TBD Meeting (3238-19)

LAS VEGAS – Recent research is offering new insights into psoriasis and alopecia in the pediatric population, a dermatologist told colleagues, and it’s time to be on the lookout for psoriasis linked to treatment with tumor necrosis factor (TNF) inhibitors.

Lawrence F. Eichenfield, MD, professor of dermatology and pediatrics, at the University of California, San Diego, offered these tips and comments in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

Psoriasis

It’s a brand new day for adult psoriasis sufferers, but it seems to be only a brand new morning for their pediatric counterparts. “Kids and teenagers were left behind in the biologic revolution,” Dr. Eichenfield said. “Only two systemic biologics have been approved for psoriasis in children.” They are ustekinumab (Stelara), approved by the Food and Drug Administration for treating psoriasis in children aged 12 years and older, and etanercept, approved for aged 4 years and older.

The good news, he said, is that “our new biologic agents are now being studied in children.”

Research is also providing new insight into pediatric psoriasis, said Dr. Eichenfield, who is also chief of pediatric and adolescent dermatology at Rady Children’s Hospital in San Diego. It’s now clear that “there’s a lot more facial involvement, and a high involvement of scalp and nail,” he noted.

It’s also clear, he said, that inflammation begins early in pediatric psoriasis. That raises the question of whether it’s a good idea to launch aggressive treatment to stop the “psoriatic march” toward cardiovascular and other medical problems down the line, he commented.

“Keep an open mind to getting aggressive in therapy,” he advised, although he acknowledged that “it’s hard to get beyond the two biologics, and only one is approved for children under 12.”

Dr. Eichenfield advised colleagues to keep an eye out for TNF inhibitor–induced psoriasis. “We’re seeing it pretty regularly,” he said, commonly in children who are treated with TNF inhibitors for rheumatoid arthritis or Crohn’s disease.

The lesions “look like dermatitis but are very psoriasiform,” he said, and research suggests this can appear after a single dose or after as many as 63 months of treatment. Topical and light therapy can be helpful. But if those treatments do not help, he said, it’s time to consider changing the biologic that the patient is taking. “Is the biologic adequately controlling their underlying disease? If not, you can help find one that would be great for their underlying disease and clear up their psoriasis.”

Alopecia

Pediatric alopecia “is a problem I see pretty regularly in practice,” Dr. Eichenfield said. When he sees patients with alopecia, he says that, “‘if your child doesn’t have 50% hair loss, you’re in the good group. It will generally heal up and never come back again.’ ”

He referred to a recent study, where investigators at the Children’s Hospital of Philadelphia retrospectively studied 125 children under age 4 years who were diagnosed with alopecia areata and followed for 2 years. Over time, those children with over 50% of hair loss initially were more likely to have worsening Severity of Alopecia Tool (SALT) scores over the follow-up period. But a high proportion of those with mild alopecia initially continued to have mild alopecia at follow-up (Pediatr Dermatol. 2019 Aug 29. doi: 10.1111/pde.13990).

Dr. Eichenfield noted that the study found that 41% of the patients also had atopic dermatitis.

He also highlighted two other recent studies on pediatric alopecia: One found that while vitamin D levels were low in a majority of children with alopecia in the study, the proportion who had a deficiency was similar to the proportion in a larger pediatric population, at about 22% in both groups (J Am Acad Dermatol. 2018 Sep;79(3):e43-e44). Supplementation doesn’t seem to help. “It’s not important to test levels,” he said.

Another study examined whether it’s a good idea to test patients for celiac disease in children with alopecia (Pediatr Dermatol. 2018 Jul;35[4]:535-8). Some parents may ask this question, but the answer, he said, is generally no.

What’s next? “We were hoping oral and topical JAK inhibitors would work well” in this population, Dr. Eichenfield said, but study findings haven’t been promising.

Still, oral tofacitinib (Xeljanz) showed some “pretty impressive” success in a recent study in four children, he noted. Based on the results, the authors wrote that “we suggest that, after proper counseling regarding the risks, including severe infection and malignancy, the use of tofacitinib may be considered for preadolescent children with AA [alopecia areata] who are experiencing psychosocial impairment” (J Am Acad Dermatol. 2019 Feb;80[2]:568-70).

In general, Dr. Eichenfield said, research on pediatric alopecia “will be secondary, especially with JAK inhibitors because of the risk of side effects. But [children will] probably tolerate them better than adults do because they have fewer medical problems.”

Meanwhile, he added, controversy continues to swirl around how to treat children over age 10 years who have lost 50% or more of their hair. “I’ve seen hundreds of kids with alopecia areata,” he said, “and I can’t predict what the course may be.”

Dr. Eichenfield reports multiple relationships (consultant or investigator) with various pharmaceutical companies, including Abbvie, Allergan, Lilly, Novartis, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Recent research is offering new insights into psoriasis and alopecia in the pediatric population, a dermatologist told colleagues, and it’s time to be on the lookout for psoriasis linked to treatment with tumor necrosis factor (TNF) inhibitors.

Lawrence F. Eichenfield, MD, professor of dermatology and pediatrics, at the University of California, San Diego, offered these tips and comments in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

Psoriasis

It’s a brand new day for adult psoriasis sufferers, but it seems to be only a brand new morning for their pediatric counterparts. “Kids and teenagers were left behind in the biologic revolution,” Dr. Eichenfield said. “Only two systemic biologics have been approved for psoriasis in children.” They are ustekinumab (Stelara), approved by the Food and Drug Administration for treating psoriasis in children aged 12 years and older, and etanercept, approved for aged 4 years and older.

The good news, he said, is that “our new biologic agents are now being studied in children.”

Research is also providing new insight into pediatric psoriasis, said Dr. Eichenfield, who is also chief of pediatric and adolescent dermatology at Rady Children’s Hospital in San Diego. It’s now clear that “there’s a lot more facial involvement, and a high involvement of scalp and nail,” he noted.

It’s also clear, he said, that inflammation begins early in pediatric psoriasis. That raises the question of whether it’s a good idea to launch aggressive treatment to stop the “psoriatic march” toward cardiovascular and other medical problems down the line, he commented.

“Keep an open mind to getting aggressive in therapy,” he advised, although he acknowledged that “it’s hard to get beyond the two biologics, and only one is approved for children under 12.”

Dr. Eichenfield advised colleagues to keep an eye out for TNF inhibitor–induced psoriasis. “We’re seeing it pretty regularly,” he said, commonly in children who are treated with TNF inhibitors for rheumatoid arthritis or Crohn’s disease.

The lesions “look like dermatitis but are very psoriasiform,” he said, and research suggests this can appear after a single dose or after as many as 63 months of treatment. Topical and light therapy can be helpful. But if those treatments do not help, he said, it’s time to consider changing the biologic that the patient is taking. “Is the biologic adequately controlling their underlying disease? If not, you can help find one that would be great for their underlying disease and clear up their psoriasis.”

Alopecia

Pediatric alopecia “is a problem I see pretty regularly in practice,” Dr. Eichenfield said. When he sees patients with alopecia, he says that, “‘if your child doesn’t have 50% hair loss, you’re in the good group. It will generally heal up and never come back again.’ ”

He referred to a recent study, where investigators at the Children’s Hospital of Philadelphia retrospectively studied 125 children under age 4 years who were diagnosed with alopecia areata and followed for 2 years. Over time, those children with over 50% of hair loss initially were more likely to have worsening Severity of Alopecia Tool (SALT) scores over the follow-up period. But a high proportion of those with mild alopecia initially continued to have mild alopecia at follow-up (Pediatr Dermatol. 2019 Aug 29. doi: 10.1111/pde.13990).

Dr. Eichenfield noted that the study found that 41% of the patients also had atopic dermatitis.

He also highlighted two other recent studies on pediatric alopecia: One found that while vitamin D levels were low in a majority of children with alopecia in the study, the proportion who had a deficiency was similar to the proportion in a larger pediatric population, at about 22% in both groups (J Am Acad Dermatol. 2018 Sep;79(3):e43-e44). Supplementation doesn’t seem to help. “It’s not important to test levels,” he said.

Another study examined whether it’s a good idea to test patients for celiac disease in children with alopecia (Pediatr Dermatol. 2018 Jul;35[4]:535-8). Some parents may ask this question, but the answer, he said, is generally no.

What’s next? “We were hoping oral and topical JAK inhibitors would work well” in this population, Dr. Eichenfield said, but study findings haven’t been promising.

Still, oral tofacitinib (Xeljanz) showed some “pretty impressive” success in a recent study in four children, he noted. Based on the results, the authors wrote that “we suggest that, after proper counseling regarding the risks, including severe infection and malignancy, the use of tofacitinib may be considered for preadolescent children with AA [alopecia areata] who are experiencing psychosocial impairment” (J Am Acad Dermatol. 2019 Feb;80[2]:568-70).

In general, Dr. Eichenfield said, research on pediatric alopecia “will be secondary, especially with JAK inhibitors because of the risk of side effects. But [children will] probably tolerate them better than adults do because they have fewer medical problems.”

Meanwhile, he added, controversy continues to swirl around how to treat children over age 10 years who have lost 50% or more of their hair. “I’ve seen hundreds of kids with alopecia areata,” he said, “and I can’t predict what the course may be.”

Dr. Eichenfield reports multiple relationships (consultant or investigator) with various pharmaceutical companies, including Abbvie, Allergan, Lilly, Novartis, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Recent research is offering new insights into psoriasis and alopecia in the pediatric population, a dermatologist told colleagues, and it’s time to be on the lookout for psoriasis linked to treatment with tumor necrosis factor (TNF) inhibitors.

Lawrence F. Eichenfield, MD, professor of dermatology and pediatrics, at the University of California, San Diego, offered these tips and comments in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

Psoriasis

It’s a brand new day for adult psoriasis sufferers, but it seems to be only a brand new morning for their pediatric counterparts. “Kids and teenagers were left behind in the biologic revolution,” Dr. Eichenfield said. “Only two systemic biologics have been approved for psoriasis in children.” They are ustekinumab (Stelara), approved by the Food and Drug Administration for treating psoriasis in children aged 12 years and older, and etanercept, approved for aged 4 years and older.

The good news, he said, is that “our new biologic agents are now being studied in children.”

Research is also providing new insight into pediatric psoriasis, said Dr. Eichenfield, who is also chief of pediatric and adolescent dermatology at Rady Children’s Hospital in San Diego. It’s now clear that “there’s a lot more facial involvement, and a high involvement of scalp and nail,” he noted.

It’s also clear, he said, that inflammation begins early in pediatric psoriasis. That raises the question of whether it’s a good idea to launch aggressive treatment to stop the “psoriatic march” toward cardiovascular and other medical problems down the line, he commented.

“Keep an open mind to getting aggressive in therapy,” he advised, although he acknowledged that “it’s hard to get beyond the two biologics, and only one is approved for children under 12.”

