Dermatology

Collagen powder may be noninferior to primary closure for healing punch biopsy–induced wounds and possibly leads to improved early cosmetic outcomes and accelerated wound maturation, according to Azam Qureshi of the University of Maryland, Baltimore, and associates.

In a small pilot study published in Journal of Drugs in Dermatology, eight volunteers (mean age, 37 years) received a 4-mm punch biopsy on each thigh. One wound was managed with primary closure, the other with daily application of collagen powder. The wounds were biopsied at 4 weeks for histopathologic analysis, and the study subjects rated pain, itch, and treatment preferences at 1, 2, 4, 6, and 12 weeks.

The size of wounds treated with collagen was reduced by 28.95% at 1 week, 55.76% at 2 weeks, and 95.94% at 4 weeks; six of the eight collagen-treated wounds were completely healed at 4 weeks. Wound size was reduced by 75.71% 1 week after the second biopsy, much faster than the initial healing. In addition to collagen, one patient required hyfrecation for hemostasis, which did not affect results; three of the eight subjects rated the collagen treatment as “annoying,” but no one rated it as “difficult,” and patients generally regarded collagen treatment as more time consuming.

The histopathologic analysis showed epidermal reepithelialization in collagen-treated wounds and wounds managed with primary closure, with more organized granulation tissue in the collagen-treated wounds. Similar pain and itch ratings were reported between wound types, and both patients and blinded dermatologists observing the study preferred the appearance of collagen-treated wounds.

“Future research elucidating the optimal duration of collagen therapy is needed, as less than 4 weeks may be sufficient. Shortened treatment courses would decrease the cost and effort required by patients. Future studies should also investigate the efficacy of collagen powder in healing larger wounds and in comparison to healing by secondary intention,” the investigators wrote.

CPN Biosciences funded the study. No authors had relevant financial disclosures.

[email protected]

SOURCE: Qureshi A et al. J Drug Dermatol. 2019;18(7):667-73

Collagen powder may be noninferior to primary closure for healing punch biopsy–induced wounds and possibly leads to improved early cosmetic outcomes and accelerated wound maturation, according to Azam Qureshi of the University of Maryland, Baltimore, and associates.

In a small pilot study published in Journal of Drugs in Dermatology, eight volunteers (mean age, 37 years) received a 4-mm punch biopsy on each thigh. One wound was managed with primary closure, the other with daily application of collagen powder. The wounds were biopsied at 4 weeks for histopathologic analysis, and the study subjects rated pain, itch, and treatment preferences at 1, 2, 4, 6, and 12 weeks.

The size of wounds treated with collagen was reduced by 28.95% at 1 week, 55.76% at 2 weeks, and 95.94% at 4 weeks; six of the eight collagen-treated wounds were completely healed at 4 weeks. Wound size was reduced by 75.71% 1 week after the second biopsy, much faster than the initial healing. In addition to collagen, one patient required hyfrecation for hemostasis, which did not affect results; three of the eight subjects rated the collagen treatment as “annoying,” but no one rated it as “difficult,” and patients generally regarded collagen treatment as more time consuming.

The histopathologic analysis showed epidermal reepithelialization in collagen-treated wounds and wounds managed with primary closure, with more organized granulation tissue in the collagen-treated wounds. Similar pain and itch ratings were reported between wound types, and both patients and blinded dermatologists observing the study preferred the appearance of collagen-treated wounds.

“Future research elucidating the optimal duration of collagen therapy is needed, as less than 4 weeks may be sufficient. Shortened treatment courses would decrease the cost and effort required by patients. Future studies should also investigate the efficacy of collagen powder in healing larger wounds and in comparison to healing by secondary intention,” the investigators wrote.

CPN Biosciences funded the study. No authors had relevant financial disclosures.

[email protected]

SOURCE: Qureshi A et al. J Drug Dermatol. 2019;18(7):667-73

Collagen powder may be noninferior to primary closure for healing punch biopsy–induced wounds and possibly leads to improved early cosmetic outcomes and accelerated wound maturation, according to Azam Qureshi of the University of Maryland, Baltimore, and associates.

In a small pilot study published in Journal of Drugs in Dermatology, eight volunteers (mean age, 37 years) received a 4-mm punch biopsy on each thigh. One wound was managed with primary closure, the other with daily application of collagen powder. The wounds were biopsied at 4 weeks for histopathologic analysis, and the study subjects rated pain, itch, and treatment preferences at 1, 2, 4, 6, and 12 weeks.

