on nearly 10 years of experience treating patients on both coasts of the United States.

They are as follows:

1. Know your clinical endpoints. “One of the things that was drilled into me during my fellowship in lasers and cosmetics at Mass General was to know your clinical endpoints and to avoid a cookbook approach,” said Dr. Jalian, who practices dermatology in Los Angeles. “You should treat based on the pathology that you’re seeing on the skin and let the endpoints be your guide. The skin will tell you what you’re doing right, and the skin will tell you what you’re doing wrong. Picking up on these cues will allow you to deliver a safe and effective treatment to your patients.”

The selection of proper treatment parameters is driven by selective photothermolysis, a microsurgery technique that uses customized wavelengths, pulse durations, and fluences to target a chromophore. “Knowing the size and shape of your target allows you to pick the right pulse duration,” he said. “This is dictated by thermal relaxation time, which is proportional to the size and shape of the target. Smaller targets require a shorter pulse width, while larger targets require a longer pulse width.”

2. Do not perform a procedure for which you cannot recognize and treat the side effects. “I can’t tell you how many times I’ve gotten referrals from outside providers with a side effect that, if it had been recognized and treated, would have been inconsequential long-term for the patient,” Dr. Jalian said. “You can only avoid complications by not firing the laser. The more you practice, the more complications you’re going to have. This is inevitable, but good practice and common sense can reduce complications significantly.”

Even the most skilled clinicians encounter side effects from time to time. “The most important thing is to form a network of physicians you trust that you can call or text when you need help in managing a particular complication,” he continued. “This happens to all of us,” he said. Don’t be afraid to phone a colleague, he advised, “and get a fresh set of eyes because oftentimes they can provide insights, especially when you’re having tunnel vision during a complication, that can ultimately result in better patient care.”

3. Don’t forget your clinical training. “Trust your clinical judgment,” Dr. Jalian said. “If something doesn’t seem right, even if it was a case referred to you by experienced practitioners, you are a clinician first and foremost, and you are allowed to make a clinical judgment on lesions.” He referred to a 2011 report in which the authors described a series of four cases where patients presented for cosmetic evaluation of vascular lesions that turned out to be more significant pathologic disease. “Trust your clinical insight because this will serve you in the long term,” he said.

4. Set realistic expectations. Patients with unrealistically high expectations are likely to express dissatisfaction with their treatment results, “no matter how good of a job you do,” Dr. Jalian said. “In addition to safely treating the patient, we strive for patient satisfaction, because with these elective procedures we’re trying to give a patient a result they’re looking for. But our No. 1 job is also to be realistic about the results we can obtain. If someone comes in wanting treatment with a skin-tightening device but clearly needs a face-lift because they have too much laxity, your job is to tell them that this is not the appropriate device for them. Learn the art of saying no. If handled correctly, the patient will often thank you before she heads out the door. Ultimately, honesty is the best policy. I may say something like, ‘I’m not telling you the answer you want to hear, I’m telling you the truth.’ That often goes over well.”

5. Use proper anesthesia. Patients come to you for results, but they’re also likely to remember how well you controlled their pain during procedures. Strategies favored by Dr. Jalian include applying extra topical anesthetic to “hot spots” and splitting up treatment sessions when tackling a large area. “Consider using adjunctive analgesics such as oral medications and nitrous oxide,” he added. Other options, he said, are cooling techniques and distraction techniques, such as the use of a stress ball, consideration of the gate control theory of pain, and “talkesthesia”(using conversation to distract the patient).

6. Obtain proper informed consent. A lack of informed consent ranks as a common reason why doctors get sued. “This happens when a physician fails to inform the patient of all medically reasonable alternatives and their risks, even for noninvasive procedures prior to administering treatment,” Dr. Jalian said. “All patients have the right to an informed consent prior to any treatment. It doesn’t necessarily have to be in a written form, but it’s important to at least have a discussion and document it for all procedures, including medical and cosmetic procedures and oral and topical treatments. Keep it simple. A written consent is ineffective if the patient does not understand material about the procedure.” Avoid the use of excessive medical terms. For example, use bruising instead of purpura, redness instead of erythema, and drooping instead of ptosis.

7. Lower the laser treatment density for darker skin types. According to Dr. Jalian, several clinical studies have demonstrated that lower densities are associated with less postinflammatory hyperpigmentation in Asian and Black patients, without sacrificing clinical outcomes. “Density determines how ‘aggressive’ a treatment is,” he said. “The greater the density, the more downtime is required.”

8. Have a vascular occlusion emergency kit on hand. At a minimum, the kit should contain at least 1,500 units of hyaluronidase, aspirin, timolol/acetazolamide, a Snellen chart, steroids, and an EpiPen.

9. Use standardized photography. Even the slightest change in lighting can manipulate your results. According to Dr. Jalian, standardized photos enable you to monitor patient progress, minimize liability, and can serve as a marketing tool “so that you can capitalize on your talent.”

10. Consider combination treatments. He combines lasers based on target and depth. For example, prior to resurfacing he often performs a pass or two with a color laser such as intense pulsed light. “Depending on what’s being done, we’ll do soft-tissue augmentation before or after treatment with certain lasers,” Dr. Jalian added. “If you’re performing a toxin treatment on the same day as a laser procedure, do not treat the lower face or neck. Do the laser procedure first and limit that to the upper third of the face.”

He reported having no relevant financial disclosures.

[email protected]

During the annual conference of the American Society for Laser Medicine and Surgery, H. Ray Jalian, MD, shared his “top 10” tips and tricks for everyday cosmetic practice, based on nearly 10 years of experience treating patients on both coasts of the United States.

They are as follows:

1. Know your clinical endpoints. “One of the things that was drilled into me during my fellowship in lasers and cosmetics at Mass General was to know your clinical endpoints and to avoid a cookbook approach,” said Dr. Jalian, who practices dermatology in Los Angeles. “You should treat based on the pathology that you’re seeing on the skin and let the endpoints be your guide. The skin will tell you what you’re doing right, and the skin will tell you what you’re doing wrong. Picking up on these cues will allow you to deliver a safe and effective treatment to your patients.”

The selection of proper treatment parameters is driven by selective photothermolysis, a microsurgery technique that uses customized wavelengths, pulse durations, and fluences to target a chromophore. “Knowing the size and shape of your target allows you to pick the right pulse duration,” he said. “This is dictated by thermal relaxation time, which is proportional to the size and shape of the target. Smaller targets require a shorter pulse width, while larger targets require a longer pulse width.”

2. Do not perform a procedure for which you cannot recognize and treat the side effects. “I can’t tell you how many times I’ve gotten referrals from outside providers with a side effect that, if it had been recognized and treated, would have been inconsequential long-term for the patient,” Dr. Jalian said. “You can only avoid complications by not firing the laser. The more you practice, the more complications you’re going to have. This is inevitable, but good practice and common sense can reduce complications significantly.”

Even the most skilled clinicians encounter side effects from time to time. “The most important thing is to form a network of physicians you trust that you can call or text when you need help in managing a particular complication,” he continued. “This happens to all of us,” he said. Don’t be afraid to phone a colleague, he advised, “and get a fresh set of eyes because oftentimes they can provide insights, especially when you’re having tunnel vision during a complication, that can ultimately result in better patient care.”

3. Don’t forget your clinical training. “Trust your clinical judgment,” Dr. Jalian said. “If something doesn’t seem right, even if it was a case referred to you by experienced practitioners, you are a clinician first and foremost, and you are allowed to make a clinical judgment on lesions.” He referred to a 2011 report in which the authors described a series of four cases where patients presented for cosmetic evaluation of vascular lesions that turned out to be more significant pathologic disease. “Trust your clinical insight because this will serve you in the long term,” he said.

4. Set realistic expectations. Patients with unrealistically high expectations are likely to express dissatisfaction with their treatment results, “no matter how good of a job you do,” Dr. Jalian said. “In addition to safely treating the patient, we strive for patient satisfaction, because with these elective procedures we’re trying to give a patient a result they’re looking for. But our No. 1 job is also to be realistic about the results we can obtain. If someone comes in wanting treatment with a skin-tightening device but clearly needs a face-lift because they have too much laxity, your job is to tell them that this is not the appropriate device for them. Learn the art of saying no. If handled correctly, the patient will often thank you before she heads out the door. Ultimately, honesty is the best policy. I may say something like, ‘I’m not telling you the answer you want to hear, I’m telling you the truth.’ That often goes over well.”

5. Use proper anesthesia. Patients come to you for results, but they’re also likely to remember how well you controlled their pain during procedures. Strategies favored by Dr. Jalian include applying extra topical anesthetic to “hot spots” and splitting up treatment sessions when tackling a large area. “Consider using adjunctive analgesics such as oral medications and nitrous oxide,” he added. Other options, he said, are cooling techniques and distraction techniques, such as the use of a stress ball, consideration of the gate control theory of pain, and “talkesthesia”(using conversation to distract the patient).

6. Obtain proper informed consent. A lack of informed consent ranks as a common reason why doctors get sued. “This happens when a physician fails to inform the patient of all medically reasonable alternatives and their risks, even for noninvasive procedures prior to administering treatment,” Dr. Jalian said. “All patients have the right to an informed consent prior to any treatment. It doesn’t necessarily have to be in a written form, but it’s important to at least have a discussion and document it for all procedures, including medical and cosmetic procedures and oral and topical treatments. Keep it simple. A written consent is ineffective if the patient does not understand material about the procedure.” Avoid the use of excessive medical terms. For example, use bruising instead of purpura, redness instead of erythema, and drooping instead of ptosis.

7. Lower the laser treatment density for darker skin types. According to Dr. Jalian, several clinical studies have demonstrated that lower densities are associated with less postinflammatory hyperpigmentation in Asian and Black patients, without sacrificing clinical outcomes. “Density determines how ‘aggressive’ a treatment is,” he said. “The greater the density, the more downtime is required.”

8. Have a vascular occlusion emergency kit on hand. At a minimum, the kit should contain at least 1,500 units of hyaluronidase, aspirin, timolol/acetazolamide, a Snellen chart, steroids, and an EpiPen.

9. Use standardized photography. Even the slightest change in lighting can manipulate your results. According to Dr. Jalian, standardized photos enable you to monitor patient progress, minimize liability, and can serve as a marketing tool “so that you can capitalize on your talent.”

10. Consider combination treatments. He combines lasers based on target and depth. For example, prior to resurfacing he often performs a pass or two with a color laser such as intense pulsed light. “Depending on what’s being done, we’ll do soft-tissue augmentation before or after treatment with certain lasers,” Dr. Jalian added. “If you’re performing a toxin treatment on the same day as a laser procedure, do not treat the lower face or neck. Do the laser procedure first and limit that to the upper third of the face.”

He reported having no relevant financial disclosures.

[email protected]

During the annual conference of the American Society for Laser Medicine and Surgery, H. Ray Jalian, MD, shared his “top 10” tips and tricks for everyday cosmetic practice, based on nearly 10 years of experience treating patients on both coasts of the United States.

They are as follows:

1. Know your clinical endpoints. “One of the things that was drilled into me during my fellowship in lasers and cosmetics at Mass General was to know your clinical endpoints and to avoid a cookbook approach,” said Dr. Jalian, who practices dermatology in Los Angeles. “You should treat based on the pathology that you’re seeing on the skin and let the endpoints be your guide. The skin will tell you what you’re doing right, and the skin will tell you what you’re doing wrong. Picking up on these cues will allow you to deliver a safe and effective treatment to your patients.”

The selection of proper treatment parameters is driven by selective photothermolysis, a microsurgery technique that uses customized wavelengths, pulse durations, and fluences to target a chromophore. “Knowing the size and shape of your target allows you to pick the right pulse duration,” he said. “This is dictated by thermal relaxation time, which is proportional to the size and shape of the target. Smaller targets require a shorter pulse width, while larger targets require a longer pulse width.”

2. Do not perform a procedure for which you cannot recognize and treat the side effects. “I can’t tell you how many times I’ve gotten referrals from outside providers with a side effect that, if it had been recognized and treated, would have been inconsequential long-term for the patient,” Dr. Jalian said. “You can only avoid complications by not firing the laser. The more you practice, the more complications you’re going to have. This is inevitable, but good practice and common sense can reduce complications significantly.”

Even the most skilled clinicians encounter side effects from time to time. “The most important thing is to form a network of physicians you trust that you can call or text when you need help in managing a particular complication,” he continued. “This happens to all of us,” he said. Don’t be afraid to phone a colleague, he advised, “and get a fresh set of eyes because oftentimes they can provide insights, especially when you’re having tunnel vision during a complication, that can ultimately result in better patient care.”

3. Don’t forget your clinical training. “Trust your clinical judgment,” Dr. Jalian said. “If something doesn’t seem right, even if it was a case referred to you by experienced practitioners, you are a clinician first and foremost, and you are allowed to make a clinical judgment on lesions.” He referred to a 2011 report in which the authors described a series of four cases where patients presented for cosmetic evaluation of vascular lesions that turned out to be more significant pathologic disease. “Trust your clinical insight because this will serve you in the long term,” he said.

4. Set realistic expectations. Patients with unrealistically high expectations are likely to express dissatisfaction with their treatment results, “no matter how good of a job you do,” Dr. Jalian said. “In addition to safely treating the patient, we strive for patient satisfaction, because with these elective procedures we’re trying to give a patient a result they’re looking for. But our No. 1 job is also to be realistic about the results we can obtain. If someone comes in wanting treatment with a skin-tightening device but clearly needs a face-lift because they have too much laxity, your job is to tell them that this is not the appropriate device for them. Learn the art of saying no. If handled correctly, the patient will often thank you before she heads out the door. Ultimately, honesty is the best policy. I may say something like, ‘I’m not telling you the answer you want to hear, I’m telling you the truth.’ That often goes over well.”

5. Use proper anesthesia. Patients come to you for results, but they’re also likely to remember how well you controlled their pain during procedures. Strategies favored by Dr. Jalian include applying extra topical anesthetic to “hot spots” and splitting up treatment sessions when tackling a large area. “Consider using adjunctive analgesics such as oral medications and nitrous oxide,” he added. Other options, he said, are cooling techniques and distraction techniques, such as the use of a stress ball, consideration of the gate control theory of pain, and “talkesthesia”(using conversation to distract the patient).