Dr. Eichenfield advised colleagues to keep an eye out for TNF inhibitor–induced psoriasis. “We’re seeing it pretty regularly,” he said, commonly in children who are treated with TNF inhibitors for rheumatoid arthritis or Crohn’s disease.

The lesions “look like dermatitis but are very psoriasiform,” he said, and research suggests this can appear after a single dose or after as many as 63 months of treatment. Topical and light therapy can be helpful. But if those treatments do not help, he said, it’s time to consider changing the biologic that the patient is taking. “Is the biologic adequately controlling their underlying disease? If not, you can help find one that would be great for their underlying disease and clear up their psoriasis.”

Alopecia

Pediatric alopecia “is a problem I see pretty regularly in practice,” Dr. Eichenfield said. When he sees patients with alopecia, he says that, “‘if your child doesn’t have 50% hair loss, you’re in the good group. It will generally heal up and never come back again.’ ”

He referred to a recent study, where investigators at the Children’s Hospital of Philadelphia retrospectively studied 125 children under age 4 years who were diagnosed with alopecia areata and followed for 2 years. Over time, those children with over 50% of hair loss initially were more likely to have worsening Severity of Alopecia Tool (SALT) scores over the follow-up period. But a high proportion of those with mild alopecia initially continued to have mild alopecia at follow-up (Pediatr Dermatol. 2019 Aug 29. doi: 10.1111/pde.13990).

Dr. Eichenfield noted that the study found that 41% of the patients also had atopic dermatitis.

He also highlighted two other recent studies on pediatric alopecia: One found that while vitamin D levels were low in a majority of children with alopecia in the study, the proportion who had a deficiency was similar to the proportion in a larger pediatric population, at about 22% in both groups (J Am Acad Dermatol. 2018 Sep;79(3):e43-e44). Supplementation doesn’t seem to help. “It’s not important to test levels,” he said.

Another study examined whether it’s a good idea to test patients for celiac disease in children with alopecia (Pediatr Dermatol. 2018 Jul;35[4]:535-8). Some parents may ask this question, but the answer, he said, is generally no.

What’s next? “We were hoping oral and topical JAK inhibitors would work well” in this population, Dr. Eichenfield said, but study findings haven’t been promising.

Still, oral tofacitinib (Xeljanz) showed some “pretty impressive” success in a recent study in four children, he noted. Based on the results, the authors wrote that “we suggest that, after proper counseling regarding the risks, including severe infection and malignancy, the use of tofacitinib may be considered for preadolescent children with AA [alopecia areata] who are experiencing psychosocial impairment” (J Am Acad Dermatol. 2019 Feb;80[2]:568-70).

In general, Dr. Eichenfield said, research on pediatric alopecia “will be secondary, especially with JAK inhibitors because of the risk of side effects. But [children will] probably tolerate them better than adults do because they have fewer medical problems.”

Meanwhile, he added, controversy continues to swirl around how to treat children over age 10 years who have lost 50% or more of their hair. “I’ve seen hundreds of kids with alopecia areata,” he said, “and I can’t predict what the course may be.”

Dr. Eichenfield reports multiple relationships (consultant or investigator) with various pharmaceutical companies, including Abbvie, Allergan, Lilly, Novartis, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – While biologics have dramatically changed the picture, drugs like methotrexate, acitretin, cyclosporine, and apremilast still have roles to play in the treatment of psoriasis, a dermatologist told colleagues.

However, caution is necessary, especially when the drugs are used in combination with biologics, Bruce E. Strober, MD, PhD, of Yale University, New Haven, Conn., and Central Connecticut Dermatology, Cromwell, Conn., said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Strober offered these tips about the proper use of these four drugs in psoriasis patients:

Acitretin (Soriatane). “This was used as monotherapy initially, but at this point in history, fewer and fewer patients are getting it as monotherapy,” he said. A dose of 25 mg/day appears to provide the best mix of efficacy and side-effect control, “although it’s not a high-efficacy drug, especially at 25 mg a day. It’s a slow-acting drug, and you may need 4 if not 6 months to see the maximum effect before you give up on it.”

What about using acitretin in combination with other therapies? Studies examining its use with phototherapy haven’t been promising, Dr. Strober said. The drug can be used with methotrexate, he said, even though the combination will worry pharmacists. “Follow the liver, and you’ll be fine” he noted. “That combination can be successful. Laboratory monitoring is not onerous: Discontinue after a few months if you’ve not seen any movement.” The drug can also be used with biologics, he said.

Apremilast (Otezla). This drug will bring about a third of patients to a Psoriasis Area and Severity Index (PASI) 75. “That’s not the most impressive efficacy. Rarely do we clear patients with this drug, and it has tolerability issues in some patients,” Dr. Strober said. Side effects can include diarrhea, nausea, headache, and depression. “Warn patients of these possibilities,” he added.

Methotrexate. “It’s very helpful and not a drug to be feared if it’s monitored correctly,” Dr. Strober said. “It’s certainly not a biologic, but it’s not a bad drug from an efficacy standpoint, and it does have efficacy in psoriatic arthritis.”

The drug’s low cost can make it a good alternative to biologics in patients with limited insurance options – such as those on Medicare – or those who don’t have insurance, he said.

“Psoriasis is often controlled at a mean dose of 15 mg/week [orally], with no test dose; start at 15-mg weekly,” he said. “It’s an interesting drug that allows you to dose weekly and still get efficacy,” especially when dosed subcutaneously.

Beware the many contraindications such as pregnancy, possible pregnancy, and high alcohol intake, he added. Dr. Strober doesn’t recommend liver biopsies to monitor hepatic effects. “It’s a poor test with risk and sampling error,” he said.

Cyclosporine. This drug is best “in severe patients in need of a quick response,” said Dr. Strober, who added that biologics are often a better option even in patients who are sensitive to price since samples and free-drug programs are available. “It’s in and out of the body quickly, and most people skip doses and get recurrence of their disease quickly,” he said.

Blood tests are a hassle for patients, he said, and “people often don’t feel great on the drug,” said Dr. Strober, who added, however, that he still does occasionally use it.

Dr. Strober reported multiple disclosures including consultant/advisory board (AbbVie, Amgen, Lilly, Pfizer, among others) and investigator relationships. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – While biologics have dramatically changed the picture, drugs like methotrexate, acitretin, cyclosporine, and apremilast still have roles to play in the treatment of psoriasis, a dermatologist told colleagues.

However, caution is necessary, especially when the drugs are used in combination with biologics, Bruce E. Strober, MD, PhD, of Yale University, New Haven, Conn., and Central Connecticut Dermatology, Cromwell, Conn., said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Strober offered these tips about the proper use of these four drugs in psoriasis patients:

Acitretin (Soriatane). “This was used as monotherapy initially, but at this point in history, fewer and fewer patients are getting it as monotherapy,” he said. A dose of 25 mg/day appears to provide the best mix of efficacy and side-effect control, “although it’s not a high-efficacy drug, especially at 25 mg a day. It’s a slow-acting drug, and you may need 4 if not 6 months to see the maximum effect before you give up on it.”

What about using acitretin in combination with other therapies? Studies examining its use with phototherapy haven’t been promising, Dr. Strober said. The drug can be used with methotrexate, he said, even though the combination will worry pharmacists. “Follow the liver, and you’ll be fine” he noted. “That combination can be successful. Laboratory monitoring is not onerous: Discontinue after a few months if you’ve not seen any movement.” The drug can also be used with biologics, he said.

Apremilast (Otezla). This drug will bring about a third of patients to a Psoriasis Area and Severity Index (PASI) 75. “That’s not the most impressive efficacy. Rarely do we clear patients with this drug, and it has tolerability issues in some patients,” Dr. Strober said. Side effects can include diarrhea, nausea, headache, and depression. “Warn patients of these possibilities,” he added.

Methotrexate. “It’s very helpful and not a drug to be feared if it’s monitored correctly,” Dr. Strober said. “It’s certainly not a biologic, but it’s not a bad drug from an efficacy standpoint, and it does have efficacy in psoriatic arthritis.”

The drug’s low cost can make it a good alternative to biologics in patients with limited insurance options – such as those on Medicare – or those who don’t have insurance, he said.

“Psoriasis is often controlled at a mean dose of 15 mg/week [orally], with no test dose; start at 15-mg weekly,” he said. “It’s an interesting drug that allows you to dose weekly and still get efficacy,” especially when dosed subcutaneously.

Beware the many contraindications such as pregnancy, possible pregnancy, and high alcohol intake, he added. Dr. Strober doesn’t recommend liver biopsies to monitor hepatic effects. “It’s a poor test with risk and sampling error,” he said.

Cyclosporine. This drug is best “in severe patients in need of a quick response,” said Dr. Strober, who added that biologics are often a better option even in patients who are sensitive to price since samples and free-drug programs are available. “It’s in and out of the body quickly, and most people skip doses and get recurrence of their disease quickly,” he said.

Blood tests are a hassle for patients, he said, and “people often don’t feel great on the drug,” said Dr. Strober, who added, however, that he still does occasionally use it.

Dr. Strober reported multiple disclosures including consultant/advisory board (AbbVie, Amgen, Lilly, Pfizer, among others) and investigator relationships. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – While biologics have dramatically changed the picture, drugs like methotrexate, acitretin, cyclosporine, and apremilast still have roles to play in the treatment of psoriasis, a dermatologist told colleagues.

However, caution is necessary, especially when the drugs are used in combination with biologics, Bruce E. Strober, MD, PhD, of Yale University, New Haven, Conn., and Central Connecticut Dermatology, Cromwell, Conn., said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Strober offered these tips about the proper use of these four drugs in psoriasis patients:

Acitretin (Soriatane). “This was used as monotherapy initially, but at this point in history, fewer and fewer patients are getting it as monotherapy,” he said. A dose of 25 mg/day appears to provide the best mix of efficacy and side-effect control, “although it’s not a high-efficacy drug, especially at 25 mg a day. It’s a slow-acting drug, and you may need 4 if not 6 months to see the maximum effect before you give up on it.”

What about using acitretin in combination with other therapies? Studies examining its use with phototherapy haven’t been promising, Dr. Strober said. The drug can be used with methotrexate, he said, even though the combination will worry pharmacists. “Follow the liver, and you’ll be fine” he noted. “That combination can be successful. Laboratory monitoring is not onerous: Discontinue after a few months if you’ve not seen any movement.” The drug can also be used with biologics, he said.

Apremilast (Otezla). This drug will bring about a third of patients to a Psoriasis Area and Severity Index (PASI) 75. “That’s not the most impressive efficacy. Rarely do we clear patients with this drug, and it has tolerability issues in some patients,” Dr. Strober said. Side effects can include diarrhea, nausea, headache, and depression. “Warn patients of these possibilities,” he added.

Methotrexate. “It’s very helpful and not a drug to be feared if it’s monitored correctly,” Dr. Strober said. “It’s certainly not a biologic, but it’s not a bad drug from an efficacy standpoint, and it does have efficacy in psoriatic arthritis.”