The size of wounds treated with collagen was reduced by 28.95% at 1 week, 55.76% at 2 weeks, and 95.94% at 4 weeks; six of the eight collagen-treated wounds were completely healed at 4 weeks. Wound size was reduced by 75.71% 1 week after the second biopsy, much faster than the initial healing. In addition to collagen, one patient required hyfrecation for hemostasis, which did not affect results; three of the eight subjects rated the collagen treatment as “annoying,” but no one rated it as “difficult,” and patients generally regarded collagen treatment as more time consuming.

The histopathologic analysis showed epidermal reepithelialization in collagen-treated wounds and wounds managed with primary closure, with more organized granulation tissue in the collagen-treated wounds. Similar pain and itch ratings were reported between wound types, and both patients and blinded dermatologists observing the study preferred the appearance of collagen-treated wounds.

“Future research elucidating the optimal duration of collagen therapy is needed, as less than 4 weeks may be sufficient. Shortened treatment courses would decrease the cost and effort required by patients. Future studies should also investigate the efficacy of collagen powder in healing larger wounds and in comparison to healing by secondary intention,” the investigators wrote.

CPN Biosciences funded the study. No authors had relevant financial disclosures.

[email protected]

SOURCE: Qureshi A et al. J Drug Dermatol. 2019;18(7):667-73

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at [email protected].

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at [email protected].

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

Nummular dermatitis, or nummular eczema, is an inflammatory skin condition that is considered to be a distinctive form of idiopathic eczema, while the term also is used to describe lesional morphology associated with other conditions.

The term nummular derives from the Latin word for “coin,” as lesions are commonly annular plaques. Lesions of nummular dermatitis can be single or multiple. The typical distribution involves the extremities and, although less common, it can affect the trunk as well. The morphology of lesions is consistent with a localized eczematous reaction, with induration, oozing, crusting, and/or scaling.

Nummular dermatitis may be associated with atopic dermatitis, or it can be an isolated condition.¹ While the pathogenesis is uncertain, instigating factors include xerotic skin, insect bites, or scratches or scrapes.¹Staphylococcus infection or colonization, contact allergies to metals such as nickel and less commonly mercury, sensitivity to formaldehyde or medicines such as neomycin, and sensitization to an environmental aeroallergen (such as Candida albicans, dust mites) are considered risk factors.²

The diagnosis of nummular dermatitis is clinical. Laboratory testing and/or biopsy generally are not necessary, although a bacterial culture can be considered in patients with exudative and/or crusted lesions to rule out impetigo as a primary process of secondary infection. In some cases, patch testing for allergic contact dermatitis may be useful.

The differential diagnosis of nummular dermatitis includes tinea corporis (ringworm), atopic dermatitis, allergic contact dermatitis, impetigo, and psoriasis. Tinea corporis usually presents as annular lesions with a distinct peripheral scaling, rather than the diffuse induration of nummular dermatitis. Potassium hydroxide preparation or fungal culture can identify tinea species. Nummular dermatitis may be seen in patients with atopic dermatitis, who should have typical history, morphology, and course consistent with standard diagnostic criteria. Allergic contact dermatitis can present with regional, localized eczematous plaques in areas exposed to contact allergens. Patterns of lesions in areas of contact and worsening with repeat exposures can be clues to this diagnosis. Impetigo can present with honey-colored crusted lesions and/or superficial erosions, or purulent pyoderma. Lesions can be single or multiple and generally appear less inflammatory than nummular dermatitis. Psoriasis lesions may be annular, are more common on extensor surfaces, and usually have more prominent overlying pinkish, silvery white or micaceous scale.

Management of nummular dermatitis requires strong anti-inflammatory medications, usually mid-potency or higher topical corticosteroids, along with moisturizers and limiting exposure to skin irritants. “Wet wraps,” with application of topical corticosteroids to wet skin with occlusive wet dressings can enhance response. Transition from higher strength topical corticosteroids to lower strength agents used intermittently can help achieve remission or cure. Management practices include less frequent bathing with lukewarm water, using hypoallergenic cleansers and detergents, and applying moisturizers frequently. If plaques do recur, they tend to do so in the same location and in some patients resolution may result in hyper or hypopigmentation. Refractory disease may be managed with intralesional steroid injections, or systemic medications such as methotrexate.³

Dr. Tracy is a research fellow in pediatric dermatology at Rady Children’s Hospital–San Diego and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Tracy nor Dr. Eichenfield have any relevant financial disclosures. Email them at [email protected].