6. Obtain proper informed consent. A lack of informed consent ranks as a common reason why doctors get sued. “This happens when a physician fails to inform the patient of all medically reasonable alternatives and their risks, even for noninvasive procedures prior to administering treatment,” Dr. Jalian said. “All patients have the right to an informed consent prior to any treatment. It doesn’t necessarily have to be in a written form, but it’s important to at least have a discussion and document it for all procedures, including medical and cosmetic procedures and oral and topical treatments. Keep it simple. A written consent is ineffective if the patient does not understand material about the procedure.” Avoid the use of excessive medical terms. For example, use bruising instead of purpura, redness instead of erythema, and drooping instead of ptosis.

7. Lower the laser treatment density for darker skin types. According to Dr. Jalian, several clinical studies have demonstrated that lower densities are associated with less postinflammatory hyperpigmentation in Asian and Black patients, without sacrificing clinical outcomes. “Density determines how ‘aggressive’ a treatment is,” he said. “The greater the density, the more downtime is required.”

8. Have a vascular occlusion emergency kit on hand. At a minimum, the kit should contain at least 1,500 units of hyaluronidase, aspirin, timolol/acetazolamide, a Snellen chart, steroids, and an EpiPen.

9. Use standardized photography. Even the slightest change in lighting can manipulate your results. According to Dr. Jalian, standardized photos enable you to monitor patient progress, minimize liability, and can serve as a marketing tool “so that you can capitalize on your talent.”

10. Consider combination treatments. He combines lasers based on target and depth. For example, prior to resurfacing he often performs a pass or two with a color laser such as intense pulsed light. “Depending on what’s being done, we’ll do soft-tissue augmentation before or after treatment with certain lasers,” Dr. Jalian added. “If you’re performing a toxin treatment on the same day as a laser procedure, do not treat the lower face or neck. Do the laser procedure first and limit that to the upper third of the face.”

He reported having no relevant financial disclosures.

[email protected]

Decorative tattooing has increased in popularity over the last decade. Multiple reactions can be seen as a result of allergic contact dermatitis/sensitivities to pigment used, photoallergic reactions, infectious processes because of contaminated ink or a nonsterile environment, or as a Koebner response.

Dermatitis is commonly seen in patients with a sensitivity to certain pigments. Mercury sulfide or cinnabar in red, chromium in green, and cobalt in blue are common offenders. Cadmium, which is used for yellow, may cause a photoallergic reaction following exposure to ultraviolet light. Other inorganic salts of metals used for tattooing include ferric hydrate for ochre, ferric oxide for brown, manganese salts for purple. Reactions may be seen within a few weeks up to years after the tattoo is placed.

Reactions are often confined to the tattoo and may present as erythematous papules or plaques, although lesions may also present as scaly and eczematous patches. Psoriasis, vitiligo, and lichen planus may Koebnerize and appear in the tattoo. Sarcoidosis may occur in tattoos and can be seen upon histopathologic examination. Allergic contact dermatitis may also be seen in people who receive temporary henna tattoos in which the henna dye is mixed with paraphenylenediamine (PPD).

Histologically, granulomatous, sarcoidal, and lichenoid patterns may be seen. A punch biopsy was performed in this patient that revealed a lichenoid and interstitial lymphohistiocytic infiltrate with red tattoo pigment. Special stains for PAS, GMS, FITE, and AFB were negative. There was no polarizable foreign material identified.

Treatment includes topical steroids, which may be ineffective, intralesional kenalog, and surgical excision. Laser must be used with caution, as it may aggravate the allergic reaction and cause a systemic reaction.

This case and photo were provided by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

Decorative tattooing has increased in popularity over the last decade. Multiple reactions can be seen as a result of allergic contact dermatitis/sensitivities to pigment used, photoallergic reactions, infectious processes because of contaminated ink or a nonsterile environment, or as a Koebner response.

Dermatitis is commonly seen in patients with a sensitivity to certain pigments. Mercury sulfide or cinnabar in red, chromium in green, and cobalt in blue are common offenders. Cadmium, which is used for yellow, may cause a photoallergic reaction following exposure to ultraviolet light. Other inorganic salts of metals used for tattooing include ferric hydrate for ochre, ferric oxide for brown, manganese salts for purple. Reactions may be seen within a few weeks up to years after the tattoo is placed.

Reactions are often confined to the tattoo and may present as erythematous papules or plaques, although lesions may also present as scaly and eczematous patches. Psoriasis, vitiligo, and lichen planus may Koebnerize and appear in the tattoo. Sarcoidosis may occur in tattoos and can be seen upon histopathologic examination. Allergic contact dermatitis may also be seen in people who receive temporary henna tattoos in which the henna dye is mixed with paraphenylenediamine (PPD).

Histologically, granulomatous, sarcoidal, and lichenoid patterns may be seen. A punch biopsy was performed in this patient that revealed a lichenoid and interstitial lymphohistiocytic infiltrate with red tattoo pigment. Special stains for PAS, GMS, FITE, and AFB were negative. There was no polarizable foreign material identified.

Treatment includes topical steroids, which may be ineffective, intralesional kenalog, and surgical excision. Laser must be used with caution, as it may aggravate the allergic reaction and cause a systemic reaction.

This case and photo were provided by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

Decorative tattooing has increased in popularity over the last decade. Multiple reactions can be seen as a result of allergic contact dermatitis/sensitivities to pigment used, photoallergic reactions, infectious processes because of contaminated ink or a nonsterile environment, or as a Koebner response.

Dermatitis is commonly seen in patients with a sensitivity to certain pigments. Mercury sulfide or cinnabar in red, chromium in green, and cobalt in blue are common offenders. Cadmium, which is used for yellow, may cause a photoallergic reaction following exposure to ultraviolet light. Other inorganic salts of metals used for tattooing include ferric hydrate for ochre, ferric oxide for brown, manganese salts for purple. Reactions may be seen within a few weeks up to years after the tattoo is placed.

Reactions are often confined to the tattoo and may present as erythematous papules or plaques, although lesions may also present as scaly and eczematous patches. Psoriasis, vitiligo, and lichen planus may Koebnerize and appear in the tattoo. Sarcoidosis may occur in tattoos and can be seen upon histopathologic examination. Allergic contact dermatitis may also be seen in people who receive temporary henna tattoos in which the henna dye is mixed with paraphenylenediamine (PPD).

Histologically, granulomatous, sarcoidal, and lichenoid patterns may be seen. A punch biopsy was performed in this patient that revealed a lichenoid and interstitial lymphohistiocytic infiltrate with red tattoo pigment. Special stains for PAS, GMS, FITE, and AFB were negative. There was no polarizable foreign material identified.

Treatment includes topical steroids, which may be ineffective, intralesional kenalog, and surgical excision. Laser must be used with caution, as it may aggravate the allergic reaction and cause a systemic reaction.

This case and photo were provided by Dr. Bilu Martin.

Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to [email protected].

The way Kelly Stankiewicz, MD, sees it, the first step in any cosmetic consultation is to be present and listen intently to the patient’s concerns.

“I can’t tell you how many times I’ve walked into a room and thought the patient would say they’re concerned about one thing, but they’re concerned about something totally different,” Dr. Stankiewicz, a dermatologist in private practice in Park City, Utah, said during the annual conference of the American Society for Laser Medicine and Surgery. “The first question I ask is, ‘What would you like to improve?’ ‘What’s bothering you?’ ‘What would you like to make look better?’ Frequently, it’s not what you think.”

Next, she tries to get a sense of their lifestyle by asking patients about their occupation, hobbies, and outdoor activities they may engage in. “Here in Park City, it’s very sunny most all the time, so treatments need to be tailored to when those outdoor activities are being done, or perhaps they can be avoided for a period of time,” she said. “This gives you an idea of what kind of downtime people will tolerate. I also like to hear about their history of cosmetic procedures. If someone has had a lot of cosmetic procedures done, you can talk with them on a more detailed level. If someone is completely unaware of treatment options, you have to keep it simple.”

Dr. Stankiewicz also reviews their personal history of cosmetic procedures when considering safety of treatment. “For instance, if somebody has had a neck lift, you want to be very cautious doing any ablative procedures along the jawline,” she said. “I also like to know if anyone has had any reactions to dermal fillers or neuromodulators that they did not like. It’s very helpful to hear from patients what’s worked for them and what hasn’t. I also like to keep my ear open for pricing concerns. Not everyone will bring up the pricing issues, but sometimes they will, and it’s an important piece of information. Lastly, it’s important to look for any warning signs like irrational behavior or unrealistic expectations. These are patients you want to try to avoid treating.”

She shared four other key components to an effective cosmetic consultation, including the examination itself, which she prefers to separate from the discussion portion of the visit. “I lean the patient back in the exam chair and shine the light on their skin, which is important for evaluating for conditions you may not have discussed that could be easily improved,” Dr. Stankiewicz said.

“If the patient is concerned about pigmented lesions, I’ll pull out my dermatoscope to make sure there isn’t any concern for skin cancer. After the examination, I’ll sit the patient up again so that there is a very distinct start and finish to the examination portion of my cosmetic consultation.”

Surgery vs. noninvasive treatments

Step three in her consultative process is to review treatment options with patients. “I never hold back if surgery is their best treatment option,” she said. “I don’t perform surgery, but I have a list of people I can refer them to.”

CasarsaGuru/Getty Images

Once she addresses the potential for surgery, she reviews noninvasive treatment options, including topical products, injectables, lasers, and chemical peels. “Everyone who comes in for a cosmetic consultation leaves with some sort of topical recommendation, even if it’s as simple as a sunscreen I think they would like or a prescription for generic tretinoin,” she said. “I always present options in a framework starting with those that require lower downtime, higher number of treatment options, and lower cost. Then I move up the scale to tell them more about treatments that require higher downtime, a lower number of treatments, but have a higher cost.”

Step four in her consultative process involves discussing her final treatment recommendations. She’ll say something like, “I’ve been through all these options with you and my final recommendation is X,” and the patient walks away with a clear understanding of the recommendations, she said. “When I leave the room after giving my final recommendation, I’ll write everything down outside of the room, or I’ll have a member of my staff write down everything I’ve said outside the room.”

Finally, she and her staff record all the relevant information for the patient as a customized handout, including the treatment options discussed, how many will be required, whether they have to come in early for numbing cream or not, and the per treatment price tag. “Once we’ve written down everything we’ve discussed, I’ll circle or I’ll star my recommended treatment,” Dr. Stankiewicz said. They also have a handout for topical products, and she checks off the topical products that she discussed with the patient. The third handout she provides to patients is a recommended skin care regimen.

Dr. Stankiewicz reported having no relevant financial disclosures.

[email protected]

The way Kelly Stankiewicz, MD, sees it, the first step in any cosmetic consultation is to be present and listen intently to the patient’s concerns.

“I can’t tell you how many times I’ve walked into a room and thought the patient would say they’re concerned about one thing, but they’re concerned about something totally different,” Dr. Stankiewicz, a dermatologist in private practice in Park City, Utah, said during the annual conference of the American Society for Laser Medicine and Surgery. “The first question I ask is, ‘What would you like to improve?’ ‘What’s bothering you?’ ‘What would you like to make look better?’ Frequently, it’s not what you think.”

Next, she tries to get a sense of their lifestyle by asking patients about their occupation, hobbies, and outdoor activities they may engage in. “Here in Park City, it’s very sunny most all the time, so treatments need to be tailored to when those outdoor activities are being done, or perhaps they can be avoided for a period of time,” she said. “This gives you an idea of what kind of downtime people will tolerate. I also like to hear about their history of cosmetic procedures. If someone has had a lot of cosmetic procedures done, you can talk with them on a more detailed level. If someone is completely unaware of treatment options, you have to keep it simple.”

Dr. Stankiewicz also reviews their personal history of cosmetic procedures when considering safety of treatment. “For instance, if somebody has had a neck lift, you want to be very cautious doing any ablative procedures along the jawline,” she said. “I also like to know if anyone has had any reactions to dermal fillers or neuromodulators that they did not like. It’s very helpful to hear from patients what’s worked for them and what hasn’t. I also like to keep my ear open for pricing concerns. Not everyone will bring up the pricing issues, but sometimes they will, and it’s an important piece of information. Lastly, it’s important to look for any warning signs like irrational behavior or unrealistic expectations. These are patients you want to try to avoid treating.”

She shared four other key components to an effective cosmetic consultation, including the examination itself, which she prefers to separate from the discussion portion of the visit. “I lean the patient back in the exam chair and shine the light on their skin, which is important for evaluating for conditions you may not have discussed that could be easily improved,” Dr. Stankiewicz said.

“If the patient is concerned about pigmented lesions, I’ll pull out my dermatoscope to make sure there isn’t any concern for skin cancer. After the examination, I’ll sit the patient up again so that there is a very distinct start and finish to the examination portion of my cosmetic consultation.”

Surgery vs. noninvasive treatments

Step three in her consultative process is to review treatment options with patients. “I never hold back if surgery is their best treatment option,” she said. “I don’t perform surgery, but I have a list of people I can refer them to.”

CasarsaGuru/Getty Images

Once she addresses the potential for surgery, she reviews noninvasive treatment options, including topical products, injectables, lasers, and chemical peels. “Everyone who comes in for a cosmetic consultation leaves with some sort of topical recommendation, even if it’s as simple as a sunscreen I think they would like or a prescription for generic tretinoin,” she said. “I always present options in a framework starting with those that require lower downtime, higher number of treatment options, and lower cost. Then I move up the scale to tell them more about treatments that require higher downtime, a lower number of treatments, but have a higher cost.”

Step four in her consultative process involves discussing her final treatment recommendations. She’ll say something like, “I’ve been through all these options with you and my final recommendation is X,” and the patient walks away with a clear understanding of the recommendations, she said. “When I leave the room after giving my final recommendation, I’ll write everything down outside of the room, or I’ll have a member of my staff write down everything I’ve said outside the room.”

Finally, she and her staff record all the relevant information for the patient as a customized handout, including the treatment options discussed, how many will be required, whether they have to come in early for numbing cream or not, and the per treatment price tag. “Once we’ve written down everything we’ve discussed, I’ll circle or I’ll star my recommended treatment,” Dr. Stankiewicz said. They also have a handout for topical products, and she checks off the topical products that she discussed with the patient. The third handout she provides to patients is a recommended skin care regimen.