The drug’s low cost can make it a good alternative to biologics in patients with limited insurance options – such as those on Medicare – or those who don’t have insurance, he said.

“Psoriasis is often controlled at a mean dose of 15 mg/week [orally], with no test dose; start at 15-mg weekly,” he said. “It’s an interesting drug that allows you to dose weekly and still get efficacy,” especially when dosed subcutaneously.

Beware the many contraindications such as pregnancy, possible pregnancy, and high alcohol intake, he added. Dr. Strober doesn’t recommend liver biopsies to monitor hepatic effects. “It’s a poor test with risk and sampling error,” he said.

Cyclosporine. This drug is best “in severe patients in need of a quick response,” said Dr. Strober, who added that biologics are often a better option even in patients who are sensitive to price since samples and free-drug programs are available. “It’s in and out of the body quickly, and most people skip doses and get recurrence of their disease quickly,” he said.

Blood tests are a hassle for patients, he said, and “people often don’t feel great on the drug,” said Dr. Strober, who added, however, that he still does occasionally use it.

Dr. Strober reported multiple disclosures including consultant/advisory board (AbbVie, Amgen, Lilly, Pfizer, among others) and investigator relationships. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Eczema is eczema is eczema, right? Maybe not. “Atopic dermatitis might not be one disease,” a dermatologist told colleagues, and treatments may need to be adjusted to reflect the age and ethnicity of patients.

More research is needed, Kenneth B. Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, said during a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “We’re probably just on the tip of the iceberg of understanding the physiology of atopic dermatitis. Hopefully, it will lead to the therapeutic advances we’ve seen in psoriasis.”

As Dr. Gordon explained, there’s a wide gap between our understanding of psoriasis and atopic dermatitis (AD). Currently, there’s only one biologic treatment for AD, he said, “and our medicines aren’t well understood.”

As for the disease itself, he said, “you might hear a renowned [expert] say, ‘This is how it works,’ and another say, ‘This is absolutely not how it works.’ ” One camp focused on the skin barrier, he said, while another camp highlighted inflammation in AD.

“Both the barrier and inflammation are important,” he said. “There are multiple cell types and cytokines that are important, but we don’t know yet the relative importance of them all. You have this cytokine soup, and we’re still trying to figure out the driving forces.”

What is clear, Dr. Gordon said, is that AD acts differently in certain patient populations. It’s not the same in pediatric versus adult patients, he said, and it’s not the same in white versus black versus Asian patients. Research, for example, suggests that Th2, Th22, and Th17 pathways appear to be important in pediatric AD, but not Th1, he said. In contrast, the Th1 pathway plays a role in white adults – but not in black adults

Different cytokines appear to play different roles in these populations, he said. “One of the key things moving forward is going to be figuring out which patients you apply these medications to,” he noted.

Dr. Gordon has multiple disclosures including honoraria or research support from Abbvie, Lilly, Novartis, Pfizer, UCB, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Eczema is eczema is eczema, right? Maybe not. “Atopic dermatitis might not be one disease,” a dermatologist told colleagues, and treatments may need to be adjusted to reflect the age and ethnicity of patients.

More research is needed, Kenneth B. Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, said during a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “We’re probably just on the tip of the iceberg of understanding the physiology of atopic dermatitis. Hopefully, it will lead to the therapeutic advances we’ve seen in psoriasis.”

As Dr. Gordon explained, there’s a wide gap between our understanding of psoriasis and atopic dermatitis (AD). Currently, there’s only one biologic treatment for AD, he said, “and our medicines aren’t well understood.”

As for the disease itself, he said, “you might hear a renowned [expert] say, ‘This is how it works,’ and another say, ‘This is absolutely not how it works.’ ” One camp focused on the skin barrier, he said, while another camp highlighted inflammation in AD.

“Both the barrier and inflammation are important,” he said. “There are multiple cell types and cytokines that are important, but we don’t know yet the relative importance of them all. You have this cytokine soup, and we’re still trying to figure out the driving forces.”

What is clear, Dr. Gordon said, is that AD acts differently in certain patient populations. It’s not the same in pediatric versus adult patients, he said, and it’s not the same in white versus black versus Asian patients. Research, for example, suggests that Th2, Th22, and Th17 pathways appear to be important in pediatric AD, but not Th1, he said. In contrast, the Th1 pathway plays a role in white adults – but not in black adults

Different cytokines appear to play different roles in these populations, he said. “One of the key things moving forward is going to be figuring out which patients you apply these medications to,” he noted.

Dr. Gordon has multiple disclosures including honoraria or research support from Abbvie, Lilly, Novartis, Pfizer, UCB, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Eczema is eczema is eczema, right? Maybe not. “Atopic dermatitis might not be one disease,” a dermatologist told colleagues, and treatments may need to be adjusted to reflect the age and ethnicity of patients.

More research is needed, Kenneth B. Gordon, MD, chair and professor of dermatology at the Medical College of Wisconsin, Milwaukee, said during a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “We’re probably just on the tip of the iceberg of understanding the physiology of atopic dermatitis. Hopefully, it will lead to the therapeutic advances we’ve seen in psoriasis.”

As Dr. Gordon explained, there’s a wide gap between our understanding of psoriasis and atopic dermatitis (AD). Currently, there’s only one biologic treatment for AD, he said, “and our medicines aren’t well understood.”

As for the disease itself, he said, “you might hear a renowned [expert] say, ‘This is how it works,’ and another say, ‘This is absolutely not how it works.’ ” One camp focused on the skin barrier, he said, while another camp highlighted inflammation in AD.

“Both the barrier and inflammation are important,” he said. “There are multiple cell types and cytokines that are important, but we don’t know yet the relative importance of them all. You have this cytokine soup, and we’re still trying to figure out the driving forces.”

What is clear, Dr. Gordon said, is that AD acts differently in certain patient populations. It’s not the same in pediatric versus adult patients, he said, and it’s not the same in white versus black versus Asian patients. Research, for example, suggests that Th2, Th22, and Th17 pathways appear to be important in pediatric AD, but not Th1, he said. In contrast, the Th1 pathway plays a role in white adults – but not in black adults

Different cytokines appear to play different roles in these populations, he said. “One of the key things moving forward is going to be figuring out which patients you apply these medications to,” he noted.

Dr. Gordon has multiple disclosures including honoraria or research support from Abbvie, Lilly, Novartis, Pfizer, UCB, and others. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Biologics are revolutionizing the treatment of atopic dermatitis (AD), but a dermatologist urged colleagues to keep in mind the value of traditional topical and systemic treatments.

Joseph F. Fowler Jr., MD, of the University of Louisville, Ky., offered these tips about AD treatment in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

• Keep the epidermal skin barrier in mind.

The epidermal skin barrier is abnormal in patients with AD, Dr. Fowler said, because of several possible factors: altered levels of natural moisturizing factor (which can be caused by a genetic mutation), imbalances between ceramides and lipids, and reduced aquaporin levels.

Enhancing the skin barrier is crucial in treating AD, he said, and products with these ingredients may help: ceramides, glycerin/glycerol (glucoside), colloidal oatmeal, and components of natural moisturizing factor.

• Expensive products are probably better.

“These products are available over the counter and via prescription,” he said. “Do they make the skin barrier stronger? The answer is they probably they do. But most do tend to be expensive, especially Rx products.”

Not all patients, of course, can afford the most expensive options. “You and your patients have to decide whether it’s better to get something like plain old Vaseline or a very inexpensive cream at Walmart that may be more accessible,” he said. “I tell patients that if the cost is not a big issue, these other products are probably better, and they will make your skin heal better and feel better. But if cost is a problem, use what you can afford.”

• Don’t forget about hypochlorous acid.

While it’s chemically similar to bleach, this product “doesn’t bleach your clothes or smell bleachy,” Dr. Fowler said. “It does have antibiotic and antipruritic effects.”

• For predictability, try methotrexate.

Methotrexate, an old workhorse in dermatology, remains an option, especially for patients who need alternatives to biologics, Dr. Fowler said. “I’ve used it much more in the last 10 years for eczema than for psoriasis and anything else. We’re used to using it, and I find it predictably effective at a dosage that’s similar to that for psoriasis.”

• Mycophenolate mofetil (CellCept) may be helpful.

Dr. Fowler’s research has shown that mycophenolate mofetil is useful in about 50% of chronic AD cases. “The problem with the drug is that you couldn’t tell which ones would get better and which ones wouldn’t.” Still, it can be an alternative to methotrexate and cyclosporine, he said.

• Cyclosporine is a short-term treatment.

“It’s like steroids on steroids,” Dr. Fowler said. “I’ve had to use it sometimes even in the age of biologics, which may not work as fast as we’d like in someone who’s really miserable.” The drug is linked to liver and kidney risks, he cautioned, and “you don’t want to be on it very long.”

• Ultraviolet light therapy can help.

This strategy works well “if they come in and get to the office and do it,” Dr. Fowler said. “We should remember it as an option.”

A patient who’s over 80 years old with bad AD has been getting narrow-band UVB treatments for at least 5 years, he said. “I just look at him every 3-4 months. Every time he says, ‘Can I keep coming and get my light treatments?’ and I say sure. At 80-plus, I’m not too worried about cutaneous malignancy or any other side effects.”

Dr. Fowler reported relationships with the speaker’s bureau of SmartPractice and ties with Asana, Johnson & Johnson, Lilly, Novartis and Pfizer. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Biologics are revolutionizing the treatment of atopic dermatitis (AD), but a dermatologist urged colleagues to keep in mind the value of traditional topical and systemic treatments.

Joseph F. Fowler Jr., MD, of the University of Louisville, Ky., offered these tips about AD treatment in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

• Keep the epidermal skin barrier in mind.

The epidermal skin barrier is abnormal in patients with AD, Dr. Fowler said, because of several possible factors: altered levels of natural moisturizing factor (which can be caused by a genetic mutation), imbalances between ceramides and lipids, and reduced aquaporin levels.

Enhancing the skin barrier is crucial in treating AD, he said, and products with these ingredients may help: ceramides, glycerin/glycerol (glucoside), colloidal oatmeal, and components of natural moisturizing factor.

• Expensive products are probably better.

“These products are available over the counter and via prescription,” he said. “Do they make the skin barrier stronger? The answer is they probably they do. But most do tend to be expensive, especially Rx products.”

Not all patients, of course, can afford the most expensive options. “You and your patients have to decide whether it’s better to get something like plain old Vaseline or a very inexpensive cream at Walmart that may be more accessible,” he said. “I tell patients that if the cost is not a big issue, these other products are probably better, and they will make your skin heal better and feel better. But if cost is a problem, use what you can afford.”

• Don’t forget about hypochlorous acid.

While it’s chemically similar to bleach, this product “doesn’t bleach your clothes or smell bleachy,” Dr. Fowler said. “It does have antibiotic and antipruritic effects.”

• For predictability, try methotrexate.

Methotrexate, an old workhorse in dermatology, remains an option, especially for patients who need alternatives to biologics, Dr. Fowler said. “I’ve used it much more in the last 10 years for eczema than for psoriasis and anything else. We’re used to using it, and I find it predictably effective at a dosage that’s similar to that for psoriasis.”

• Mycophenolate mofetil (CellCept) may be helpful.

Dr. Fowler’s research has shown that mycophenolate mofetil is useful in about 50% of chronic AD cases. “The problem with the drug is that you couldn’t tell which ones would get better and which ones wouldn’t.” Still, it can be an alternative to methotrexate and cyclosporine, he said.

• Cyclosporine is a short-term treatment.

“It’s like steroids on steroids,” Dr. Fowler said. “I’ve had to use it sometimes even in the age of biologics, which may not work as fast as we’d like in someone who’s really miserable.” The drug is linked to liver and kidney risks, he cautioned, and “you don’t want to be on it very long.”

• Ultraviolet light therapy can help.

This strategy works well “if they come in and get to the office and do it,” Dr. Fowler said. “We should remember it as an option.”

A patient who’s over 80 years old with bad AD has been getting narrow-band UVB treatments for at least 5 years, he said. “I just look at him every 3-4 months. Every time he says, ‘Can I keep coming and get my light treatments?’ and I say sure. At 80-plus, I’m not too worried about cutaneous malignancy or any other side effects.”

Dr. Fowler reported relationships with the speaker’s bureau of SmartPractice and ties with Asana, Johnson & Johnson, Lilly, Novartis and Pfizer. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Biologics are revolutionizing the treatment of atopic dermatitis (AD), but a dermatologist urged colleagues to keep in mind the value of traditional topical and systemic treatments.

Joseph F. Fowler Jr., MD, of the University of Louisville, Ky., offered these tips about AD treatment in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar:

• Keep the epidermal skin barrier in mind.

The epidermal skin barrier is abnormal in patients with AD, Dr. Fowler said, because of several possible factors: altered levels of natural moisturizing factor (which can be caused by a genetic mutation), imbalances between ceramides and lipids, and reduced aquaporin levels.

Enhancing the skin barrier is crucial in treating AD, he said, and products with these ingredients may help: ceramides, glycerin/glycerol (glucoside), colloidal oatmeal, and components of natural moisturizing factor.

• Expensive products are probably better.

“These products are available over the counter and via prescription,” he said. “Do they make the skin barrier stronger? The answer is they probably they do. But most do tend to be expensive, especially Rx products.”

Not all patients, of course, can afford the most expensive options. “You and your patients have to decide whether it’s better to get something like plain old Vaseline or a very inexpensive cream at Walmart that may be more accessible,” he said. “I tell patients that if the cost is not a big issue, these other products are probably better, and they will make your skin heal better and feel better. But if cost is a problem, use what you can afford.”

• Don’t forget about hypochlorous acid.

While it’s chemically similar to bleach, this product “doesn’t bleach your clothes or smell bleachy,” Dr. Fowler said. “It does have antibiotic and antipruritic effects.”

• For predictability, try methotrexate.

Methotrexate, an old workhorse in dermatology, remains an option, especially for patients who need alternatives to biologics, Dr. Fowler said. “I’ve used it much more in the last 10 years for eczema than for psoriasis and anything else. We’re used to using it, and I find it predictably effective at a dosage that’s similar to that for psoriasis.”

• Mycophenolate mofetil (CellCept) may be helpful.

Dr. Fowler’s research has shown that mycophenolate mofetil is useful in about 50% of chronic AD cases. “The problem with the drug is that you couldn’t tell which ones would get better and which ones wouldn’t.” Still, it can be an alternative to methotrexate and cyclosporine, he said.

• Cyclosporine is a short-term treatment.

“It’s like steroids on steroids,” Dr. Fowler said. “I’ve had to use it sometimes even in the age of biologics, which may not work as fast as we’d like in someone who’s really miserable.” The drug is linked to liver and kidney risks, he cautioned, and “you don’t want to be on it very long.”

• Ultraviolet light therapy can help.

This strategy works well “if they come in and get to the office and do it,” Dr. Fowler said. “We should remember it as an option.”

A patient who’s over 80 years old with bad AD has been getting narrow-band UVB treatments for at least 5 years, he said. “I just look at him every 3-4 months. Every time he says, ‘Can I keep coming and get my light treatments?’ and I say sure. At 80-plus, I’m not too worried about cutaneous malignancy or any other side effects.”

Dr. Fowler reported relationships with the speaker’s bureau of SmartPractice and ties with Asana, Johnson & Johnson, Lilly, Novartis and Pfizer. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – The patient, a 61-year-old man, came to see a dermatologist here about subcutaneous masses on his left arm, abdomen, and on both thighs.

It didn’t take long for Curt Samlaska, MD, of the University of Nevada, Reno, to link the masses to the patient’s daily regimen of seven insulin injections.

But diagnosing the condition required more than asking a few questions. At first, the man appeared to suffer from lipohypertrophy – a lump caused by an accumulation of fat at the site of insulin injections. But, Dr. Samlaska told colleagues, the patient had a different condition that’s barely been discussed in the dermatologic literature – insulin-derived amyloidosis, also known as “insulin ball.”

“It’s probably much more prevalent than we currently appreciate,” said Dr. Samlaska, who spoke in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “Many cases are not [fully] evaluated and thought to be lipohypertrophy.”

Dr. Samlaska’s patient had suffered from diabetes since age 23 and tightly controls his blood sugar through seven daily injections. He injects short-acting insulin into his arms and abdomen, and long-acting insulin into his thighs.

The masses began appearing about 10 years ago, he told Dr. Samlaska, and he’s suffered more pain while injecting them over time. But the masses are easier to grasp during injections, and the patient’s body did not offer many other sites for injections.

According to Dr. Samlaska, there are about 75 case reports of insulin ball in the medical literature, almost all in endocrinology journals. Ninety percent have a single lump, most commonly in the abdomen, and most have poor glycemic control, he said. (His patient is an outlier.)

Research suggests that insulin balls absorb about 34% of the insulin that’s injected, meaning that patients must inject more than usual to get the same effect. Be careful to advise patients about this, Dr. Samlaska said, because they might try alternative injection sites and get a sudden unexpected flood of insulin – potentially causing hypoglycemia.

He added that another drug – the HIV fusion inhibitor enfuvirtide – also has been linked to amyloidosis.

Pathology can offer insight into whether a mass is an insulin ball or a case of lipohypertrophy, he said. “They’re difficult to distinguish on clinical grounds,” he said, although lipohypertrophy masses are firmer, and they shrink when patients stop injecting insulin. Insulin balls do not.

The treatment for insulin balls is surgical excision, he said. “It’s very easy to do. With the extrusion technique, it comes out like a cheese, like a cyst.”

He said his patient was scheduled to soon undergo excision treatment.

Dr. Samlaska reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – The patient, a 61-year-old man, came to see a dermatologist here about subcutaneous masses on his left arm, abdomen, and on both thighs.

It didn’t take long for Curt Samlaska, MD, of the University of Nevada, Reno, to link the masses to the patient’s daily regimen of seven insulin injections.

But diagnosing the condition required more than asking a few questions. At first, the man appeared to suffer from lipohypertrophy – a lump caused by an accumulation of fat at the site of insulin injections. But, Dr. Samlaska told colleagues, the patient had a different condition that’s barely been discussed in the dermatologic literature – insulin-derived amyloidosis, also known as “insulin ball.”

“It’s probably much more prevalent than we currently appreciate,” said Dr. Samlaska, who spoke in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “Many cases are not [fully] evaluated and thought to be lipohypertrophy.”

Dr. Samlaska’s patient had suffered from diabetes since age 23 and tightly controls his blood sugar through seven daily injections. He injects short-acting insulin into his arms and abdomen, and long-acting insulin into his thighs.

The masses began appearing about 10 years ago, he told Dr. Samlaska, and he’s suffered more pain while injecting them over time. But the masses are easier to grasp during injections, and the patient’s body did not offer many other sites for injections.

According to Dr. Samlaska, there are about 75 case reports of insulin ball in the medical literature, almost all in endocrinology journals. Ninety percent have a single lump, most commonly in the abdomen, and most have poor glycemic control, he said. (His patient is an outlier.)

Research suggests that insulin balls absorb about 34% of the insulin that’s injected, meaning that patients must inject more than usual to get the same effect. Be careful to advise patients about this, Dr. Samlaska said, because they might try alternative injection sites and get a sudden unexpected flood of insulin – potentially causing hypoglycemia.

He added that another drug – the HIV fusion inhibitor enfuvirtide – also has been linked to amyloidosis.

Pathology can offer insight into whether a mass is an insulin ball or a case of lipohypertrophy, he said. “They’re difficult to distinguish on clinical grounds,” he said, although lipohypertrophy masses are firmer, and they shrink when patients stop injecting insulin. Insulin balls do not.

The treatment for insulin balls is surgical excision, he said. “It’s very easy to do. With the extrusion technique, it comes out like a cheese, like a cyst.”

He said his patient was scheduled to soon undergo excision treatment.

Dr. Samlaska reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – The patient, a 61-year-old man, came to see a dermatologist here about subcutaneous masses on his left arm, abdomen, and on both thighs.

It didn’t take long for Curt Samlaska, MD, of the University of Nevada, Reno, to link the masses to the patient’s daily regimen of seven insulin injections.

But diagnosing the condition required more than asking a few questions. At first, the man appeared to suffer from lipohypertrophy – a lump caused by an accumulation of fat at the site of insulin injections. But, Dr. Samlaska told colleagues, the patient had a different condition that’s barely been discussed in the dermatologic literature – insulin-derived amyloidosis, also known as “insulin ball.”

“It’s probably much more prevalent than we currently appreciate,” said Dr. Samlaska, who spoke in a presentation at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar. “Many cases are not [fully] evaluated and thought to be lipohypertrophy.”

Dr. Samlaska’s patient had suffered from diabetes since age 23 and tightly controls his blood sugar through seven daily injections. He injects short-acting insulin into his arms and abdomen, and long-acting insulin into his thighs.

The masses began appearing about 10 years ago, he told Dr. Samlaska, and he’s suffered more pain while injecting them over time. But the masses are easier to grasp during injections, and the patient’s body did not offer many other sites for injections.

According to Dr. Samlaska, there are about 75 case reports of insulin ball in the medical literature, almost all in endocrinology journals. Ninety percent have a single lump, most commonly in the abdomen, and most have poor glycemic control, he said. (His patient is an outlier.)

Research suggests that insulin balls absorb about 34% of the insulin that’s injected, meaning that patients must inject more than usual to get the same effect. Be careful to advise patients about this, Dr. Samlaska said, because they might try alternative injection sites and get a sudden unexpected flood of insulin – potentially causing hypoglycemia.

He added that another drug – the HIV fusion inhibitor enfuvirtide – also has been linked to amyloidosis.