Dr. Stankiewicz reported having no relevant financial disclosures.

[email protected]

The way Kelly Stankiewicz, MD, sees it, the first step in any cosmetic consultation is to be present and listen intently to the patient’s concerns.

“I can’t tell you how many times I’ve walked into a room and thought the patient would say they’re concerned about one thing, but they’re concerned about something totally different,” Dr. Stankiewicz, a dermatologist in private practice in Park City, Utah, said during the annual conference of the American Society for Laser Medicine and Surgery. “The first question I ask is, ‘What would you like to improve?’ ‘What’s bothering you?’ ‘What would you like to make look better?’ Frequently, it’s not what you think.”

Next, she tries to get a sense of their lifestyle by asking patients about their occupation, hobbies, and outdoor activities they may engage in. “Here in Park City, it’s very sunny most all the time, so treatments need to be tailored to when those outdoor activities are being done, or perhaps they can be avoided for a period of time,” she said. “This gives you an idea of what kind of downtime people will tolerate. I also like to hear about their history of cosmetic procedures. If someone has had a lot of cosmetic procedures done, you can talk with them on a more detailed level. If someone is completely unaware of treatment options, you have to keep it simple.”

Dr. Stankiewicz also reviews their personal history of cosmetic procedures when considering safety of treatment. “For instance, if somebody has had a neck lift, you want to be very cautious doing any ablative procedures along the jawline,” she said. “I also like to know if anyone has had any reactions to dermal fillers or neuromodulators that they did not like. It’s very helpful to hear from patients what’s worked for them and what hasn’t. I also like to keep my ear open for pricing concerns. Not everyone will bring up the pricing issues, but sometimes they will, and it’s an important piece of information. Lastly, it’s important to look for any warning signs like irrational behavior or unrealistic expectations. These are patients you want to try to avoid treating.”

She shared four other key components to an effective cosmetic consultation, including the examination itself, which she prefers to separate from the discussion portion of the visit. “I lean the patient back in the exam chair and shine the light on their skin, which is important for evaluating for conditions you may not have discussed that could be easily improved,” Dr. Stankiewicz said.

“If the patient is concerned about pigmented lesions, I’ll pull out my dermatoscope to make sure there isn’t any concern for skin cancer. After the examination, I’ll sit the patient up again so that there is a very distinct start and finish to the examination portion of my cosmetic consultation.”

Surgery vs. noninvasive treatments

Step three in her consultative process is to review treatment options with patients. “I never hold back if surgery is their best treatment option,” she said. “I don’t perform surgery, but I have a list of people I can refer them to.”

CasarsaGuru/Getty Images

Once she addresses the potential for surgery, she reviews noninvasive treatment options, including topical products, injectables, lasers, and chemical peels. “Everyone who comes in for a cosmetic consultation leaves with some sort of topical recommendation, even if it’s as simple as a sunscreen I think they would like or a prescription for generic tretinoin,” she said. “I always present options in a framework starting with those that require lower downtime, higher number of treatment options, and lower cost. Then I move up the scale to tell them more about treatments that require higher downtime, a lower number of treatments, but have a higher cost.”

Step four in her consultative process involves discussing her final treatment recommendations. She’ll say something like, “I’ve been through all these options with you and my final recommendation is X,” and the patient walks away with a clear understanding of the recommendations, she said. “When I leave the room after giving my final recommendation, I’ll write everything down outside of the room, or I’ll have a member of my staff write down everything I’ve said outside the room.”

Finally, she and her staff record all the relevant information for the patient as a customized handout, including the treatment options discussed, how many will be required, whether they have to come in early for numbing cream or not, and the per treatment price tag. “Once we’ve written down everything we’ve discussed, I’ll circle or I’ll star my recommended treatment,” Dr. Stankiewicz said. They also have a handout for topical products, and she checks off the topical products that she discussed with the patient. The third handout she provides to patients is a recommended skin care regimen.

Dr. Stankiewicz reported having no relevant financial disclosures.

[email protected]

A 2,940-nm and 1,470-nm hybrid fractional laser was found to be safe and effective for treating the genitourinary syndrome of menopause (GSM), results from a pilot trial showed.

“The genitourinary syndrome of menopause causes suffering in breast cancer survivors and postmenopausal women,” Jill S. Waibel, MD, said during the annual conference of the American Society for Laser Medicine and Surgery. A common side effect for breast cancer survivors is early onset of menopause that is brought on by treatment, specifically aromatase-inhibitor therapies, she noted.

The symptoms of GSM include discomfort during sex, impaired sexual function, burning or sensation or irritation of the genital area, vaginal constriction, frequent urinary tract infections, urinary incontinence, and vaginal laxity, said Dr. Waibel, owner and medical director of the Miami Dermatology and Laser Institute. Nonhormonal treatments have included OTC vaginal lubricants, OTC moisturizers, low-dose vaginal estrogen – which increases the risk of breast cancer – and systemic estrogen therapy, which also can increase the risk of breast and endometrial cancer. “So, we need a healthy, nondrug option,” she said.

The objective of the pilot study was to determine the safety and efficacy of the diVa hybrid fractional laser as a treatment for symptoms of genitourinary syndrome of menopause, early menopause after breast cancer, or vaginal atrophy. The laser applies tunable nonablative (1,470-nm) and ablative (2,940-nm) wavelengths to the same microscopic treatment zone to maximize results and reduce downtime. The device features a motorized precision guidance system and calibrated rotation for homogeneous pulsing.

“The 2,940-nm wavelength is used to ablate to a depth of 0-800 micrometers while the 1,470-nm wavelength is used to coagulate the epithelium and the lamina propria at a depth of 100-700 micrometers,” said Dr. Waibel, who is also subsection chief of dermatology at Baptist Hospital of Miami. “This combination is used for epithelial tissue to heal quickly and the lamina propria to remodel slowly over time, laying down more collagen in tissue.” Each procedure is delivered via a single-use dilator, which expands the vaginal canal for increased treatment area. “The tip length is 5.5 cm and the diameter is 1 cm,” she said. “The clear tip acts as a hygienic barrier between the tip and the handpiece.”

Study participants included 25 women between the ages of 40 and 70 with early menopause after breast cancer or vaginal atrophy: 20 in the treatment arm and 5 in the sham-treatment arm. Dr. Waibel performed three procedures 2 weeks apart. An ob.gyn. assessed the primary endpoints, which included the Vaginal Health Index Scale (VHIS), the Vaginal Maturation Index (VMI), the Female Sexual Function Index (FSFI) questionnaire, and the Day-to-Day Impact of Vaginal Aging (DIVA) questionnaire. Secondary endpoints were histology and a satisfaction questionnaire.

Of the women in the treated group, there were data available for 19 at 3 months follow-up and 17 at 6 months follow-up. Based on the results in these patients, there were statistically significant improvements in nearly all domains of the FSFI treatment arm at 3 and 6 months when compared to baseline, especially arousal (P values of .05 at 3 months and .01 at 6 months) and lubrication (P values of .009 at three months and .001 at 6 months).

Between 3 and 6 months, patients in the treatment arm experienced improvements in four dimensions of the DIVA questionnaire: daily activities (P value of .01 at 3 months to .010 at 6 months), emotional well-being (P value of .06 at 3 months to .014 at 6 months), sexual function (P value of .30 at 3 months to .003 at 6 months), and self-concept/body image (P value of .002 at 3 months to .001 at 6 months).

As for satisfaction, a majority of those in the treatment arm were “somewhat satisfied” with the treatment and would “somewhat likely” repeat and recommend the treatment to friends and family, Dr. Waibel said. Results among the women in the control arm, who were also surveyed, were in the similar range, she noted. (No other results for women in the control arm were available.)

Following treatments, histology revealed that the collagen was denser, fibroblasts were more dense, and vascularity was more notable. No adverse events were observed. “The hybrid fractional laser is safe and effective for treating GSM, early menopause after breast cancer, or vaginal atrophy,” Dr. Waibel concluded. Further studies are important to improve the understanding of “laser dosimetry, frequency of treatments, and longevity of effect. Collaboration between ob.gyns. and dermatologists is important as we learn about laser therapy in GSM.”

Dr. Waibel disclosed that she is a member of the advisory board of Sciton, which manufactures the diVa laser. She has also conducted clinical trials for many other device and pharmaceutical companies.

[email protected]

A 2,940-nm and 1,470-nm hybrid fractional laser was found to be safe and effective for treating the genitourinary syndrome of menopause (GSM), results from a pilot trial showed.

“The genitourinary syndrome of menopause causes suffering in breast cancer survivors and postmenopausal women,” Jill S. Waibel, MD, said during the annual conference of the American Society for Laser Medicine and Surgery. A common side effect for breast cancer survivors is early onset of menopause that is brought on by treatment, specifically aromatase-inhibitor therapies, she noted.

The symptoms of GSM include discomfort during sex, impaired sexual function, burning or sensation or irritation of the genital area, vaginal constriction, frequent urinary tract infections, urinary incontinence, and vaginal laxity, said Dr. Waibel, owner and medical director of the Miami Dermatology and Laser Institute. Nonhormonal treatments have included OTC vaginal lubricants, OTC moisturizers, low-dose vaginal estrogen – which increases the risk of breast cancer – and systemic estrogen therapy, which also can increase the risk of breast and endometrial cancer. “So, we need a healthy, nondrug option,” she said.

The objective of the pilot study was to determine the safety and efficacy of the diVa hybrid fractional laser as a treatment for symptoms of genitourinary syndrome of menopause, early menopause after breast cancer, or vaginal atrophy. The laser applies tunable nonablative (1,470-nm) and ablative (2,940-nm) wavelengths to the same microscopic treatment zone to maximize results and reduce downtime. The device features a motorized precision guidance system and calibrated rotation for homogeneous pulsing.

“The 2,940-nm wavelength is used to ablate to a depth of 0-800 micrometers while the 1,470-nm wavelength is used to coagulate the epithelium and the lamina propria at a depth of 100-700 micrometers,” said Dr. Waibel, who is also subsection chief of dermatology at Baptist Hospital of Miami. “This combination is used for epithelial tissue to heal quickly and the lamina propria to remodel slowly over time, laying down more collagen in tissue.” Each procedure is delivered via a single-use dilator, which expands the vaginal canal for increased treatment area. “The tip length is 5.5 cm and the diameter is 1 cm,” she said. “The clear tip acts as a hygienic barrier between the tip and the handpiece.”

Study participants included 25 women between the ages of 40 and 70 with early menopause after breast cancer or vaginal atrophy: 20 in the treatment arm and 5 in the sham-treatment arm. Dr. Waibel performed three procedures 2 weeks apart. An ob.gyn. assessed the primary endpoints, which included the Vaginal Health Index Scale (VHIS), the Vaginal Maturation Index (VMI), the Female Sexual Function Index (FSFI) questionnaire, and the Day-to-Day Impact of Vaginal Aging (DIVA) questionnaire. Secondary endpoints were histology and a satisfaction questionnaire.

Of the women in the treated group, there were data available for 19 at 3 months follow-up and 17 at 6 months follow-up. Based on the results in these patients, there were statistically significant improvements in nearly all domains of the FSFI treatment arm at 3 and 6 months when compared to baseline, especially arousal (P values of .05 at 3 months and .01 at 6 months) and lubrication (P values of .009 at three months and .001 at 6 months).

Between 3 and 6 months, patients in the treatment arm experienced improvements in four dimensions of the DIVA questionnaire: daily activities (P value of .01 at 3 months to .010 at 6 months), emotional well-being (P value of .06 at 3 months to .014 at 6 months), sexual function (P value of .30 at 3 months to .003 at 6 months), and self-concept/body image (P value of .002 at 3 months to .001 at 6 months).

As for satisfaction, a majority of those in the treatment arm were “somewhat satisfied” with the treatment and would “somewhat likely” repeat and recommend the treatment to friends and family, Dr. Waibel said. Results among the women in the control arm, who were also surveyed, were in the similar range, she noted. (No other results for women in the control arm were available.)

Following treatments, histology revealed that the collagen was denser, fibroblasts were more dense, and vascularity was more notable. No adverse events were observed. “The hybrid fractional laser is safe and effective for treating GSM, early menopause after breast cancer, or vaginal atrophy,” Dr. Waibel concluded. Further studies are important to improve the understanding of “laser dosimetry, frequency of treatments, and longevity of effect. Collaboration between ob.gyns. and dermatologists is important as we learn about laser therapy in GSM.”

Dr. Waibel disclosed that she is a member of the advisory board of Sciton, which manufactures the diVa laser. She has also conducted clinical trials for many other device and pharmaceutical companies.

[email protected]

A 2,940-nm and 1,470-nm hybrid fractional laser was found to be safe and effective for treating the genitourinary syndrome of menopause (GSM), results from a pilot trial showed.

“The genitourinary syndrome of menopause causes suffering in breast cancer survivors and postmenopausal women,” Jill S. Waibel, MD, said during the annual conference of the American Society for Laser Medicine and Surgery. A common side effect for breast cancer survivors is early onset of menopause that is brought on by treatment, specifically aromatase-inhibitor therapies, she noted.

The symptoms of GSM include discomfort during sex, impaired sexual function, burning or sensation or irritation of the genital area, vaginal constriction, frequent urinary tract infections, urinary incontinence, and vaginal laxity, said Dr. Waibel, owner and medical director of the Miami Dermatology and Laser Institute. Nonhormonal treatments have included OTC vaginal lubricants, OTC moisturizers, low-dose vaginal estrogen – which increases the risk of breast cancer – and systemic estrogen therapy, which also can increase the risk of breast and endometrial cancer. “So, we need a healthy, nondrug option,” she said.

The objective of the pilot study was to determine the safety and efficacy of the diVa hybrid fractional laser as a treatment for symptoms of genitourinary syndrome of menopause, early menopause after breast cancer, or vaginal atrophy. The laser applies tunable nonablative (1,470-nm) and ablative (2,940-nm) wavelengths to the same microscopic treatment zone to maximize results and reduce downtime. The device features a motorized precision guidance system and calibrated rotation for homogeneous pulsing.