Pathology can offer insight into whether a mass is an insulin ball or a case of lipohypertrophy, he said. “They’re difficult to distinguish on clinical grounds,” he said, although lipohypertrophy masses are firmer, and they shrink when patients stop injecting insulin. Insulin balls do not.

The treatment for insulin balls is surgical excision, he said. “It’s very easy to do. With the extrusion technique, it comes out like a cheese, like a cyst.”

He said his patient was scheduled to soon undergo excision treatment.

Dr. Samlaska reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Be alert for hidden cases of hyperhidrosis in patients, Seemal R. Desai, MD, said during a presentation on this topic at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

During an examination for another condition, he said, patients may be “sweating and dripping.” However, “you look over that diagnosis because that’s not what they’re there for,” said Dr. Desai, a dermatologist at the University of Texas Southwestern Medical Center in Dallas.

He described one of his patients, who only revealed that she suffered from “horrible, devastating” hyperhidrosis after he’d treated her for years for melasma. The sweating especially affected her because it prevented her from wearing the skin-exposing clothing of her Indian culture.

Delays in treatment are common in hyperhidrosis, which is believed to affect 5% of the world’s population. According to Dr. Desai, research suggests that 85% of patients with hyperhidrosis wait more than 3 years to bring it up with doctors, and half wait more than a decade.

There are many treatments for hyperhidrosis. Some are fairly simple: over-the-counter or prescription antiperspirants, said Dr. Desai, who likes the over-the-counter brand Certain Dri), iontophoresis (application of electric current), topical anticholinergics (including glycopyrronium tosylate cloth wipes, recently approved by the FDA for topical treatment of primary axillary hyperhidrosis for ages 9 years and older), and systemic management. Others are minimally invasive: Botox injections and the miraDry medical device (which relies on thermolysis). And surgical strategies may be an option for severe cases.

On its website, the International Hyperhidrosis Society provides a chart of options for hyperhidrosis in various parts of the body. Treatments tend to focus on the underarms, however, and “we’ve got huge unmet needs for patient options,” Dr. Desai said.
 

• During his presentation, he provided the following pearls regarding hyperhidrosis treatments:
• Distinguish between antiperspirants, which block sweating, and deodorants, which cover up body odor. “Sometimes I get caught up in the middle of a busy office visit and use these terms interchangeably. They’re really different, but patients and the public tend to equate those together,” he commented.
• Make sure patients understand how to properly use antiperspirants and explain that antiperspirants must be applied to dry skin. “Antiperspirant is forming a clog in the drain” to prevent the release of sweat, he said. “If you apply it to wet skin, you will block that chemical reaction in the duct.”
• Massage in the antiperspirant, he advises, and don’t occlude the skin. Apply twice daily, including before bedtime. “They can use antiperspirant on the hands and the bottom of the feet,”Dr. Desai said. “You want to ensure that they’re using the spray on the surface and in the web space. They can also use antiperspirants on the face, but avoid contact with the eyes.”
• Be careful if you prescribe glycopyrronium cloths off label. These wipes are helpful and they can be used outside the FDA-approved use in the underarms, said Dr. Desai, who said he has palmar hyperhidrosis and has successfully used them on his palms, but he hasn’t found them to be helpful on the soles of his feet.

Dr. Desai recommends 5-minute applications on the palms because the treatment can irritate the face and eyes.

Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, told the audience about the case of a teacher who touched his eyes after applying the treatment. He went to school, felt ill, and ended up in an emergency department because he had an enlarged pupil. “You just have to tell people this can happen,” she said.

Dr. Desai reported no relevant disclosures.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Be alert for hidden cases of hyperhidrosis in patients, Seemal R. Desai, MD, said during a presentation on this topic at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

During an examination for another condition, he said, patients may be “sweating and dripping.” However, “you look over that diagnosis because that’s not what they’re there for,” said Dr. Desai, a dermatologist at the University of Texas Southwestern Medical Center in Dallas.

He described one of his patients, who only revealed that she suffered from “horrible, devastating” hyperhidrosis after he’d treated her for years for melasma. The sweating especially affected her because it prevented her from wearing the skin-exposing clothing of her Indian culture.

Delays in treatment are common in hyperhidrosis, which is believed to affect 5% of the world’s population. According to Dr. Desai, research suggests that 85% of patients with hyperhidrosis wait more than 3 years to bring it up with doctors, and half wait more than a decade.

There are many treatments for hyperhidrosis. Some are fairly simple: over-the-counter or prescription antiperspirants, said Dr. Desai, who likes the over-the-counter brand Certain Dri), iontophoresis (application of electric current), topical anticholinergics (including glycopyrronium tosylate cloth wipes, recently approved by the FDA for topical treatment of primary axillary hyperhidrosis for ages 9 years and older), and systemic management. Others are minimally invasive: Botox injections and the miraDry medical device (which relies on thermolysis). And surgical strategies may be an option for severe cases.

On its website, the International Hyperhidrosis Society provides a chart of options for hyperhidrosis in various parts of the body. Treatments tend to focus on the underarms, however, and “we’ve got huge unmet needs for patient options,” Dr. Desai said.
 

• During his presentation, he provided the following pearls regarding hyperhidrosis treatments:
• Distinguish between antiperspirants, which block sweating, and deodorants, which cover up body odor. “Sometimes I get caught up in the middle of a busy office visit and use these terms interchangeably. They’re really different, but patients and the public tend to equate those together,” he commented.
• Make sure patients understand how to properly use antiperspirants and explain that antiperspirants must be applied to dry skin. “Antiperspirant is forming a clog in the drain” to prevent the release of sweat, he said. “If you apply it to wet skin, you will block that chemical reaction in the duct.”
• Massage in the antiperspirant, he advises, and don’t occlude the skin. Apply twice daily, including before bedtime. “They can use antiperspirant on the hands and the bottom of the feet,”Dr. Desai said. “You want to ensure that they’re using the spray on the surface and in the web space. They can also use antiperspirants on the face, but avoid contact with the eyes.”
• Be careful if you prescribe glycopyrronium cloths off label. These wipes are helpful and they can be used outside the FDA-approved use in the underarms, said Dr. Desai, who said he has palmar hyperhidrosis and has successfully used them on his palms, but he hasn’t found them to be helpful on the soles of his feet.

Dr. Desai recommends 5-minute applications on the palms because the treatment can irritate the face and eyes.

Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, told the audience about the case of a teacher who touched his eyes after applying the treatment. He went to school, felt ill, and ended up in an emergency department because he had an enlarged pupil. “You just have to tell people this can happen,” she said.

Dr. Desai reported no relevant disclosures.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Be alert for hidden cases of hyperhidrosis in patients, Seemal R. Desai, MD, said during a presentation on this topic at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

During an examination for another condition, he said, patients may be “sweating and dripping.” However, “you look over that diagnosis because that’s not what they’re there for,” said Dr. Desai, a dermatologist at the University of Texas Southwestern Medical Center in Dallas.

He described one of his patients, who only revealed that she suffered from “horrible, devastating” hyperhidrosis after he’d treated her for years for melasma. The sweating especially affected her because it prevented her from wearing the skin-exposing clothing of her Indian culture.

Delays in treatment are common in hyperhidrosis, which is believed to affect 5% of the world’s population. According to Dr. Desai, research suggests that 85% of patients with hyperhidrosis wait more than 3 years to bring it up with doctors, and half wait more than a decade.

There are many treatments for hyperhidrosis. Some are fairly simple: over-the-counter or prescription antiperspirants, said Dr. Desai, who likes the over-the-counter brand Certain Dri), iontophoresis (application of electric current), topical anticholinergics (including glycopyrronium tosylate cloth wipes, recently approved by the FDA for topical treatment of primary axillary hyperhidrosis for ages 9 years and older), and systemic management. Others are minimally invasive: Botox injections and the miraDry medical device (which relies on thermolysis). And surgical strategies may be an option for severe cases.

On its website, the International Hyperhidrosis Society provides a chart of options for hyperhidrosis in various parts of the body. Treatments tend to focus on the underarms, however, and “we’ve got huge unmet needs for patient options,” Dr. Desai said.
 

• During his presentation, he provided the following pearls regarding hyperhidrosis treatments:
• Distinguish between antiperspirants, which block sweating, and deodorants, which cover up body odor. “Sometimes I get caught up in the middle of a busy office visit and use these terms interchangeably. They’re really different, but patients and the public tend to equate those together,” he commented.
• Make sure patients understand how to properly use antiperspirants and explain that antiperspirants must be applied to dry skin. “Antiperspirant is forming a clog in the drain” to prevent the release of sweat, he said. “If you apply it to wet skin, you will block that chemical reaction in the duct.”
• Massage in the antiperspirant, he advises, and don’t occlude the skin. Apply twice daily, including before bedtime. “They can use antiperspirant on the hands and the bottom of the feet,”Dr. Desai said. “You want to ensure that they’re using the spray on the surface and in the web space. They can also use antiperspirants on the face, but avoid contact with the eyes.”
• Be careful if you prescribe glycopyrronium cloths off label. These wipes are helpful and they can be used outside the FDA-approved use in the underarms, said Dr. Desai, who said he has palmar hyperhidrosis and has successfully used them on his palms, but he hasn’t found them to be helpful on the soles of his feet.

Dr. Desai recommends 5-minute applications on the palms because the treatment can irritate the face and eyes.

Linda F. Stein Gold, MD, of Henry Ford Health System in Detroit, told the audience about the case of a teacher who touched his eyes after applying the treatment. He went to school, felt ill, and ended up in an emergency department because he had an enlarged pupil. “You just have to tell people this can happen,” she said.

Dr. Desai reported no relevant disclosures.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – It is important to think outside the box and consider whether secondary causes of hyperhidrosis are at play when a patient complains of sweating too much, a dermatologist told his colleagues.

“Look at where the patient fits into the sweating paradigm,” advised Seemal R. Desai, MD, of University of Texas Southwestern Medical Center in Dallas, and consider factors such as where and how often patients are oversweating.

In cases of secondary hyperhidrosis – those that are caused by another condition – “the key is to really find the underlying cause of the problem and not just try to treat the sweating,” said Dr. Desai, who spoke in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

According to Dr. Desai, the answers to several questions can help pinpoint a diagnosis of primary hyperhidrosis (also known as focal or primary focal hyperhidrosis) or secondary hyperhidrosis:

• Where does the sweating occur?

Sweating occurs over large parts of the body in patients with secondary hyperhidrosis, Dr. Desai said, although it is typically limited to certain areas, such as the armpits, palms, or soles in the primary form.

• When did the sweating begin?

When sweating begins in adulthood, he said, there’s a good chance that it has a secondary cause. Sweating that began in childhood is more likely to be the primary form.

• How does sweating occur at night?

Dr. Desai advised: “Ask about sleep patterns. Do you sweat during your sleep or wake up feeling like you’re sweating?” Sweating throughout a sleep cycle – not “night sweats” that are brief in nature – indicate a probable secondary cause, he said.

According to Dr. Desai, the causes of secondary hyperhidrosis are numerous, including hypoglycemia, neural tumors, and cardiovascular conditions. “Typically, if I’m trying to figure out why a patient is having generalized sweating, the No. 1 cause is medications.”

Dr. Desai reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – It is important to think outside the box and consider whether secondary causes of hyperhidrosis are at play when a patient complains of sweating too much, a dermatologist told his colleagues.

“Look at where the patient fits into the sweating paradigm,” advised Seemal R. Desai, MD, of University of Texas Southwestern Medical Center in Dallas, and consider factors such as where and how often patients are oversweating.

In cases of secondary hyperhidrosis – those that are caused by another condition – “the key is to really find the underlying cause of the problem and not just try to treat the sweating,” said Dr. Desai, who spoke in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

According to Dr. Desai, the answers to several questions can help pinpoint a diagnosis of primary hyperhidrosis (also known as focal or primary focal hyperhidrosis) or secondary hyperhidrosis:

• Where does the sweating occur?

Sweating occurs over large parts of the body in patients with secondary hyperhidrosis, Dr. Desai said, although it is typically limited to certain areas, such as the armpits, palms, or soles in the primary form.

• When did the sweating begin?

When sweating begins in adulthood, he said, there’s a good chance that it has a secondary cause. Sweating that began in childhood is more likely to be the primary form.

• How does sweating occur at night?

Dr. Desai advised: “Ask about sleep patterns. Do you sweat during your sleep or wake up feeling like you’re sweating?” Sweating throughout a sleep cycle – not “night sweats” that are brief in nature – indicate a probable secondary cause, he said.

According to Dr. Desai, the causes of secondary hyperhidrosis are numerous, including hypoglycemia, neural tumors, and cardiovascular conditions. “Typically, if I’m trying to figure out why a patient is having generalized sweating, the No. 1 cause is medications.”

Dr. Desai reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – It is important to think outside the box and consider whether secondary causes of hyperhidrosis are at play when a patient complains of sweating too much, a dermatologist told his colleagues.

“Look at where the patient fits into the sweating paradigm,” advised Seemal R. Desai, MD, of University of Texas Southwestern Medical Center in Dallas, and consider factors such as where and how often patients are oversweating.

In cases of secondary hyperhidrosis – those that are caused by another condition – “the key is to really find the underlying cause of the problem and not just try to treat the sweating,” said Dr. Desai, who spoke in a presentation at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

According to Dr. Desai, the answers to several questions can help pinpoint a diagnosis of primary hyperhidrosis (also known as focal or primary focal hyperhidrosis) or secondary hyperhidrosis:

• Where does the sweating occur?

Sweating occurs over large parts of the body in patients with secondary hyperhidrosis, Dr. Desai said, although it is typically limited to certain areas, such as the armpits, palms, or soles in the primary form.

• When did the sweating begin?

When sweating begins in adulthood, he said, there’s a good chance that it has a secondary cause. Sweating that began in childhood is more likely to be the primary form.

• How does sweating occur at night?

Dr. Desai advised: “Ask about sleep patterns. Do you sweat during your sleep or wake up feeling like you’re sweating?” Sweating throughout a sleep cycle – not “night sweats” that are brief in nature – indicate a probable secondary cause, he said.

According to Dr. Desai, the causes of secondary hyperhidrosis are numerous, including hypoglycemia, neural tumors, and cardiovascular conditions. “Typically, if I’m trying to figure out why a patient is having generalized sweating, the No. 1 cause is medications.”

Dr. Desai reported no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Merkel cell carcinoma, an extremely rare form of skin cancer, is often caused by a subclinical virus that routinely inhabits the skin. Now, a serum test of virus antibody levels is offering insight into the state of the disease, according to one dermatologist.

“If you have these antibodies, you have a better prognosis. You can follow those antibodies to test for recurrence or progression,” Isaac Brownell, MD, PhD, of the Dermatology Branch of the National Institutes of Health said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The cancer appears in the skin’s Merkel cells, which contribute to our sense of touch by helping us to discriminate textures. “When you put your hand in your pocket, and you can tell the difference between the front and back of a quarter,” he said, “you’re using the Merkel cells in your fingertips.”

Only about 2,500 cases of Merkel cell carcinoma appear in the United States each year, Dr. Brownell said. It appears more often in elderly white patients, is more common in men than women, and is more likely among immunosuppressed patients, whose risk is increased 15- to 20-fold. Cases are more common in sunnier regions – at least in men – and lesions frequently appear on the head, face, and neck.

Five-year survival is estimated at 51% if the cancer is localized, according to a 2016 study of 9,387 cases that Dr. Brownell highlighted. But survival declines dramatically if it has spread to lymph nodes or distant sites (Ann Surg Oncol. 2016 Oct;23[11]:3564-71).

In recent years, researchers have linked 80% of Merkel cell carcinoma cases to the Merkel cell polyomavirus, he said. The virus normally inhabits our skin with no ill effects, he said. “We all have this virus on our skin. It’s everywhere, and even children have antibodies,” he said. But mutations can lead to Merkel cell carcinoma.

Does it matter if cases are polyomavirus positive or polyomavirus negative? Not really, Dr. Brownell said, since the presence of the virus doesn’t appear to affect overall prognosis. However, he said, serum antibody testing can be helpful in polyomavirus-positive patients because it offers insight into prognosis and tumor burden. For example, “if the baseline titer falls and then starts to go up, they’re likely to have a recurrence, and you’ll want to look out for that,” he said.

Dr. Brownell offered another bit of advice: Be prepared to respond to patients who worry that they have a contagious virus and could be a danger to others. The proper answer, he said, is this: “You don’t have to worry about infecting people. Your tumor is not making the virus, you’re not infectious, and we have the virus on us already.”

For more information about the antibody test, visit merkelcell.org/sero.

Dr. Brownell reported having no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Merkel cell carcinoma, an extremely rare form of skin cancer, is often caused by a subclinical virus that routinely inhabits the skin. Now, a serum test of virus antibody levels is offering insight into the state of the disease, according to one dermatologist.

“If you have these antibodies, you have a better prognosis. You can follow those antibodies to test for recurrence or progression,” Isaac Brownell, MD, PhD, of the Dermatology Branch of the National Institutes of Health said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The cancer appears in the skin’s Merkel cells, which contribute to our sense of touch by helping us to discriminate textures. “When you put your hand in your pocket, and you can tell the difference between the front and back of a quarter,” he said, “you’re using the Merkel cells in your fingertips.”

Only about 2,500 cases of Merkel cell carcinoma appear in the United States each year, Dr. Brownell said. It appears more often in elderly white patients, is more common in men than women, and is more likely among immunosuppressed patients, whose risk is increased 15- to 20-fold. Cases are more common in sunnier regions – at least in men – and lesions frequently appear on the head, face, and neck.

Five-year survival is estimated at 51% if the cancer is localized, according to a 2016 study of 9,387 cases that Dr. Brownell highlighted. But survival declines dramatically if it has spread to lymph nodes or distant sites (Ann Surg Oncol. 2016 Oct;23[11]:3564-71).

In recent years, researchers have linked 80% of Merkel cell carcinoma cases to the Merkel cell polyomavirus, he said. The virus normally inhabits our skin with no ill effects, he said. “We all have this virus on our skin. It’s everywhere, and even children have antibodies,” he said. But mutations can lead to Merkel cell carcinoma.

Does it matter if cases are polyomavirus positive or polyomavirus negative? Not really, Dr. Brownell said, since the presence of the virus doesn’t appear to affect overall prognosis. However, he said, serum antibody testing can be helpful in polyomavirus-positive patients because it offers insight into prognosis and tumor burden. For example, “if the baseline titer falls and then starts to go up, they’re likely to have a recurrence, and you’ll want to look out for that,” he said.

Dr. Brownell offered another bit of advice: Be prepared to respond to patients who worry that they have a contagious virus and could be a danger to others. The proper answer, he said, is this: “You don’t have to worry about infecting people. Your tumor is not making the virus, you’re not infectious, and we have the virus on us already.”

For more information about the antibody test, visit merkelcell.org/sero.

Dr. Brownell reported having no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Merkel cell carcinoma, an extremely rare form of skin cancer, is often caused by a subclinical virus that routinely inhabits the skin. Now, a serum test of virus antibody levels is offering insight into the state of the disease, according to one dermatologist.

“If you have these antibodies, you have a better prognosis. You can follow those antibodies to test for recurrence or progression,” Isaac Brownell, MD, PhD, of the Dermatology Branch of the National Institutes of Health said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

The cancer appears in the skin’s Merkel cells, which contribute to our sense of touch by helping us to discriminate textures. “When you put your hand in your pocket, and you can tell the difference between the front and back of a quarter,” he said, “you’re using the Merkel cells in your fingertips.”

Only about 2,500 cases of Merkel cell carcinoma appear in the United States each year, Dr. Brownell said. It appears more often in elderly white patients, is more common in men than women, and is more likely among immunosuppressed patients, whose risk is increased 15- to 20-fold. Cases are more common in sunnier regions – at least in men – and lesions frequently appear on the head, face, and neck.

Five-year survival is estimated at 51% if the cancer is localized, according to a 2016 study of 9,387 cases that Dr. Brownell highlighted. But survival declines dramatically if it has spread to lymph nodes or distant sites (Ann Surg Oncol. 2016 Oct;23[11]:3564-71).

In recent years, researchers have linked 80% of Merkel cell carcinoma cases to the Merkel cell polyomavirus, he said. The virus normally inhabits our skin with no ill effects, he said. “We all have this virus on our skin. It’s everywhere, and even children have antibodies,” he said. But mutations can lead to Merkel cell carcinoma.

Does it matter if cases are polyomavirus positive or polyomavirus negative? Not really, Dr. Brownell said, since the presence of the virus doesn’t appear to affect overall prognosis. However, he said, serum antibody testing can be helpful in polyomavirus-positive patients because it offers insight into prognosis and tumor burden. For example, “if the baseline titer falls and then starts to go up, they’re likely to have a recurrence, and you’ll want to look out for that,” he said.

Dr. Brownell offered another bit of advice: Be prepared to respond to patients who worry that they have a contagious virus and could be a danger to others. The proper answer, he said, is this: “You don’t have to worry about infecting people. Your tumor is not making the virus, you’re not infectious, and we have the virus on us already.”

For more information about the antibody test, visit merkelcell.org/sero.

Dr. Brownell reported having no relevant disclosures. SDEF and this news organization are owned by the same parent company.

LAS VEGAS – When she brings up dermatomyositis in the context of dermatology, Alisa Femia, MD, often hears from trainees and medical students who assume that this is a condition for rheumatologists to diagnose and treat. That’s not true: Dermatologists need to watch for this potentially fatal connective tissue disorder because they may see it first, she said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

“A fifth are clinically amyopathic,” and they may not initially see a rheumatologist, said Dr. Femia, director of inpatient dermatology at the department of dermatology, New York University. “They have normal muscle enzymes and no muscle weakness. It really puts them in our care as dermatologists.”