“The 2,940-nm wavelength is used to ablate to a depth of 0-800 micrometers while the 1,470-nm wavelength is used to coagulate the epithelium and the lamina propria at a depth of 100-700 micrometers,” said Dr. Waibel, who is also subsection chief of dermatology at Baptist Hospital of Miami. “This combination is used for epithelial tissue to heal quickly and the lamina propria to remodel slowly over time, laying down more collagen in tissue.” Each procedure is delivered via a single-use dilator, which expands the vaginal canal for increased treatment area. “The tip length is 5.5 cm and the diameter is 1 cm,” she said. “The clear tip acts as a hygienic barrier between the tip and the handpiece.”

Study participants included 25 women between the ages of 40 and 70 with early menopause after breast cancer or vaginal atrophy: 20 in the treatment arm and 5 in the sham-treatment arm. Dr. Waibel performed three procedures 2 weeks apart. An ob.gyn. assessed the primary endpoints, which included the Vaginal Health Index Scale (VHIS), the Vaginal Maturation Index (VMI), the Female Sexual Function Index (FSFI) questionnaire, and the Day-to-Day Impact of Vaginal Aging (DIVA) questionnaire. Secondary endpoints were histology and a satisfaction questionnaire.

Of the women in the treated group, there were data available for 19 at 3 months follow-up and 17 at 6 months follow-up. Based on the results in these patients, there were statistically significant improvements in nearly all domains of the FSFI treatment arm at 3 and 6 months when compared to baseline, especially arousal (P values of .05 at 3 months and .01 at 6 months) and lubrication (P values of .009 at three months and .001 at 6 months).

Between 3 and 6 months, patients in the treatment arm experienced improvements in four dimensions of the DIVA questionnaire: daily activities (P value of .01 at 3 months to .010 at 6 months), emotional well-being (P value of .06 at 3 months to .014 at 6 months), sexual function (P value of .30 at 3 months to .003 at 6 months), and self-concept/body image (P value of .002 at 3 months to .001 at 6 months).

As for satisfaction, a majority of those in the treatment arm were “somewhat satisfied” with the treatment and would “somewhat likely” repeat and recommend the treatment to friends and family, Dr. Waibel said. Results among the women in the control arm, who were also surveyed, were in the similar range, she noted. (No other results for women in the control arm were available.)

Following treatments, histology revealed that the collagen was denser, fibroblasts were more dense, and vascularity was more notable. No adverse events were observed. “The hybrid fractional laser is safe and effective for treating GSM, early menopause after breast cancer, or vaginal atrophy,” Dr. Waibel concluded. Further studies are important to improve the understanding of “laser dosimetry, frequency of treatments, and longevity of effect. Collaboration between ob.gyns. and dermatologists is important as we learn about laser therapy in GSM.”

Dr. Waibel disclosed that she is a member of the advisory board of Sciton, which manufactures the diVa laser. She has also conducted clinical trials for many other device and pharmaceutical companies.

[email protected]

I just completed the third edition of my Cosmetic Dermatology textbook (McGraw Hill), which will come out later this year. Although writing it is a huge effort, I really enjoy all the basic science. While I was working on the book, I was most surprised by the findings on cellular senescence and autophagy, and I would like to share what I learned. These will be buzz words in the skin care field in the future.

Right now, it is too early, and we don’t know enough yet, to have cosmeceuticals that affect cellular senescence and autophagy. But, it’s not too early to learn about this research, to avoid falling prey to any pseudoscience that invariably ends up affecting cosmeceuticals on the market. The following is a brief primer on cellular senescence, skin aging, and cosmeceuticals; it represents what we currently know.
 

Cell phases

Keratinocytes and fibroblasts go through five different phases: stem, proliferation, differentiation, senescence, and apoptosis. The difference between apoptotic cells and senescent cells is that apoptotic cells are not viable and are eliminated, while senescent cells, even though they have gone into cell cycle arrest, remain functional and are not eliminated from the skin.

What are senescent cells?

Senescent cells have lost the ability to proliferate but have not undergone apoptosis. Senescent human skin fibroblasts in cell culture lose the youthful spindlelike shape and become enlarged and flattened.¹ Their lysosomes and mitochondria lose functionality.² The presence of senescent cells is associated with increased aging and seems to speed aging.
 

Senescent cells and skin aging

Senescent cells are increased in the age-related phenotype³ because of an age-related decline of senescent cell removal systems, such as the immune system⁴ and the autophagy-lysosomal pathway.⁵ Senescent cells are deleterious because they develop into a senescence-associated secretory phenotype (SASP), which is believed to be one of the major causes of aging. SASP cells communicate with nearby cells using proinflammatory cytokines, which include catabolic modulators such as Matrix metalloproteinases. They are known to release growth factors, cytokines, chemokines, matrix-modeling enzymes, lipids, and extracellular vesicles. The last are lipid bilayer-lined vesicles that can transport functional RNA and microRNA and facilitate other modes of communication between cells.⁶

The SASP is likely a natural tumor suppressive mode employed by cells to prevent cells with cancerous mutations from undergoing replication;⁷ however, when it comes to aging, the deleterious effects of SASP outweigh the beneficial effects. For example, SASP contributes to a prolonged state of inflammation, known as “inflammaging,”⁸ which is detrimental to the skin’s appearance. Human fibroblasts that have assumed the SASP secrete proinflammatory cytokines and MMPs and release reactive oxygen species,^9,10 resulting in degradation of the surrounding extracellular matrix (ECM). Loss of the ECM leads to fibroblast compaction and reduced DNA synthesis, all caused by SASPs.⁹
 

What causes cellular senescence?

Activation of the nuclear factor-erythroid 2-related transcription factor 2 (NRF2) induces cellular senescence via direct targeting of certain ECM genes. NRF2 is a key regulator of the skin’s antioxidant defense system, which controls the transcription of genes encoding reactive oxygen species–detoxifying enzymes and various other antioxidant proteins.¹¹ Loss of mitochondrial autophagy also induces senescence, as do activation of the TP53 gene, inactivity of SIRT-1, and short telomeres.

Cellular senescence and skin aging

Timely clearance of senescent cells before they create too much damage postpones the onset and severity of age-related diseases and extends the life span of mice.^12,6 Antiaging treatments should focus on decreasing the number of senescent cells and reverting senescent cells to the more juvenile forms: proliferating or differentiating cells as an approach to prevent skin aging.¹³ Restoration of the lysosomal-mitochondrial axis has been shown to revert SASP back to a juvenile status. Normalization of the lysosomal-mitochondrial axis is a prerequisite to reverse senescence.¹⁴

Cellular senescence, autophagy, the lysosomal-mitochondrial axis, and cosmeceuticals

Autophagy is the important process of organelles, like mitochondria,¹⁵ self-digesting their cytoplasmic material into lysosomes for degradation. Mitochondrial autophagy is very important in slowing the aging process because damaged mitochondria generate free radicals. As you can imagine, much research is focused on this area, but it is too early for any research to translate to efficacious cosmeceuticals.

Conclusion

To summarize, activation of sirtuin-1 (SIRT-1) has been shown to extend the lifespan of mammals, as does caloric restriction.¹⁶ This extension occurs because SIRT-1 decreases senescence and activates autophagy.

Although we do not yet know whether topical skincare products could affect senescence or autophagy, there are data to show that oral resveratrol16 and melatonin¹⁷ activate SIRT-1 and increase autophagy. I am closely watching this research and will let you know if there are any similar data on topical cosmeceuticals targeting senescence or autophagy. Stay tuned!
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at [email protected].

References

1. Papadopoulou A et al. Biogerontology. 2020 Dec;21(6):695-708.

2. López-Otin C et al. Cell. 2013 June 6;153, 1194–217.

3. Yoon J E et al. Theranostics. 2018 Sep 9;8(17):4620-32.

4. Rodier F, Campisi J. J Cell Biol. 2011 Feb 21;192(4):547-56.

5. Dutta D et al. Circ Res. 2012 Apr 13;110(8):1125-38.

6. Terlecki-Zaniewicz L et al. J Invest Dermatol. 2019 Dec;139(12):2425-36.e5.

7. Campisi J et al. Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40.

8. Franceschi C and Campisi J. J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1:S4-9.

9. Nelson G et al. Aging Cell. 2012 Apr;11(2):345-9.

10. Passos JF et al. PLoS Biol. 2007 May;5(5):e110.

11. Hiebert P et al. Dev Cell.  2018 Jul 16;46(2):145-61.e10.

12. Baker DJ et al. Nature. 2016 Feb 11:530(7589):184-9.

13. Mavrogonatou E et al. Matrix Biol. 2019 Jan;75-76:27-42.

14. Park JT et al. Ageing Res Rev. 2018 Nov;47:176-82.

15. Levine B and Kroemer G. Cell. 2019 Jan 10;176(1-2):11-42.

16. Morselli E et al. Cell Death Dis. 2010;1(1):e10.

17. Lee JH et al. Oncotarget. 2016 Mar 15;7(11):12075-88.

I just completed the third edition of my Cosmetic Dermatology textbook (McGraw Hill), which will come out later this year. Although writing it is a huge effort, I really enjoy all the basic science. While I was working on the book, I was most surprised by the findings on cellular senescence and autophagy, and I would like to share what I learned. These will be buzz words in the skin care field in the future.

Right now, it is too early, and we don’t know enough yet, to have cosmeceuticals that affect cellular senescence and autophagy. But, it’s not too early to learn about this research, to avoid falling prey to any pseudoscience that invariably ends up affecting cosmeceuticals on the market. The following is a brief primer on cellular senescence, skin aging, and cosmeceuticals; it represents what we currently know.
 

Cell phases

Keratinocytes and fibroblasts go through five different phases: stem, proliferation, differentiation, senescence, and apoptosis. The difference between apoptotic cells and senescent cells is that apoptotic cells are not viable and are eliminated, while senescent cells, even though they have gone into cell cycle arrest, remain functional and are not eliminated from the skin.

What are senescent cells?

Senescent cells have lost the ability to proliferate but have not undergone apoptosis. Senescent human skin fibroblasts in cell culture lose the youthful spindlelike shape and become enlarged and flattened.¹ Their lysosomes and mitochondria lose functionality.² The presence of senescent cells is associated with increased aging and seems to speed aging.
 

Senescent cells and skin aging

Senescent cells are increased in the age-related phenotype³ because of an age-related decline of senescent cell removal systems, such as the immune system⁴ and the autophagy-lysosomal pathway.⁵ Senescent cells are deleterious because they develop into a senescence-associated secretory phenotype (SASP), which is believed to be one of the major causes of aging. SASP cells communicate with nearby cells using proinflammatory cytokines, which include catabolic modulators such as Matrix metalloproteinases. They are known to release growth factors, cytokines, chemokines, matrix-modeling enzymes, lipids, and extracellular vesicles. The last are lipid bilayer-lined vesicles that can transport functional RNA and microRNA and facilitate other modes of communication between cells.⁶

The SASP is likely a natural tumor suppressive mode employed by cells to prevent cells with cancerous mutations from undergoing replication;⁷ however, when it comes to aging, the deleterious effects of SASP outweigh the beneficial effects. For example, SASP contributes to a prolonged state of inflammation, known as “inflammaging,”⁸ which is detrimental to the skin’s appearance. Human fibroblasts that have assumed the SASP secrete proinflammatory cytokines and MMPs and release reactive oxygen species,^9,10 resulting in degradation of the surrounding extracellular matrix (ECM). Loss of the ECM leads to fibroblast compaction and reduced DNA synthesis, all caused by SASPs.⁹
 

What causes cellular senescence?

Activation of the nuclear factor-erythroid 2-related transcription factor 2 (NRF2) induces cellular senescence via direct targeting of certain ECM genes. NRF2 is a key regulator of the skin’s antioxidant defense system, which controls the transcription of genes encoding reactive oxygen species–detoxifying enzymes and various other antioxidant proteins.¹¹ Loss of mitochondrial autophagy also induces senescence, as do activation of the TP53 gene, inactivity of SIRT-1, and short telomeres.

Cellular senescence and skin aging

Timely clearance of senescent cells before they create too much damage postpones the onset and severity of age-related diseases and extends the life span of mice.^12,6 Antiaging treatments should focus on decreasing the number of senescent cells and reverting senescent cells to the more juvenile forms: proliferating or differentiating cells as an approach to prevent skin aging.¹³ Restoration of the lysosomal-mitochondrial axis has been shown to revert SASP back to a juvenile status. Normalization of the lysosomal-mitochondrial axis is a prerequisite to reverse senescence.¹⁴

Cellular senescence, autophagy, the lysosomal-mitochondrial axis, and cosmeceuticals

Autophagy is the important process of organelles, like mitochondria,¹⁵ self-digesting their cytoplasmic material into lysosomes for degradation. Mitochondrial autophagy is very important in slowing the aging process because damaged mitochondria generate free radicals. As you can imagine, much research is focused on this area, but it is too early for any research to translate to efficacious cosmeceuticals.

Conclusion

To summarize, activation of sirtuin-1 (SIRT-1) has been shown to extend the lifespan of mammals, as does caloric restriction.¹⁶ This extension occurs because SIRT-1 decreases senescence and activates autophagy.

Although we do not yet know whether topical skincare products could affect senescence or autophagy, there are data to show that oral resveratrol16 and melatonin¹⁷ activate SIRT-1 and increase autophagy. I am closely watching this research and will let you know if there are any similar data on topical cosmeceuticals targeting senescence or autophagy. Stay tuned!
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at [email protected].

References

1. Papadopoulou A et al. Biogerontology. 2020 Dec;21(6):695-708.

2. López-Otin C et al. Cell. 2013 June 6;153, 1194–217.

3. Yoon J E et al. Theranostics. 2018 Sep 9;8(17):4620-32.

4. Rodier F, Campisi J. J Cell Biol. 2011 Feb 21;192(4):547-56.

5. Dutta D et al. Circ Res. 2012 Apr 13;110(8):1125-38.

6. Terlecki-Zaniewicz L et al. J Invest Dermatol. 2019 Dec;139(12):2425-36.e5.

7. Campisi J et al. Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40.

8. Franceschi C and Campisi J. J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1:S4-9.

9. Nelson G et al. Aging Cell. 2012 Apr;11(2):345-9.

10. Passos JF et al. PLoS Biol. 2007 May;5(5):e110.

11. Hiebert P et al. Dev Cell.  2018 Jul 16;46(2):145-61.e10.

12. Baker DJ et al. Nature. 2016 Feb 11:530(7589):184-9.

13. Mavrogonatou E et al. Matrix Biol. 2019 Jan;75-76:27-42.

14. Park JT et al. Ageing Res Rev. 2018 Nov;47:176-82.

15. Levine B and Kroemer G. Cell. 2019 Jan 10;176(1-2):11-42.

16. Morselli E et al. Cell Death Dis. 2010;1(1):e10.

17. Lee JH et al. Oncotarget. 2016 Mar 15;7(11):12075-88.

I just completed the third edition of my Cosmetic Dermatology textbook (McGraw Hill), which will come out later this year. Although writing it is a huge effort, I really enjoy all the basic science. While I was working on the book, I was most surprised by the findings on cellular senescence and autophagy, and I would like to share what I learned. These will be buzz words in the skin care field in the future.

Right now, it is too early, and we don’t know enough yet, to have cosmeceuticals that affect cellular senescence and autophagy. But, it’s not too early to learn about this research, to avoid falling prey to any pseudoscience that invariably ends up affecting cosmeceuticals on the market. The following is a brief primer on cellular senescence, skin aging, and cosmeceuticals; it represents what we currently know.
 

Cell phases

Keratinocytes and fibroblasts go through five different phases: stem, proliferation, differentiation, senescence, and apoptosis. The difference between apoptotic cells and senescent cells is that apoptotic cells are not viable and are eliminated, while senescent cells, even though they have gone into cell cycle arrest, remain functional and are not eliminated from the skin.

What are senescent cells?

Senescent cells have lost the ability to proliferate but have not undergone apoptosis. Senescent human skin fibroblasts in cell culture lose the youthful spindlelike shape and become enlarged and flattened.¹ Their lysosomes and mitochondria lose functionality.² The presence of senescent cells is associated with increased aging and seems to speed aging.
 

Senescent cells and skin aging

Senescent cells are increased in the age-related phenotype³ because of an age-related decline of senescent cell removal systems, such as the immune system⁴ and the autophagy-lysosomal pathway.⁵ Senescent cells are deleterious because they develop into a senescence-associated secretory phenotype (SASP), which is believed to be one of the major causes of aging. SASP cells communicate with nearby cells using proinflammatory cytokines, which include catabolic modulators such as Matrix metalloproteinases. They are known to release growth factors, cytokines, chemokines, matrix-modeling enzymes, lipids, and extracellular vesicles. The last are lipid bilayer-lined vesicles that can transport functional RNA and microRNA and facilitate other modes of communication between cells.⁶

The SASP is likely a natural tumor suppressive mode employed by cells to prevent cells with cancerous mutations from undergoing replication;⁷ however, when it comes to aging, the deleterious effects of SASP outweigh the beneficial effects. For example, SASP contributes to a prolonged state of inflammation, known as “inflammaging,”⁸ which is detrimental to the skin’s appearance. Human fibroblasts that have assumed the SASP secrete proinflammatory cytokines and MMPs and release reactive oxygen species,^9,10 resulting in degradation of the surrounding extracellular matrix (ECM). Loss of the ECM leads to fibroblast compaction and reduced DNA synthesis, all caused by SASPs.⁹
 

What causes cellular senescence?

Activation of the nuclear factor-erythroid 2-related transcription factor 2 (NRF2) induces cellular senescence via direct targeting of certain ECM genes. NRF2 is a key regulator of the skin’s antioxidant defense system, which controls the transcription of genes encoding reactive oxygen species–detoxifying enzymes and various other antioxidant proteins.¹¹ Loss of mitochondrial autophagy also induces senescence, as do activation of the TP53 gene, inactivity of SIRT-1, and short telomeres.

Cellular senescence and skin aging

Timely clearance of senescent cells before they create too much damage postpones the onset and severity of age-related diseases and extends the life span of mice.^12,6 Antiaging treatments should focus on decreasing the number of senescent cells and reverting senescent cells to the more juvenile forms: proliferating or differentiating cells as an approach to prevent skin aging.¹³ Restoration of the lysosomal-mitochondrial axis has been shown to revert SASP back to a juvenile status. Normalization of the lysosomal-mitochondrial axis is a prerequisite to reverse senescence.¹⁴

Cellular senescence, autophagy, the lysosomal-mitochondrial axis, and cosmeceuticals

Autophagy is the important process of organelles, like mitochondria,¹⁵ self-digesting their cytoplasmic material into lysosomes for degradation. Mitochondrial autophagy is very important in slowing the aging process because damaged mitochondria generate free radicals. As you can imagine, much research is focused on this area, but it is too early for any research to translate to efficacious cosmeceuticals.

Conclusion

To summarize, activation of sirtuin-1 (SIRT-1) has been shown to extend the lifespan of mammals, as does caloric restriction.¹⁶ This extension occurs because SIRT-1 decreases senescence and activates autophagy.

Although we do not yet know whether topical skincare products could affect senescence or autophagy, there are data to show that oral resveratrol16 and melatonin¹⁷ activate SIRT-1 and increase autophagy. I am closely watching this research and will let you know if there are any similar data on topical cosmeceuticals targeting senescence or autophagy. Stay tuned!
 

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur who practices in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann has written two textbooks and a New York Times Best Sellers book for consumers. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Revance, Evolus, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a company that independently tests skin care products and makes recommendations to physicians on which skin care technologies are best. Write to her at [email protected].

References

1. Papadopoulou A et al. Biogerontology. 2020 Dec;21(6):695-708.

2. López-Otin C et al. Cell. 2013 June 6;153, 1194–217.

3. Yoon J E et al. Theranostics. 2018 Sep 9;8(17):4620-32.

4. Rodier F, Campisi J. J Cell Biol. 2011 Feb 21;192(4):547-56.

5. Dutta D et al. Circ Res. 2012 Apr 13;110(8):1125-38.

6. Terlecki-Zaniewicz L et al. J Invest Dermatol. 2019 Dec;139(12):2425-36.e5.

7. Campisi J et al. Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40.

8. Franceschi C and Campisi J. J Gerontol A Biol Sci Med Sci. 2014 Jun;69 Suppl 1:S4-9.

9. Nelson G et al. Aging Cell. 2012 Apr;11(2):345-9.

10. Passos JF et al. PLoS Biol. 2007 May;5(5):e110.

11. Hiebert P et al. Dev Cell.  2018 Jul 16;46(2):145-61.e10.

12. Baker DJ et al. Nature. 2016 Feb 11:530(7589):184-9.

13. Mavrogonatou E et al. Matrix Biol. 2019 Jan;75-76:27-42.

14. Park JT et al. Ageing Res Rev. 2018 Nov;47:176-82.

15. Levine B and Kroemer G. Cell. 2019 Jan 10;176(1-2):11-42.

16. Morselli E et al. Cell Death Dis. 2010;1(1):e10.

17. Lee JH et al. Oncotarget. 2016 Mar 15;7(11):12075-88.

A federal judge in Texas has dismissed a lawsuit from 117 Houston Methodist Hospital workers who refused to get a COVID-19 vaccine and said it was illegal to require them to do so.

In the ruling issued June 12, U.S. District Judge Lynn Hughes upheld the hospital’s policy and said the vaccination requirement didn’t break any federal laws.

“This is not coercion,” Judge Hughes wrote in the ruling.

“Methodist is trying to do their business of saving lives without giving them the COVID-19 virus,” he wrote. “It is a choice made to keep staff, patients, and their families safer.”

In April, the Houston Methodist Hospital system announced a policy that required employees to be vaccinated by June 7 or request an exemption. After the deadline, 178 of 26,000 employees refused to get inoculated and were placed on suspension without pay. The employees said the vaccine was unsafe and “experimental.” In his ruling, Judge Hughes said their claim was false and irrelevant.

“Texas law only protects employees from being terminated for refusing to commit an act carrying criminal penalties to the worker,” he wrote. “Receiving a COVID-19 vaccination is not an illegal act, and it carries no criminal penalties.”

He denounced the “press-release style of the complaint” and the comparison of the hospital’s vaccine policy to forced experimentation by the Nazis against Jewish people during the Holocaust.

“Equating the injection requirement to medical experimentation in concentration camps is reprehensible,” he wrote. “Nazi doctors conducted medical experiments on victims that caused pain, mutilation, permanent disability, and in many cases, death.”

Judge Hughes also said that employees can “freely choose” to accept or refuse a COVID-19 vaccine. If they refuse, they “simply need to work somewhere else,” he wrote.

“If a worker refuses an assignment, changed office, earlier start time, or other directive, he may be properly fired,” Judge Hughes said. “Every employment includes limits on the worker’s behavior in exchange for his remuneration. This is all part of the bargain.”

The ruling could set a precedent for similar COVID-19 vaccine lawsuits across the country, NPR reported. Houston Methodist was one of the first hospitals to require staff to be vaccinated. After the ruling on June 12, the hospital system wrote in a statement that it was “pleased and reassured” that Judge Hughes dismissed a “frivolous lawsuit.”

The hospital system will begin to terminate the 178 employees who were suspended if they don’t get a vaccine by June 21.

Jennifer Bridges, a nurse who has led the campaign against the vaccine policy, said she and the other plaintiffs will appeal the decision, according to KHOU.

“We’re OK with this decision. We are appealing. This will be taken all the way to the Supreme Court,” she told the news station. “This is far from over. This is literally only the beginning.”

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

A federal judge in Texas has dismissed a lawsuit from 117 Houston Methodist Hospital workers who refused to get a COVID-19 vaccine and said it was illegal to require them to do so.

In the ruling issued June 12, U.S. District Judge Lynn Hughes upheld the hospital’s policy and said the vaccination requirement didn’t break any federal laws.

“This is not coercion,” Judge Hughes wrote in the ruling.

“Methodist is trying to do their business of saving lives without giving them the COVID-19 virus,” he wrote. “It is a choice made to keep staff, patients, and their families safer.”

In April, the Houston Methodist Hospital system announced a policy that required employees to be vaccinated by June 7 or request an exemption. After the deadline, 178 of 26,000 employees refused to get inoculated and were placed on suspension without pay. The employees said the vaccine was unsafe and “experimental.” In his ruling, Judge Hughes said their claim was false and irrelevant.

“Texas law only protects employees from being terminated for refusing to commit an act carrying criminal penalties to the worker,” he wrote. “Receiving a COVID-19 vaccination is not an illegal act, and it carries no criminal penalties.”

He denounced the “press-release style of the complaint” and the comparison of the hospital’s vaccine policy to forced experimentation by the Nazis against Jewish people during the Holocaust.

“Equating the injection requirement to medical experimentation in concentration camps is reprehensible,” he wrote. “Nazi doctors conducted medical experiments on victims that caused pain, mutilation, permanent disability, and in many cases, death.”

Judge Hughes also said that employees can “freely choose” to accept or refuse a COVID-19 vaccine. If they refuse, they “simply need to work somewhere else,” he wrote.

“If a worker refuses an assignment, changed office, earlier start time, or other directive, he may be properly fired,” Judge Hughes said. “Every employment includes limits on the worker’s behavior in exchange for his remuneration. This is all part of the bargain.”

The ruling could set a precedent for similar COVID-19 vaccine lawsuits across the country, NPR reported. Houston Methodist was one of the first hospitals to require staff to be vaccinated. After the ruling on June 12, the hospital system wrote in a statement that it was “pleased and reassured” that Judge Hughes dismissed a “frivolous lawsuit.”

The hospital system will begin to terminate the 178 employees who were suspended if they don’t get a vaccine by June 21.

Jennifer Bridges, a nurse who has led the campaign against the vaccine policy, said she and the other plaintiffs will appeal the decision, according to KHOU.

“We’re OK with this decision. We are appealing. This will be taken all the way to the Supreme Court,” she told the news station. “This is far from over. This is literally only the beginning.”

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

A federal judge in Texas has dismissed a lawsuit from 117 Houston Methodist Hospital workers who refused to get a COVID-19 vaccine and said it was illegal to require them to do so.

In the ruling issued June 12, U.S. District Judge Lynn Hughes upheld the hospital’s policy and said the vaccination requirement didn’t break any federal laws.

“This is not coercion,” Judge Hughes wrote in the ruling.

“Methodist is trying to do their business of saving lives without giving them the COVID-19 virus,” he wrote. “It is a choice made to keep staff, patients, and their families safer.”

In April, the Houston Methodist Hospital system announced a policy that required employees to be vaccinated by June 7 or request an exemption. After the deadline, 178 of 26,000 employees refused to get inoculated and were placed on suspension without pay. The employees said the vaccine was unsafe and “experimental.” In his ruling, Judge Hughes said their claim was false and irrelevant.

“Texas law only protects employees from being terminated for refusing to commit an act carrying criminal penalties to the worker,” he wrote. “Receiving a COVID-19 vaccination is not an illegal act, and it carries no criminal penalties.”

He denounced the “press-release style of the complaint” and the comparison of the hospital’s vaccine policy to forced experimentation by the Nazis against Jewish people during the Holocaust.

“Equating the injection requirement to medical experimentation in concentration camps is reprehensible,” he wrote. “Nazi doctors conducted medical experiments on victims that caused pain, mutilation, permanent disability, and in many cases, death.”

Judge Hughes also said that employees can “freely choose” to accept or refuse a COVID-19 vaccine. If they refuse, they “simply need to work somewhere else,” he wrote.

“If a worker refuses an assignment, changed office, earlier start time, or other directive, he may be properly fired,” Judge Hughes said. “Every employment includes limits on the worker’s behavior in exchange for his remuneration. This is all part of the bargain.”

The ruling could set a precedent for similar COVID-19 vaccine lawsuits across the country, NPR reported. Houston Methodist was one of the first hospitals to require staff to be vaccinated. After the ruling on June 12, the hospital system wrote in a statement that it was “pleased and reassured” that Judge Hughes dismissed a “frivolous lawsuit.”

The hospital system will begin to terminate the 178 employees who were suspended if they don’t get a vaccine by June 21.

Jennifer Bridges, a nurse who has led the campaign against the vaccine policy, said she and the other plaintiffs will appeal the decision, according to KHOU.