The challenge is that patient presentations can be subtle, but the stakes may be high, she added. “If we catch them early and treat some of these patients aggressively, we can save their lives.”

During the presentation, Dr. Femia provided these pearls for diagnosing dermatomyositis:

• Don’t rely on tests like biopsies to absolutely tell you what’s going on. “Clinical examination is the most important test to establish the diagnosis,” she said. “If you’re suspecting dermatomyositis ... get the patient in a gown [for a full-body exam] and look for all the signs that might not be as prominent as they are in our textbooks.”
• Look for the “butterfly” rash on the midface that is unique because it spares the nasolabial folds. “It looks like someone took an eraser and wiped out those areas,” Dr. Femia said. “This is important to help us nail down the diagnosis.”
• Other telltale signs, she said, include erythema on the extensor surfaces of digits, severe itching in the scalp, and a rash on the eyelids.
• Be aware of pulmonary involvement, including interstitial lung disease. In some cases, patients and their physicians wrongly believe that patients with dermatomyositis have asthma or pneumonia. “Pulmonologists are not necessarily aware of lung disease associated with dermatomyositis,” she said.

It’s wise to refer patients with dermatomyositis for malignancy and lung disease screening even if they don’t show signs of muscular involvement. “There’s no significant difference in rates of malignancy or lung disease in classic versus amyopathic dermatomyositis.”

Keep the MDA5 form of dermatomyositis in mind, Dr. Femia said. Anti–melanoma differentiation–associated gene 5 dermatomyositis is linked to rapidly progressive interstitial lung disease, alopecia, arthritis and oral lacerations. “Initially, it can have features of lupus, and the patient can be on immunosuppressive therapy, which mitigates diagnostic findings.”

Dr. Femia disclosed serving as principal investigator for a clinical trial in cutaneous dermatomyositis therapy.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – When she brings up dermatomyositis in the context of dermatology, Alisa Femia, MD, often hears from trainees and medical students who assume that this is a condition for rheumatologists to diagnose and treat. That’s not true: Dermatologists need to watch for this potentially fatal connective tissue disorder because they may see it first, she said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

“A fifth are clinically amyopathic,” and they may not initially see a rheumatologist, said Dr. Femia, director of inpatient dermatology at the department of dermatology, New York University. “They have normal muscle enzymes and no muscle weakness. It really puts them in our care as dermatologists.”

The challenge is that patient presentations can be subtle, but the stakes may be high, she added. “If we catch them early and treat some of these patients aggressively, we can save their lives.”

During the presentation, Dr. Femia provided these pearls for diagnosing dermatomyositis:

• Don’t rely on tests like biopsies to absolutely tell you what’s going on. “Clinical examination is the most important test to establish the diagnosis,” she said. “If you’re suspecting dermatomyositis ... get the patient in a gown [for a full-body exam] and look for all the signs that might not be as prominent as they are in our textbooks.”
• Look for the “butterfly” rash on the midface that is unique because it spares the nasolabial folds. “It looks like someone took an eraser and wiped out those areas,” Dr. Femia said. “This is important to help us nail down the diagnosis.”
• Other telltale signs, she said, include erythema on the extensor surfaces of digits, severe itching in the scalp, and a rash on the eyelids.
• Be aware of pulmonary involvement, including interstitial lung disease. In some cases, patients and their physicians wrongly believe that patients with dermatomyositis have asthma or pneumonia. “Pulmonologists are not necessarily aware of lung disease associated with dermatomyositis,” she said.

It’s wise to refer patients with dermatomyositis for malignancy and lung disease screening even if they don’t show signs of muscular involvement. “There’s no significant difference in rates of malignancy or lung disease in classic versus amyopathic dermatomyositis.”

Keep the MDA5 form of dermatomyositis in mind, Dr. Femia said. Anti–melanoma differentiation–associated gene 5 dermatomyositis is linked to rapidly progressive interstitial lung disease, alopecia, arthritis and oral lacerations. “Initially, it can have features of lupus, and the patient can be on immunosuppressive therapy, which mitigates diagnostic findings.”

Dr. Femia disclosed serving as principal investigator for a clinical trial in cutaneous dermatomyositis therapy.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – When she brings up dermatomyositis in the context of dermatology, Alisa Femia, MD, often hears from trainees and medical students who assume that this is a condition for rheumatologists to diagnose and treat. That’s not true: Dermatologists need to watch for this potentially fatal connective tissue disorder because they may see it first, she said at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

“A fifth are clinically amyopathic,” and they may not initially see a rheumatologist, said Dr. Femia, director of inpatient dermatology at the department of dermatology, New York University. “They have normal muscle enzymes and no muscle weakness. It really puts them in our care as dermatologists.”

The challenge is that patient presentations can be subtle, but the stakes may be high, she added. “If we catch them early and treat some of these patients aggressively, we can save their lives.”

During the presentation, Dr. Femia provided these pearls for diagnosing dermatomyositis:

• Don’t rely on tests like biopsies to absolutely tell you what’s going on. “Clinical examination is the most important test to establish the diagnosis,” she said. “If you’re suspecting dermatomyositis ... get the patient in a gown [for a full-body exam] and look for all the signs that might not be as prominent as they are in our textbooks.”
• Look for the “butterfly” rash on the midface that is unique because it spares the nasolabial folds. “It looks like someone took an eraser and wiped out those areas,” Dr. Femia said. “This is important to help us nail down the diagnosis.”
• Other telltale signs, she said, include erythema on the extensor surfaces of digits, severe itching in the scalp, and a rash on the eyelids.
• Be aware of pulmonary involvement, including interstitial lung disease. In some cases, patients and their physicians wrongly believe that patients with dermatomyositis have asthma or pneumonia. “Pulmonologists are not necessarily aware of lung disease associated with dermatomyositis,” she said.

It’s wise to refer patients with dermatomyositis for malignancy and lung disease screening even if they don’t show signs of muscular involvement. “There’s no significant difference in rates of malignancy or lung disease in classic versus amyopathic dermatomyositis.”

Keep the MDA5 form of dermatomyositis in mind, Dr. Femia said. Anti–melanoma differentiation–associated gene 5 dermatomyositis is linked to rapidly progressive interstitial lung disease, alopecia, arthritis and oral lacerations. “Initially, it can have features of lupus, and the patient can be on immunosuppressive therapy, which mitigates diagnostic findings.”

Dr. Femia disclosed serving as principal investigator for a clinical trial in cutaneous dermatomyositis therapy.

SDEF and this news organization are owned by the same parent company.

LAS VEGAS – Based on the best available data to date, certolizumab pegol is likely the best treatment choice for women with psoriasis who become pregnant, Francisco A. Kerdel, BSc, MBBS, said at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Doug Brunk/MDedge News

Dr. Kerdel, professor and vice chair of the department of dermatology at Florida International University, Miami, noted that, while tumor necrosis factor (TNF)–alpha inhibitors are category B drugs, inadequate data exist regarding lactation and exposure throughout pregnancy. “Rates of malformations and spontaneous abortions with therapy are similar to those in the general population, higher concentrations of infliximab and adalimumab have been found in infant and cord blood, compared with certolizumab pegol,” an anti-TNF biologic, he said.

In a prospective, postmarketing, multicenter pharmacokinetic study, researchers found a lack of placental transfer of certolizumab pegol during pregnancy (Ann Rheum Dis. 2018;77:228-33). Specifically, certolizumab levels were below the lower limit of quantification (less than 0.032 mcg/mL) in 13 of 14 infant samples at birth and in all infant samples at weeks 4 and 8. Only one infant had a minimal certolizumab level at birth (infant/mother ratio of 0.0009). No antibodies were detected at any time point during the study. Safety data in mothers were in line with the known safety profile of certolizumab and pregnancy profile of these underlying diseases. Adverse events experienced by the infants did not show any patterns or clusters of events suggesting a specific safety signal in children.

In a separate postmarketing pharmacokinetic study, investigators evaluated the transfer of certolizumab into breast milk (Ann Rheum Dis. 2017;76:1890-6). They found that the average daily infant dose of certolizumab was minimal. Specifically, the highest concentration of certolizumab in breast milk (0.0758 mcg/mL) was less than 1% of the expected mean plasma trough concentration of a therapeutic dose.

How do TNF-alpha inhibitors fare in the pediatric population? In a retrospective study of 390 children with psoriasis treated at 20 centers in the United States, Canada, and Europe, researchers evaluated the safety of systemic agents (JAMA Dermatol. 2017;153[11]:1147-57). Most (69%) were prescribed methotrexate, followed by biologics, acitretin, cyclosporine, and fumaric acid. Drug discontinuation (because of adverse events), which is sometimes used as an efficacy parameter, occurred in 12% of those who were on methotrexate, compared with 3% of those on biologics, 67% of those on acitretin, and 68% of those on fumaric acid.

At the other end of the age spectrum, biologic therapy is generally effective and well tolerated in elderly patients. “Sometimes, they may be more effective than other traditional drugs,” Dr. Kerdel said. “We’re a little bit concerned about immunosenescence, which can increase the risk for severe infections and malignancies. And, 90% of elderly patients with psoriasis may have comorbidities that need to be taken into account when treating psoriasis.”

Other factors come into play when choosing the right anti-TNF agent, including weight. While clinical trials show efficacy across weight groups, infliximab has weight-based dosing, “which may make it a better choice,” Dr. Kerdel said. “Patients taking etanercept may need a biweekly dose.”

Treatment flexibility also comes into play. For example, stopping therapy because of an infection or surgery may be problematic in drugs with a long half-life. Then there’s the issue of patient preference. “Some people don’t want to be injected frequently,” he said. “Some people don’t want to be injected at all and may require a simpler dosing regimen.”

Optimizing anti-TNF-alpha treatment starts with recognizing that there is a loss of response over time, Dr. Kerdel said, “or there may not be a response at all.” Contributing factors may include immunogenicity, suboptimal dosing, and poor patient adherence. In order to optimize treatment, clinicians can try switching agents or combination therapy, and explore continuous versus intermittent dosing.

“We really don’t have good data on the best protocol for switching treatment after failure of an anti-TNF-alpha agent,” he added. In cases of primary and secondary treatment failure, there is no consensus or guidelines on which second-line agent to use, nor good data on which measures to use.

No evidence-based guidelines are available for screening and monitoring patients receiving biologic therapy for psoriasis, either. “Evidence is strongest [grade B] for tuberculosis screening in patients treated with biologic agents,” Dr. Kerdel said. “Among known hepatitis B virus carriers, consider monitoring liver function tests and viral load [grade C]. High-grade evidence is lacking to support other routine testing. Physicians should use clinical judgment when screening and monitoring patients.”