“We’re OK with this decision. We are appealing. This will be taken all the way to the Supreme Court,” she told the news station. “This is far from over. This is literally only the beginning.”

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

The Comparison

A Pink scaling plaques and erythematous erosions in the antecubital fossae of a 6-year-old White boy.

B Violaceous, hyperpigmented, nummular plaques on the back and extensor surface of the right arm of a 16-month-old Black girl.

C Atopic dermatitis and follicular prominence/accentuation on the neck of a young Black girl.

Epidemiology

People of African descent have the highest atopic dermatitis prevalence and severity.

Key clinical features in people with darker skin tones include:

• follicular prominence
• papular morphology
• prurigo nodules
• hyperpigmented, violaceous-brown or gray plaques instead of erythematous plaques
• lichenification
• treatment resistant.^1,2

Worth noting
Postinflammatory hyperpigmentation and postinflammatory hypopigmentation may be more distressing to the patient/family than the atopic dermatitis itself.

Health disparity highlight
In the United States, patients with skin of color are more likely to be hospitalized with severe atopic dermatitis, have more substantial out-ofpocket costs, be underinsured, and have an increased number of missed days of work. Limited access to outpatient health care plays a role in exacerbating this health disparity.^3,4

The Comparison

A Pink scaling plaques and erythematous erosions in the antecubital fossae of a 6-year-old White boy.

B Violaceous, hyperpigmented, nummular plaques on the back and extensor surface of the right arm of a 16-month-old Black girl.

C Atopic dermatitis and follicular prominence/accentuation on the neck of a young Black girl.

Epidemiology

People of African descent have the highest atopic dermatitis prevalence and severity.

Key clinical features in people with darker skin tones include:

• follicular prominence
• papular morphology
• prurigo nodules
• hyperpigmented, violaceous-brown or gray plaques instead of erythematous plaques
• lichenification
• treatment resistant.^1,2

Worth noting
Postinflammatory hyperpigmentation and postinflammatory hypopigmentation may be more distressing to the patient/family than the atopic dermatitis itself.

Health disparity highlight
In the United States, patients with skin of color are more likely to be hospitalized with severe atopic dermatitis, have more substantial out-ofpocket costs, be underinsured, and have an increased number of missed days of work. Limited access to outpatient health care plays a role in exacerbating this health disparity.^3,4

The Comparison

A Pink scaling plaques and erythematous erosions in the antecubital fossae of a 6-year-old White boy.

B Violaceous, hyperpigmented, nummular plaques on the back and extensor surface of the right arm of a 16-month-old Black girl.

C Atopic dermatitis and follicular prominence/accentuation on the neck of a young Black girl.

Epidemiology

People of African descent have the highest atopic dermatitis prevalence and severity.

Key clinical features in people with darker skin tones include:

• follicular prominence
• papular morphology
• prurigo nodules
• hyperpigmented, violaceous-brown or gray plaques instead of erythematous plaques
• lichenification
• treatment resistant.^1,2

Worth noting
Postinflammatory hyperpigmentation and postinflammatory hypopigmentation may be more distressing to the patient/family than the atopic dermatitis itself.

Health disparity highlight
In the United States, patients with skin of color are more likely to be hospitalized with severe atopic dermatitis, have more substantial out-ofpocket costs, be underinsured, and have an increased number of missed days of work. Limited access to outpatient health care plays a role in exacerbating this health disparity.^3,4

The U.S. Occupational Safety and Health Administration issued its long-awaited Emergency Temporary Standard (ETS) for COVID-19 June 10, surprising many by including only health care workers in the new emergency workplace safety rules.

“The ETS is an overdue step toward protecting health care workers, especially those working in long-term care facilities and home health care who are at greatly increased risk of infection,” said George Washington University, Washington, professor and former Obama administration Assistant Secretary of Labor David Michaels, PhD, MPH. “OSHA’s failure to issue a COVID-specific standard in other high-risk industries, like meat and poultry processing, corrections, homeless shelters, and retail establishments is disappointing. If exposure is not controlled in these workplaces, they will continue to be important drivers of infections.”

With the new regulations in place, about 10.3 million health care workers at hospitals, nursing homes, and assisted living facilities, as well as emergency responders and home health care workers, should be guaranteed protection standards that replace former guidance.

The new protections include supplying personal protective equipment and ensuring proper usage (for example, mandatory seal checks on respirators); screening everyone who enters the facility for COVID-19; ensuring proper ventilation; and establishing physical distancing requirements (6 feet) for unvaccinated workers. It also requires employers to give workers time off for vaccination. An antiretaliation clause could shield workers who complain about unsafe conditions.

“The science tells us that health care workers, particularly those who come into regular contact with the virus, are most at risk at this point in the pandemic,” Labor Secretary Marty Walsh said on a press call. “So following an extensive review of the science and data, OSHA determined that a health care–specific safety requirement will make the biggest impact.”

But questions remain, said James Brudney, JD, a professor at Fordham Law School in New York and former chief counsel of the U.S. Senate Subcommittee on Labor. The standard doesn’t amplify or address existing rules regarding a right to refuse unsafe work, for example, so employees may still feel they are risking their jobs to complain, despite the antiretaliation clause.

And although vaccinated employees don’t have to adhere to the same distancing and masking standards in many instances, the standard doesn’t spell out how employers should determine their workers’ vaccination status – instead leaving that determination to employers through their own policies and procedures. (California’s state OSHA office rules specify the mechanism for documentation of vaccination.)

The Trump administration did not issue an ETS, saying OSHA’s general duty clause sufficed. President Joe Biden took the opposite approach, calling for an investigation into an ETS on his first day in office. But the process took months longer than promised.

“I know it’s been a long time coming,” Mr. Walsh acknowledged. “Our health care workers from the very beginning have been put at risk.

While health care unions had asked for mandated safety standards sooner, National Nurses United, the country’s largest labor union for registered nurses, still welcomed the rules.

“An ETS is a major step toward requiring accountability for hospitals who consistently put their budget goals and profits over our health and safety,” Zenei Triunfo-Cortez, RN, one of NNU’s three presidents, said in a statement June 9 anticipating the publication of the rules.

The rules do not apply to retail pharmacies, ambulatory care settings that screen nonemployees for COVID-19, or certain other settings in which all employees are vaccinated and people with suspected or confirmed COVID-19 cannot enter.

The agency said it will work with states that have already issued local regulations, including two states that issued temporary standards of their own, Virginia and California.

Employers will have 2 weeks to comply with most of the regulations after they’re published in the Federal Register. The standards will expire in 6 months but could then become permanent, as Virginia’s did in January.

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

The U.S. Occupational Safety and Health Administration issued its long-awaited Emergency Temporary Standard (ETS) for COVID-19 June 10, surprising many by including only health care workers in the new emergency workplace safety rules.

“The ETS is an overdue step toward protecting health care workers, especially those working in long-term care facilities and home health care who are at greatly increased risk of infection,” said George Washington University, Washington, professor and former Obama administration Assistant Secretary of Labor David Michaels, PhD, MPH. “OSHA’s failure to issue a COVID-specific standard in other high-risk industries, like meat and poultry processing, corrections, homeless shelters, and retail establishments is disappointing. If exposure is not controlled in these workplaces, they will continue to be important drivers of infections.”

With the new regulations in place, about 10.3 million health care workers at hospitals, nursing homes, and assisted living facilities, as well as emergency responders and home health care workers, should be guaranteed protection standards that replace former guidance.

The new protections include supplying personal protective equipment and ensuring proper usage (for example, mandatory seal checks on respirators); screening everyone who enters the facility for COVID-19; ensuring proper ventilation; and establishing physical distancing requirements (6 feet) for unvaccinated workers. It also requires employers to give workers time off for vaccination. An antiretaliation clause could shield workers who complain about unsafe conditions.

“The science tells us that health care workers, particularly those who come into regular contact with the virus, are most at risk at this point in the pandemic,” Labor Secretary Marty Walsh said on a press call. “So following an extensive review of the science and data, OSHA determined that a health care–specific safety requirement will make the biggest impact.”

But questions remain, said James Brudney, JD, a professor at Fordham Law School in New York and former chief counsel of the U.S. Senate Subcommittee on Labor. The standard doesn’t amplify or address existing rules regarding a right to refuse unsafe work, for example, so employees may still feel they are risking their jobs to complain, despite the antiretaliation clause.

And although vaccinated employees don’t have to adhere to the same distancing and masking standards in many instances, the standard doesn’t spell out how employers should determine their workers’ vaccination status – instead leaving that determination to employers through their own policies and procedures. (California’s state OSHA office rules specify the mechanism for documentation of vaccination.)

The Trump administration did not issue an ETS, saying OSHA’s general duty clause sufficed. President Joe Biden took the opposite approach, calling for an investigation into an ETS on his first day in office. But the process took months longer than promised.

“I know it’s been a long time coming,” Mr. Walsh acknowledged. “Our health care workers from the very beginning have been put at risk.

While health care unions had asked for mandated safety standards sooner, National Nurses United, the country’s largest labor union for registered nurses, still welcomed the rules.

“An ETS is a major step toward requiring accountability for hospitals who consistently put their budget goals and profits over our health and safety,” Zenei Triunfo-Cortez, RN, one of NNU’s three presidents, said in a statement June 9 anticipating the publication of the rules.

The rules do not apply to retail pharmacies, ambulatory care settings that screen nonemployees for COVID-19, or certain other settings in which all employees are vaccinated and people with suspected or confirmed COVID-19 cannot enter.

The agency said it will work with states that have already issued local regulations, including two states that issued temporary standards of their own, Virginia and California.

Employers will have 2 weeks to comply with most of the regulations after they’re published in the Federal Register. The standards will expire in 6 months but could then become permanent, as Virginia’s did in January.

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

The U.S. Occupational Safety and Health Administration issued its long-awaited Emergency Temporary Standard (ETS) for COVID-19 June 10, surprising many by including only health care workers in the new emergency workplace safety rules.

“The ETS is an overdue step toward protecting health care workers, especially those working in long-term care facilities and home health care who are at greatly increased risk of infection,” said George Washington University, Washington, professor and former Obama administration Assistant Secretary of Labor David Michaels, PhD, MPH. “OSHA’s failure to issue a COVID-specific standard in other high-risk industries, like meat and poultry processing, corrections, homeless shelters, and retail establishments is disappointing. If exposure is not controlled in these workplaces, they will continue to be important drivers of infections.”

With the new regulations in place, about 10.3 million health care workers at hospitals, nursing homes, and assisted living facilities, as well as emergency responders and home health care workers, should be guaranteed protection standards that replace former guidance.

The new protections include supplying personal protective equipment and ensuring proper usage (for example, mandatory seal checks on respirators); screening everyone who enters the facility for COVID-19; ensuring proper ventilation; and establishing physical distancing requirements (6 feet) for unvaccinated workers. It also requires employers to give workers time off for vaccination. An antiretaliation clause could shield workers who complain about unsafe conditions.

“The science tells us that health care workers, particularly those who come into regular contact with the virus, are most at risk at this point in the pandemic,” Labor Secretary Marty Walsh said on a press call. “So following an extensive review of the science and data, OSHA determined that a health care–specific safety requirement will make the biggest impact.”

But questions remain, said James Brudney, JD, a professor at Fordham Law School in New York and former chief counsel of the U.S. Senate Subcommittee on Labor. The standard doesn’t amplify or address existing rules regarding a right to refuse unsafe work, for example, so employees may still feel they are risking their jobs to complain, despite the antiretaliation clause.

And although vaccinated employees don’t have to adhere to the same distancing and masking standards in many instances, the standard doesn’t spell out how employers should determine their workers’ vaccination status – instead leaving that determination to employers through their own policies and procedures. (California’s state OSHA office rules specify the mechanism for documentation of vaccination.)

The Trump administration did not issue an ETS, saying OSHA’s general duty clause sufficed. President Joe Biden took the opposite approach, calling for an investigation into an ETS on his first day in office. But the process took months longer than promised.

“I know it’s been a long time coming,” Mr. Walsh acknowledged. “Our health care workers from the very beginning have been put at risk.

While health care unions had asked for mandated safety standards sooner, National Nurses United, the country’s largest labor union for registered nurses, still welcomed the rules.

“An ETS is a major step toward requiring accountability for hospitals who consistently put their budget goals and profits over our health and safety,” Zenei Triunfo-Cortez, RN, one of NNU’s three presidents, said in a statement June 9 anticipating the publication of the rules.

The rules do not apply to retail pharmacies, ambulatory care settings that screen nonemployees for COVID-19, or certain other settings in which all employees are vaccinated and people with suspected or confirmed COVID-19 cannot enter.

The agency said it will work with states that have already issued local regulations, including two states that issued temporary standards of their own, Virginia and California.

Employers will have 2 weeks to comply with most of the regulations after they’re published in the Federal Register. The standards will expire in 6 months but could then become permanent, as Virginia’s did in January.

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

The Diagnosis: Degos Disease 

The pathophysiology of Degos disease (malignant atrophic papulosis) is unknown.¹ Histopathology demonstrates a wedge-shaped area of dermal necrosis with edema and mucin deposition extending from the papillary dermis to the deep reticular dermis. Occluded vessels, thrombosis, and perivascular lymphocytic infiltrates also may be seen, particularly at the dermal subcutaneous junction and at the periphery of the wedge-shaped infarction. The vascular damage that occurs may be the result of vasculitis, coagulopathy, or endothelial cell dysfunction.¹  

Patients typically present with small, round, erythematous papules that eventually develop atrophic porcelain white centers and telangiectatic rims. These lesions most commonly occur on the trunk and arms. In the benign form of atrophic papulosis, only the skin is involved; however, systemic involvement of the gastrointestinal tract and central nervous system can occur, resulting in bowel perforation and stroke, respectively.¹ Although there is no definitive treatment of Degos disease, successful therapy with aspirin or dipyridamole has been reported.¹ Eculizumab, a monoclonal antibody that binds C5, and treprostinil, a prostacyclin analog, are emerging treatment options.^2,3 The differential diagnosis of Degos disease may include granuloma annulare, guttate extragenital lichen sclerosus, livedoid vasculopathy, and lymphomatoid papulosis.  

Granuloma annulare may clinically mimic the erythematous papules seen in early Degos disease, and histopathology can be used to distinguish between these two disease processes. Localized granuloma annulare is the most common variant and clinically presents as pink papules and plaques in an annular configuration.⁴ Histopathology demonstrates an unremarkable epidermis; however, the dermis contains degenerated collagen surrounded by palisading histiocytes as well as lymphocytes. Similar to Degos disease, increased mucin is seen within these areas of degeneration, but occluded vessels and thrombosis typically are not seen (Figure 1).^4,5  

Guttate extragenital lichen sclerosus initially presents as polygonal, bluish white papules that coalesce into plaques.⁶ Over time, these lesions become more atrophic and may mimic Degos disease but appear differently on histopathology. Histopathology of lichen sclerosus classically demonstrates atrophy of the epidermis with loss of the rete ridges and vacuolar surface changes. Homogenization of the superficial/papillary dermis with an underlying bandlike lymphocytic infiltrate also is seen (Figure 2).⁶

Livedoid vasculopathy is characterized by chronic recurrent ulceration of the legs secondary to thrombosis and subsequent ischemia. In the initial phase of this disease, livedo reticularis is seen followed by the development of ulcerations. As these ulcerations heal, they leave behind porcelain white scars referred to as atrophie blanche.⁷ The areas of scarring in livedoid vasculopathy are broad and angulated, differentiating them from the small, round, porcelain white macules in end-stage Degos disease. Histopathology demonstrates thrombosis and fibrin occlusion of the upper and mid dermal vessels. Very minimal perivascular infiltrate typically is seen, but when it is present, the infiltrate mostly is lymphocytic. Hyalinization of the vessel walls also is seen, particularly in the atrophie blanche stage (Figure 3).⁷  

Lymphomatoid papulosis classically presents with pruritic red papules that often spontaneously involute. After resolution of the primary lesions, atrophic varioliform scars may be left behind that can resemble Degos disease.⁸ Classically, there are 5 histopathologic subtypes: A, B, C, D, and E. Type A is the most common type of lymphomatoid papulosis, and histopathology demonstrates a dermal lymphocytic infiltrate that consists of cells arranged in small clusters. Numerous medium- to large-sized atypical lymphocytes with prominent nucleoli and abundant cytoplasm are seen, and mitotic figures are common (Figure 4).⁸ 

Our case was particularly interesting because the patient was 2 to 3 weeks pregnant. Degos disease in pregnancy appears to be quite exceptional. A PubMed search of articles indexed for MEDLINE using the terms Degos disease and pregnancy revealed only 4 other cases reported in the literature.^9-12 With the exception of a single case that was complicated by severe abdominal pain requiring labor induction, the other reported cases resulted in uncomplicated pregnancies.^9-12 Conversely, our patient's pregnancy was complicated by gestational hypertension and fetal hydrops requiring a preterm cesarean delivery. Furthermore, the infant had multiple complications, which were attributed to both placental insufficiency and a coagulopathic state.  

Our patient also was found to have a heterozygous factor V Leiden mutation on workup. A PubMed search using the terms factor V Leiden mutation and Degos disease revealed 2 other cases of factor V Leiden mutation-associated Degos disease.^13,14 The importance of factor V Leiden mutations in patients with Degos disease currently is unclear. 

The Diagnosis: Degos Disease 

The pathophysiology of Degos disease (malignant atrophic papulosis) is unknown.¹ Histopathology demonstrates a wedge-shaped area of dermal necrosis with edema and mucin deposition extending from the papillary dermis to the deep reticular dermis. Occluded vessels, thrombosis, and perivascular lymphocytic infiltrates also may be seen, particularly at the dermal subcutaneous junction and at the periphery of the wedge-shaped infarction. The vascular damage that occurs may be the result of vasculitis, coagulopathy, or endothelial cell dysfunction.¹  

Patients typically present with small, round, erythematous papules that eventually develop atrophic porcelain white centers and telangiectatic rims. These lesions most commonly occur on the trunk and arms. In the benign form of atrophic papulosis, only the skin is involved; however, systemic involvement of the gastrointestinal tract and central nervous system can occur, resulting in bowel perforation and stroke, respectively.¹ Although there is no definitive treatment of Degos disease, successful therapy with aspirin or dipyridamole has been reported.¹ Eculizumab, a monoclonal antibody that binds C5, and treprostinil, a prostacyclin analog, are emerging treatment options.^2,3 The differential diagnosis of Degos disease may include granuloma annulare, guttate extragenital lichen sclerosus, livedoid vasculopathy, and lymphomatoid papulosis.  

Granuloma annulare may clinically mimic the erythematous papules seen in early Degos disease, and histopathology can be used to distinguish between these two disease processes. Localized granuloma annulare is the most common variant and clinically presents as pink papules and plaques in an annular configuration.⁴ Histopathology demonstrates an unremarkable epidermis; however, the dermis contains degenerated collagen surrounded by palisading histiocytes as well as lymphocytes. Similar to Degos disease, increased mucin is seen within these areas of degeneration, but occluded vessels and thrombosis typically are not seen (Figure 1).^4,5  

Guttate extragenital lichen sclerosus initially presents as polygonal, bluish white papules that coalesce into plaques.⁶ Over time, these lesions become more atrophic and may mimic Degos disease but appear differently on histopathology. Histopathology of lichen sclerosus classically demonstrates atrophy of the epidermis with loss of the rete ridges and vacuolar surface changes. Homogenization of the superficial/papillary dermis with an underlying bandlike lymphocytic infiltrate also is seen (Figure 2).⁶

Livedoid vasculopathy is characterized by chronic recurrent ulceration of the legs secondary to thrombosis and subsequent ischemia. In the initial phase of this disease, livedo reticularis is seen followed by the development of ulcerations. As these ulcerations heal, they leave behind porcelain white scars referred to as atrophie blanche.⁷ The areas of scarring in livedoid vasculopathy are broad and angulated, differentiating them from the small, round, porcelain white macules in end-stage Degos disease. Histopathology demonstrates thrombosis and fibrin occlusion of the upper and mid dermal vessels. Very minimal perivascular infiltrate typically is seen, but when it is present, the infiltrate mostly is lymphocytic. Hyalinization of the vessel walls also is seen, particularly in the atrophie blanche stage (Figure 3).⁷  

Lymphomatoid papulosis classically presents with pruritic red papules that often spontaneously involute. After resolution of the primary lesions, atrophic varioliform scars may be left behind that can resemble Degos disease.⁸ Classically, there are 5 histopathologic subtypes: A, B, C, D, and E. Type A is the most common type of lymphomatoid papulosis, and histopathology demonstrates a dermal lymphocytic infiltrate that consists of cells arranged in small clusters. Numerous medium- to large-sized atypical lymphocytes with prominent nucleoli and abundant cytoplasm are seen, and mitotic figures are common (Figure 4).⁸ 

Our case was particularly interesting because the patient was 2 to 3 weeks pregnant. Degos disease in pregnancy appears to be quite exceptional. A PubMed search of articles indexed for MEDLINE using the terms Degos disease and pregnancy revealed only 4 other cases reported in the literature.^9-12 With the exception of a single case that was complicated by severe abdominal pain requiring labor induction, the other reported cases resulted in uncomplicated pregnancies.^9-12 Conversely, our patient's pregnancy was complicated by gestational hypertension and fetal hydrops requiring a preterm cesarean delivery. Furthermore, the infant had multiple complications, which were attributed to both placental insufficiency and a coagulopathic state.  

Our patient also was found to have a heterozygous factor V Leiden mutation on workup. A PubMed search using the terms factor V Leiden mutation and Degos disease revealed 2 other cases of factor V Leiden mutation-associated Degos disease.^13,14 The importance of factor V Leiden mutations in patients with Degos disease currently is unclear. 

The Diagnosis: Degos Disease 

The pathophysiology of Degos disease (malignant atrophic papulosis) is unknown.¹ Histopathology demonstrates a wedge-shaped area of dermal necrosis with edema and mucin deposition extending from the papillary dermis to the deep reticular dermis. Occluded vessels, thrombosis, and perivascular lymphocytic infiltrates also may be seen, particularly at the dermal subcutaneous junction and at the periphery of the wedge-shaped infarction. The vascular damage that occurs may be the result of vasculitis, coagulopathy, or endothelial cell dysfunction.¹  

Patients typically present with small, round, erythematous papules that eventually develop atrophic porcelain white centers and telangiectatic rims. These lesions most commonly occur on the trunk and arms. In the benign form of atrophic papulosis, only the skin is involved; however, systemic involvement of the gastrointestinal tract and central nervous system can occur, resulting in bowel perforation and stroke, respectively.¹ Although there is no definitive treatment of Degos disease, successful therapy with aspirin or dipyridamole has been reported.¹ Eculizumab, a monoclonal antibody that binds C5, and treprostinil, a prostacyclin analog, are emerging treatment options.^2,3 The differential diagnosis of Degos disease may include granuloma annulare, guttate extragenital lichen sclerosus, livedoid vasculopathy, and lymphomatoid papulosis.  

Granuloma annulare may clinically mimic the erythematous papules seen in early Degos disease, and histopathology can be used to distinguish between these two disease processes. Localized granuloma annulare is the most common variant and clinically presents as pink papules and plaques in an annular configuration.⁴ Histopathology demonstrates an unremarkable epidermis; however, the dermis contains degenerated collagen surrounded by palisading histiocytes as well as lymphocytes. Similar to Degos disease, increased mucin is seen within these areas of degeneration, but occluded vessels and thrombosis typically are not seen (Figure 1).^4,5  

Guttate extragenital lichen sclerosus initially presents as polygonal, bluish white papules that coalesce into plaques.⁶ Over time, these lesions become more atrophic and may mimic Degos disease but appear differently on histopathology. Histopathology of lichen sclerosus classically demonstrates atrophy of the epidermis with loss of the rete ridges and vacuolar surface changes. Homogenization of the superficial/papillary dermis with an underlying bandlike lymphocytic infiltrate also is seen (Figure 2).⁶

Livedoid vasculopathy is characterized by chronic recurrent ulceration of the legs secondary to thrombosis and subsequent ischemia. In the initial phase of this disease, livedo reticularis is seen followed by the development of ulcerations. As these ulcerations heal, they leave behind porcelain white scars referred to as atrophie blanche.⁷ The areas of scarring in livedoid vasculopathy are broad and angulated, differentiating them from the small, round, porcelain white macules in end-stage Degos disease. Histopathology demonstrates thrombosis and fibrin occlusion of the upper and mid dermal vessels. Very minimal perivascular infiltrate typically is seen, but when it is present, the infiltrate mostly is lymphocytic. Hyalinization of the vessel walls also is seen, particularly in the atrophie blanche stage (Figure 3).⁷  

Lymphomatoid papulosis classically presents with pruritic red papules that often spontaneously involute. After resolution of the primary lesions, atrophic varioliform scars may be left behind that can resemble Degos disease.⁸ Classically, there are 5 histopathologic subtypes: A, B, C, D, and E. Type A is the most common type of lymphomatoid papulosis, and histopathology demonstrates a dermal lymphocytic infiltrate that consists of cells arranged in small clusters. Numerous medium- to large-sized atypical lymphocytes with prominent nucleoli and abundant cytoplasm are seen, and mitotic figures are common (Figure 4).⁸ 

Our case was particularly interesting because the patient was 2 to 3 weeks pregnant. Degos disease in pregnancy appears to be quite exceptional. A PubMed search of articles indexed for MEDLINE using the terms Degos disease and pregnancy revealed only 4 other cases reported in the literature.^9-12 With the exception of a single case that was complicated by severe abdominal pain requiring labor induction, the other reported cases resulted in uncomplicated pregnancies.^9-12 Conversely, our patient's pregnancy was complicated by gestational hypertension and fetal hydrops requiring a preterm cesarean delivery. Furthermore, the infant had multiple complications, which were attributed to both placental insufficiency and a coagulopathic state.  

Our patient also was found to have a heterozygous factor V Leiden mutation on workup. A PubMed search using the terms factor V Leiden mutation and Degos disease revealed 2 other cases of factor V Leiden mutation-associated Degos disease.^13,14 The importance of factor V Leiden mutations in patients with Degos disease currently is unclear. 

In the first clinical trial of a topical histone deacetylase (HDAC) inhibitor, remetinostat showed clinical efficacy across several basal cell carcinoma (BCC) tumor types, according to research presented at the annual meeting of the Society for Investigative Dermatology.

“Our results demonstrate a clinically significant decrease in tumor size in response to 6 weeks of topical 1% remetinostat therapy in 70% of per-protocol tumors, with 55% reaching complete pathological resolution,” James M. Kilgour, MD, a postdoctoral research fellow at the Sarin Lab at Stanford (Calif.) University, said at the meeting.

Surgical excision is the preferred treatment for BCC, but there is still a need for noninvasive treatment options, Dr. Kilgour said. “Given the potential morbidity associated with excision, particularly for patients experiencing multiple or recurrent tumors, such as the immunosuppressed or patients with Gorlin syndrome, an effective and tolerable topical therapy would be a significant benefit,” he noted.

Previously, in an in silico screen experiment, Dr. Kilgour and colleagues identified HDAC inhibitors as a “top predicted therapeutic” for BCC treatment, and found that in mice studies, HDAC inhibitors were able to suppress the growth of BCC cell lines and BCC allografts.

Remetinostat, a pan-HDAC inhibitor, is being investigated as a treatment for cutaneous T-cell lymphoma.

HDAC inhibitors are thought to “alter expression of key oncogenes and tumor suppressors through epigenetic modification of histone and nonhistone proteins,” he noted.

To evaluate the efficacy of topical remetinostat for BCC, the investigators enrolled 30 patients with 49 BCC tumors in a phase 2, open-label, single-arm trial. Participants had tumors that were greater than 5 mm in diameter and had been referred to surgery at Stanford before enrollment. Patients were a mean of 59 years old, 63% were men, and 90% were White; 59.2% of participants had tumors with a diameter greater than 10 mm, the rest had tumors with a diameter of 10 mm or less.

After the tumors were photographed and measured, participants received 6 weeks of topical remetinostat therapy, followed by final measurement and photography of the tumors at 8 weeks and surgical excision. Topical remetinostat 1% gel was applied three times per day under bandage occlusion.