He concluded his presentation by noting that there are a number of biosimilar agents available or in the pipeline for infliximab, adalimumab, and etanercept. This raises a number of questions for current and future consideration. For one, “will biosimilars show the same long-term efficacy and safety as the innovator products?” he asked. “Real-world, postmarketing, and registry data are needed. Will biosimilar agents offer significant cost benefits? Will biosimilar labeling be adequately transparent? Will we find biomarkers to help us target biologic agents to specific patients and subtypes of psoriasis?”

Dr. Kerdel reported that he is a member of the speaker’s bureau for AbbVie, Amgen, Celgene, Janssen, Novartis, Lilly, Leo, Ortho, and Novartis. He has also received grant/research support from AbbVie, Amgen, AstraZeneca, Celgene, Janssen, Leo, Lilly, Menlo Therapeutics, Novartis, Pfizer, and XBiotech.

SDEF and this news organization are owned by the same parent company.

dbrunk@mdedge.com

LAS VEGAS – Based on the best available data to date, certolizumab pegol is likely the best treatment choice for women with psoriasis who become pregnant, Francisco A. Kerdel, BSc, MBBS, said at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Doug Brunk/MDedge News

Dr. Kerdel, professor and vice chair of the department of dermatology at Florida International University, Miami, noted that, while tumor necrosis factor (TNF)–alpha inhibitors are category B drugs, inadequate data exist regarding lactation and exposure throughout pregnancy. “Rates of malformations and spontaneous abortions with therapy are similar to those in the general population, higher concentrations of infliximab and adalimumab have been found in infant and cord blood, compared with certolizumab pegol,” an anti-TNF biologic, he said.

In a prospective, postmarketing, multicenter pharmacokinetic study, researchers found a lack of placental transfer of certolizumab pegol during pregnancy (Ann Rheum Dis. 2018;77:228-33). Specifically, certolizumab levels were below the lower limit of quantification (less than 0.032 mcg/mL) in 13 of 14 infant samples at birth and in all infant samples at weeks 4 and 8. Only one infant had a minimal certolizumab level at birth (infant/mother ratio of 0.0009). No antibodies were detected at any time point during the study. Safety data in mothers were in line with the known safety profile of certolizumab and pregnancy profile of these underlying diseases. Adverse events experienced by the infants did not show any patterns or clusters of events suggesting a specific safety signal in children.

In a separate postmarketing pharmacokinetic study, investigators evaluated the transfer of certolizumab into breast milk (Ann Rheum Dis. 2017;76:1890-6). They found that the average daily infant dose of certolizumab was minimal. Specifically, the highest concentration of certolizumab in breast milk (0.0758 mcg/mL) was less than 1% of the expected mean plasma trough concentration of a therapeutic dose.

How do TNF-alpha inhibitors fare in the pediatric population? In a retrospective study of 390 children with psoriasis treated at 20 centers in the United States, Canada, and Europe, researchers evaluated the safety of systemic agents (JAMA Dermatol. 2017;153[11]:1147-57). Most (69%) were prescribed methotrexate, followed by biologics, acitretin, cyclosporine, and fumaric acid. Drug discontinuation (because of adverse events), which is sometimes used as an efficacy parameter, occurred in 12% of those who were on methotrexate, compared with 3% of those on biologics, 67% of those on acitretin, and 68% of those on fumaric acid.

At the other end of the age spectrum, biologic therapy is generally effective and well tolerated in elderly patients. “Sometimes, they may be more effective than other traditional drugs,” Dr. Kerdel said. “We’re a little bit concerned about immunosenescence, which can increase the risk for severe infections and malignancies. And, 90% of elderly patients with psoriasis may have comorbidities that need to be taken into account when treating psoriasis.”

Other factors come into play when choosing the right anti-TNF agent, including weight. While clinical trials show efficacy across weight groups, infliximab has weight-based dosing, “which may make it a better choice,” Dr. Kerdel said. “Patients taking etanercept may need a biweekly dose.”

Treatment flexibility also comes into play. For example, stopping therapy because of an infection or surgery may be problematic in drugs with a long half-life. Then there’s the issue of patient preference. “Some people don’t want to be injected frequently,” he said. “Some people don’t want to be injected at all and may require a simpler dosing regimen.”

Optimizing anti-TNF-alpha treatment starts with recognizing that there is a loss of response over time, Dr. Kerdel said, “or there may not be a response at all.” Contributing factors may include immunogenicity, suboptimal dosing, and poor patient adherence. In order to optimize treatment, clinicians can try switching agents or combination therapy, and explore continuous versus intermittent dosing.

“We really don’t have good data on the best protocol for switching treatment after failure of an anti-TNF-alpha agent,” he added. In cases of primary and secondary treatment failure, there is no consensus or guidelines on which second-line agent to use, nor good data on which measures to use.

No evidence-based guidelines are available for screening and monitoring patients receiving biologic therapy for psoriasis, either. “Evidence is strongest [grade B] for tuberculosis screening in patients treated with biologic agents,” Dr. Kerdel said. “Among known hepatitis B virus carriers, consider monitoring liver function tests and viral load [grade C]. High-grade evidence is lacking to support other routine testing. Physicians should use clinical judgment when screening and monitoring patients.”

He concluded his presentation by noting that there are a number of biosimilar agents available or in the pipeline for infliximab, adalimumab, and etanercept. This raises a number of questions for current and future consideration. For one, “will biosimilars show the same long-term efficacy and safety as the innovator products?” he asked. “Real-world, postmarketing, and registry data are needed. Will biosimilar agents offer significant cost benefits? Will biosimilar labeling be adequately transparent? Will we find biomarkers to help us target biologic agents to specific patients and subtypes of psoriasis?”

Dr. Kerdel reported that he is a member of the speaker’s bureau for AbbVie, Amgen, Celgene, Janssen, Novartis, Lilly, Leo, Ortho, and Novartis. He has also received grant/research support from AbbVie, Amgen, AstraZeneca, Celgene, Janssen, Leo, Lilly, Menlo Therapeutics, Novartis, Pfizer, and XBiotech.

SDEF and this news organization are owned by the same parent company.

dbrunk@mdedge.com

LAS VEGAS – Based on the best available data to date, certolizumab pegol is likely the best treatment choice for women with psoriasis who become pregnant, Francisco A. Kerdel, BSc, MBBS, said at the Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Doug Brunk/MDedge News

Dr. Kerdel, professor and vice chair of the department of dermatology at Florida International University, Miami, noted that, while tumor necrosis factor (TNF)–alpha inhibitors are category B drugs, inadequate data exist regarding lactation and exposure throughout pregnancy. “Rates of malformations and spontaneous abortions with therapy are similar to those in the general population, higher concentrations of infliximab and adalimumab have been found in infant and cord blood, compared with certolizumab pegol,” an anti-TNF biologic, he said.

In a prospective, postmarketing, multicenter pharmacokinetic study, researchers found a lack of placental transfer of certolizumab pegol during pregnancy (Ann Rheum Dis. 2018;77:228-33). Specifically, certolizumab levels were below the lower limit of quantification (less than 0.032 mcg/mL) in 13 of 14 infant samples at birth and in all infant samples at weeks 4 and 8. Only one infant had a minimal certolizumab level at birth (infant/mother ratio of 0.0009). No antibodies were detected at any time point during the study. Safety data in mothers were in line with the known safety profile of certolizumab and pregnancy profile of these underlying diseases. Adverse events experienced by the infants did not show any patterns or clusters of events suggesting a specific safety signal in children.

In a separate postmarketing pharmacokinetic study, investigators evaluated the transfer of certolizumab into breast milk (Ann Rheum Dis. 2017;76:1890-6). They found that the average daily infant dose of certolizumab was minimal. Specifically, the highest concentration of certolizumab in breast milk (0.0758 mcg/mL) was less than 1% of the expected mean plasma trough concentration of a therapeutic dose.

How do TNF-alpha inhibitors fare in the pediatric population? In a retrospective study of 390 children with psoriasis treated at 20 centers in the United States, Canada, and Europe, researchers evaluated the safety of systemic agents (JAMA Dermatol. 2017;153[11]:1147-57). Most (69%) were prescribed methotrexate, followed by biologics, acitretin, cyclosporine, and fumaric acid. Drug discontinuation (because of adverse events), which is sometimes used as an efficacy parameter, occurred in 12% of those who were on methotrexate, compared with 3% of those on biologics, 67% of those on acitretin, and 68% of those on fumaric acid.

At the other end of the age spectrum, biologic therapy is generally effective and well tolerated in elderly patients. “Sometimes, they may be more effective than other traditional drugs,” Dr. Kerdel said. “We’re a little bit concerned about immunosenescence, which can increase the risk for severe infections and malignancies. And, 90% of elderly patients with psoriasis may have comorbidities that need to be taken into account when treating psoriasis.”

Other factors come into play when choosing the right anti-TNF agent, including weight. While clinical trials show efficacy across weight groups, infliximab has weight-based dosing, “which may make it a better choice,” Dr. Kerdel said. “Patients taking etanercept may need a biweekly dose.”

Treatment flexibility also comes into play. For example, stopping therapy because of an infection or surgery may be problematic in drugs with a long half-life. Then there’s the issue of patient preference. “Some people don’t want to be injected frequently,” he said. “Some people don’t want to be injected at all and may require a simpler dosing regimen.”

Optimizing anti-TNF-alpha treatment starts with recognizing that there is a loss of response over time, Dr. Kerdel said, “or there may not be a response at all.” Contributing factors may include immunogenicity, suboptimal dosing, and poor patient adherence. In order to optimize treatment, clinicians can try switching agents or combination therapy, and explore continuous versus intermittent dosing.

“We really don’t have good data on the best protocol for switching treatment after failure of an anti-TNF-alpha agent,” he added. In cases of primary and secondary treatment failure, there is no consensus or guidelines on which second-line agent to use, nor good data on which measures to use.

No evidence-based guidelines are available for screening and monitoring patients receiving biologic therapy for psoriasis, either. “Evidence is strongest [grade B] for tuberculosis screening in patients treated with biologic agents,” Dr. Kerdel said. “Among known hepatitis B virus carriers, consider monitoring liver function tests and viral load [grade C]. High-grade evidence is lacking to support other routine testing. Physicians should use clinical judgment when screening and monitoring patients.”

He concluded his presentation by noting that there are a number of biosimilar agents available or in the pipeline for infliximab, adalimumab, and etanercept. This raises a number of questions for current and future consideration. For one, “will biosimilars show the same long-term efficacy and safety as the innovator products?” he asked. “Real-world, postmarketing, and registry data are needed. Will biosimilar agents offer significant cost benefits? Will biosimilar labeling be adequately transparent? Will we find biomarkers to help us target biologic agents to specific patients and subtypes of psoriasis?”

Dr. Kerdel reported that he is a member of the speaker’s bureau for AbbVie, Amgen, Celgene, Janssen, Novartis, Lilly, Leo, Ortho, and Novartis. He has also received grant/research support from AbbVie, Amgen, AstraZeneca, Celgene, Janssen, Leo, Lilly, Menlo Therapeutics, Novartis, Pfizer, and XBiotech.

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dbrunk@mdedge.com