Overall, 25 participants with 33 tumors were included in the per-protocol analysis. At 8 weeks, there was at least a 30% decrease in diameter from baseline for 69.7% of tumors in these patients, with 17 of 33 tumors showing a complete response by week 8.

Regarding tumor subtypes, there was a 100% overall response rate for the 6 superficial BCC tumors (1 partial response, 5 complete responses), a 68.2% ORR for the 22 nodular tumors (5 partial responses, 10 complete responses), and a 66.7% ORR for the 3 infiltrative tumors (no partial responses, 2 complete responses). There were no partial or complete responses for the two micronodular tumors.

Most adverse events in the study were localized drug reactions, with no serious or systemic adverse events, Dr. Kilgour noted, with 10 tumors demonstrating either no reaction or a grade 1 reaction, and 23 tumors having a grade 2 or grade 3 response.

The investigators also used imaging (ImageJ) software to evaluate the average decrease in cross-sectional tumor area. The results of the analysis showed an average decrease at 8 weeks from baseline of 71.5%. In addition, histological assessment at 8 weeks demonstrated that 54.8% of tumors had complete pathological resolution.

“In the future, we advocate for a follow-up blinded, randomized, controlled trial of remetinostat with greater participant diversity,” Dr. Kilgour said. “Specifically, greater power is needed to understand which histological subtypes of BCC will respond best to the treatment and we need to understand the long-term durability of tumor resolution.”

 

Remetinostat promising as topical BCC therapy

In an interview, Beth G. Goldstein, MD, a dermatologist and Mohs surgeon in Chapel Hill, N.C., noted that the preliminary study was “an exciting report of a safe, well-tolerated nonsurgical option for patients with superficial BCCs on the trunk and extremities,” which has potential to be used in the future for nonsuperficial BCCs. The study shows that superficial BCCs can respond at a rate of 100% on nonfacial areas, said Dr. Goldstein, who was not involved in the research. “These lesions can be quite large with higher chances of recurrence and difficulty with wound care.

“This type of directed therapy hopefully continues to be perfected for treatment of BCC that avoids scarring and is well tolerated,” she added.

Dr. Goldstein commented that complete pathological resolution of 54.8% “was still unacceptably low for the remaining tumor types.” For those cases, she said remetinostat could possibly “provide a topical option as an adjunctive treatment for potentially reducing the size of the BCC prior to surgical removal,” as an alternative to a systemic therapy like vismodegib (Erivedge).

Dr. Goldstein said the strengths of the study were in the variety of tumors, close follow-up with histologic evaluation and safety signals. In terms of limitations, she said whether there were any cases of Gorlin syndrome was not clear. In addition, at least 30% of BCCs have a mixed tumor type on Mohs surgery that differs from the original biopsy, and “there was no mention if the residual tumor remained with the same histology,” she said.

In the future, a large, randomized trial is warranted to stratify for Gorlin syndrome, patients who are immunosuppressed, and additional tumor types that were underrepresented in this study, such as micronodular tumors, Dr. Goldstein said. Future studies also should examine how remetinostat impacts BCC in facial areas, the effect of multiple applications, and how the therapy performs as an adjunctive treatment before surgery.

This study was funded by Medivir, the Damon Runyon Foundation, National Cancer Institute, an American Skin Association Hambrick Medical Student grant, and Stanford Medical Scholars. Dr. Kilgour and Dr. Goldstein reported no relevant financial disclosures.

In the first clinical trial of a topical histone deacetylase (HDAC) inhibitor, remetinostat showed clinical efficacy across several basal cell carcinoma (BCC) tumor types, according to research presented at the annual meeting of the Society for Investigative Dermatology.

“Our results demonstrate a clinically significant decrease in tumor size in response to 6 weeks of topical 1% remetinostat therapy in 70% of per-protocol tumors, with 55% reaching complete pathological resolution,” James M. Kilgour, MD, a postdoctoral research fellow at the Sarin Lab at Stanford (Calif.) University, said at the meeting.

Surgical excision is the preferred treatment for BCC, but there is still a need for noninvasive treatment options, Dr. Kilgour said. “Given the potential morbidity associated with excision, particularly for patients experiencing multiple or recurrent tumors, such as the immunosuppressed or patients with Gorlin syndrome, an effective and tolerable topical therapy would be a significant benefit,” he noted.

Previously, in an in silico screen experiment, Dr. Kilgour and colleagues identified HDAC inhibitors as a “top predicted therapeutic” for BCC treatment, and found that in mice studies, HDAC inhibitors were able to suppress the growth of BCC cell lines and BCC allografts.

Remetinostat, a pan-HDAC inhibitor, is being investigated as a treatment for cutaneous T-cell lymphoma.

HDAC inhibitors are thought to “alter expression of key oncogenes and tumor suppressors through epigenetic modification of histone and nonhistone proteins,” he noted.

To evaluate the efficacy of topical remetinostat for BCC, the investigators enrolled 30 patients with 49 BCC tumors in a phase 2, open-label, single-arm trial. Participants had tumors that were greater than 5 mm in diameter and had been referred to surgery at Stanford before enrollment. Patients were a mean of 59 years old, 63% were men, and 90% were White; 59.2% of participants had tumors with a diameter greater than 10 mm, the rest had tumors with a diameter of 10 mm or less.

After the tumors were photographed and measured, participants received 6 weeks of topical remetinostat therapy, followed by final measurement and photography of the tumors at 8 weeks and surgical excision. Topical remetinostat 1% gel was applied three times per day under bandage occlusion.

Overall, 25 participants with 33 tumors were included in the per-protocol analysis. At 8 weeks, there was at least a 30% decrease in diameter from baseline for 69.7% of tumors in these patients, with 17 of 33 tumors showing a complete response by week 8.

Regarding tumor subtypes, there was a 100% overall response rate for the 6 superficial BCC tumors (1 partial response, 5 complete responses), a 68.2% ORR for the 22 nodular tumors (5 partial responses, 10 complete responses), and a 66.7% ORR for the 3 infiltrative tumors (no partial responses, 2 complete responses). There were no partial or complete responses for the two micronodular tumors.

Most adverse events in the study were localized drug reactions, with no serious or systemic adverse events, Dr. Kilgour noted, with 10 tumors demonstrating either no reaction or a grade 1 reaction, and 23 tumors having a grade 2 or grade 3 response.

The investigators also used imaging (ImageJ) software to evaluate the average decrease in cross-sectional tumor area. The results of the analysis showed an average decrease at 8 weeks from baseline of 71.5%. In addition, histological assessment at 8 weeks demonstrated that 54.8% of tumors had complete pathological resolution.

“In the future, we advocate for a follow-up blinded, randomized, controlled trial of remetinostat with greater participant diversity,” Dr. Kilgour said. “Specifically, greater power is needed to understand which histological subtypes of BCC will respond best to the treatment and we need to understand the long-term durability of tumor resolution.”

 

Remetinostat promising as topical BCC therapy

In an interview, Beth G. Goldstein, MD, a dermatologist and Mohs surgeon in Chapel Hill, N.C., noted that the preliminary study was “an exciting report of a safe, well-tolerated nonsurgical option for patients with superficial BCCs on the trunk and extremities,” which has potential to be used in the future for nonsuperficial BCCs. The study shows that superficial BCCs can respond at a rate of 100% on nonfacial areas, said Dr. Goldstein, who was not involved in the research. “These lesions can be quite large with higher chances of recurrence and difficulty with wound care.

“This type of directed therapy hopefully continues to be perfected for treatment of BCC that avoids scarring and is well tolerated,” she added.

Dr. Goldstein commented that complete pathological resolution of 54.8% “was still unacceptably low for the remaining tumor types.” For those cases, she said remetinostat could possibly “provide a topical option as an adjunctive treatment for potentially reducing the size of the BCC prior to surgical removal,” as an alternative to a systemic therapy like vismodegib (Erivedge).

Dr. Goldstein said the strengths of the study were in the variety of tumors, close follow-up with histologic evaluation and safety signals. In terms of limitations, she said whether there were any cases of Gorlin syndrome was not clear. In addition, at least 30% of BCCs have a mixed tumor type on Mohs surgery that differs from the original biopsy, and “there was no mention if the residual tumor remained with the same histology,” she said.

In the future, a large, randomized trial is warranted to stratify for Gorlin syndrome, patients who are immunosuppressed, and additional tumor types that were underrepresented in this study, such as micronodular tumors, Dr. Goldstein said. Future studies also should examine how remetinostat impacts BCC in facial areas, the effect of multiple applications, and how the therapy performs as an adjunctive treatment before surgery.

This study was funded by Medivir, the Damon Runyon Foundation, National Cancer Institute, an American Skin Association Hambrick Medical Student grant, and Stanford Medical Scholars. Dr. Kilgour and Dr. Goldstein reported no relevant financial disclosures.

In the first clinical trial of a topical histone deacetylase (HDAC) inhibitor, remetinostat showed clinical efficacy across several basal cell carcinoma (BCC) tumor types, according to research presented at the annual meeting of the Society for Investigative Dermatology.

“Our results demonstrate a clinically significant decrease in tumor size in response to 6 weeks of topical 1% remetinostat therapy in 70% of per-protocol tumors, with 55% reaching complete pathological resolution,” James M. Kilgour, MD, a postdoctoral research fellow at the Sarin Lab at Stanford (Calif.) University, said at the meeting.

Surgical excision is the preferred treatment for BCC, but there is still a need for noninvasive treatment options, Dr. Kilgour said. “Given the potential morbidity associated with excision, particularly for patients experiencing multiple or recurrent tumors, such as the immunosuppressed or patients with Gorlin syndrome, an effective and tolerable topical therapy would be a significant benefit,” he noted.

Previously, in an in silico screen experiment, Dr. Kilgour and colleagues identified HDAC inhibitors as a “top predicted therapeutic” for BCC treatment, and found that in mice studies, HDAC inhibitors were able to suppress the growth of BCC cell lines and BCC allografts.

Remetinostat, a pan-HDAC inhibitor, is being investigated as a treatment for cutaneous T-cell lymphoma.

HDAC inhibitors are thought to “alter expression of key oncogenes and tumor suppressors through epigenetic modification of histone and nonhistone proteins,” he noted.

To evaluate the efficacy of topical remetinostat for BCC, the investigators enrolled 30 patients with 49 BCC tumors in a phase 2, open-label, single-arm trial. Participants had tumors that were greater than 5 mm in diameter and had been referred to surgery at Stanford before enrollment. Patients were a mean of 59 years old, 63% were men, and 90% were White; 59.2% of participants had tumors with a diameter greater than 10 mm, the rest had tumors with a diameter of 10 mm or less.

After the tumors were photographed and measured, participants received 6 weeks of topical remetinostat therapy, followed by final measurement and photography of the tumors at 8 weeks and surgical excision. Topical remetinostat 1% gel was applied three times per day under bandage occlusion.

Overall, 25 participants with 33 tumors were included in the per-protocol analysis. At 8 weeks, there was at least a 30% decrease in diameter from baseline for 69.7% of tumors in these patients, with 17 of 33 tumors showing a complete response by week 8.

Regarding tumor subtypes, there was a 100% overall response rate for the 6 superficial BCC tumors (1 partial response, 5 complete responses), a 68.2% ORR for the 22 nodular tumors (5 partial responses, 10 complete responses), and a 66.7% ORR for the 3 infiltrative tumors (no partial responses, 2 complete responses). There were no partial or complete responses for the two micronodular tumors.

Most adverse events in the study were localized drug reactions, with no serious or systemic adverse events, Dr. Kilgour noted, with 10 tumors demonstrating either no reaction or a grade 1 reaction, and 23 tumors having a grade 2 or grade 3 response.

The investigators also used imaging (ImageJ) software to evaluate the average decrease in cross-sectional tumor area. The results of the analysis showed an average decrease at 8 weeks from baseline of 71.5%. In addition, histological assessment at 8 weeks demonstrated that 54.8% of tumors had complete pathological resolution.

“In the future, we advocate for a follow-up blinded, randomized, controlled trial of remetinostat with greater participant diversity,” Dr. Kilgour said. “Specifically, greater power is needed to understand which histological subtypes of BCC will respond best to the treatment and we need to understand the long-term durability of tumor resolution.”

 

Remetinostat promising as topical BCC therapy

In an interview, Beth G. Goldstein, MD, a dermatologist and Mohs surgeon in Chapel Hill, N.C., noted that the preliminary study was “an exciting report of a safe, well-tolerated nonsurgical option for patients with superficial BCCs on the trunk and extremities,” which has potential to be used in the future for nonsuperficial BCCs. The study shows that superficial BCCs can respond at a rate of 100% on nonfacial areas, said Dr. Goldstein, who was not involved in the research. “These lesions can be quite large with higher chances of recurrence and difficulty with wound care.

“This type of directed therapy hopefully continues to be perfected for treatment of BCC that avoids scarring and is well tolerated,” she added.

Dr. Goldstein commented that complete pathological resolution of 54.8% “was still unacceptably low for the remaining tumor types.” For those cases, she said remetinostat could possibly “provide a topical option as an adjunctive treatment for potentially reducing the size of the BCC prior to surgical removal,” as an alternative to a systemic therapy like vismodegib (Erivedge).

Dr. Goldstein said the strengths of the study were in the variety of tumors, close follow-up with histologic evaluation and safety signals. In terms of limitations, she said whether there were any cases of Gorlin syndrome was not clear. In addition, at least 30% of BCCs have a mixed tumor type on Mohs surgery that differs from the original biopsy, and “there was no mention if the residual tumor remained with the same histology,” she said.

In the future, a large, randomized trial is warranted to stratify for Gorlin syndrome, patients who are immunosuppressed, and additional tumor types that were underrepresented in this study, such as micronodular tumors, Dr. Goldstein said. Future studies also should examine how remetinostat impacts BCC in facial areas, the effect of multiple applications, and how the therapy performs as an adjunctive treatment before surgery.

This study was funded by Medivir, the Damon Runyon Foundation, National Cancer Institute, an American Skin Association Hambrick Medical Student grant, and Stanford Medical Scholars. Dr. Kilgour and Dr. Goldstein reported no relevant financial disclosures.