References

1. Pediatr Dermatol. 2012 Sep-Oct;29(5):580-3.

2. American Academy of Dermatology. Nummular Dermatitis Overview

3. Pediatr Dermatol. 2018 Sep;35(5):611-5.

The number of pregnancies among women taking isotretinoin has decreased since the introduction of the iPledge program, but pregnancy, abortions, and fetal defects associated with isotretinoin exposure are still occurring in women of reproductive age, according to a retrospective study published in JAMA Dermatology.

In 2006, the Food and Drug Administration implemented the iPledge program, with requirements that include women of childbearing age having a negative pregnancy test and evidence of using two forms of contraception monthly to use isotretinoin, a teratogen. “Although the number of pregnancy-related adverse events for patients taking isotretinoin has decreased since 2006, pregnancies, abortions, and fetal defects associated with isotretinoin exposure continue to be a problem,” Elizabeth Tkachenko, BS, from the University of Massachusetts Medical School, Worcester, and coauthors concluded. “Further research is required to determine the most efficacious system to reduce complications for patients and administrative requirements for physicians while at the same time maintaining access to this important drug.” (iPledge followed other Risk Evaluation and Mitigation Strategy systems for isotretinoin.)

She and her colleagues performed a retrospective evaluation of pregnancy-related adverse events related to isotretinoin that had occurred between January 1997 and December 2017 using the FDA Adverse Event Reporting System (FAERS), which receives reports from prescribers, consumers, and pharmaceutical manufacturers. While there could be many different classification terms for each individual, any number of adverse events reported by an individual was counted as one pregnancy. Ms. Tkachenko and colleagues classified abortions, pregnancies during contraception use, and pregnancy-related defects into separate subgroups for analysis.

From 1997 to 2017, there were 6,740 pregnancies among women (mean age, 24.6 years) during treatment with isotretinoin reported to FAERS, with 7 reports in 1997, and a peak of 768 pregnancies in 2006. Almost 70% (4,647) of the pregnancies were reported after iPledge was introduced. Between 2011 and 2017, there were 218-310 pregnancy reports each year.

Of the total number of pregnancy reports during the study period, 1,896 were abortions (28.1% of the total); 10.9% of the total number of pregnancy reports were spontaneous abortions (733). The number of abortions peaked in 2008, with 291 reports, of which 85% were therapeutic abortions. Also peaking in 2008 was the number of reports of pregnancies while taking a contraceptive (64). After 2008, pregnancies and abortions dropped.

Fetal defects peaked in 2000, with 34 cases reported, and dropped to four or fewer reports annually after 2008.

“Our findings demonstrate that reports of pregnancy among women taking isotretinoin are concentrated among those aged 20 to 29 years, peaked in 2006, and have been consistent since 2011,” the authors wrote.

Limitations of the study, they noted, include limitations of FAERS data and possible reporting fatigue among doctors and patients. The total number of isotretinoin courses prescribed to this patient population is also unknown, which affected their ability to determine the true rate of pregnancy-related adverse events, they noted.

The other authors for this study were from Harvard Medical School and the departments of dermatology at Brigham and Women’s Hospital, both in Boston, as well as the University of Pennsylvania, Philadelphia. One author reported support from an award by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health and salary support from a Pfizer Fellowship in Dermatology Patient Oriented Research grant to the trustees of the University of Pennsylvania. The other authors reported no relevant conflicts of interest.

SOURCE: Tkachenko E et al. JAMA Dermatol. 2019. doi: 10.1001/jamadermatol.2019.1388.

The number of pregnancies among women taking isotretinoin has decreased since the introduction of the iPledge program, but pregnancy, abortions, and fetal defects associated with isotretinoin exposure are still occurring in women of reproductive age, according to a retrospective study published in JAMA Dermatology.

In 2006, the Food and Drug Administration implemented the iPledge program, with requirements that include women of childbearing age having a negative pregnancy test and evidence of using two forms of contraception monthly to use isotretinoin, a teratogen. “Although the number of pregnancy-related adverse events for patients taking isotretinoin has decreased since 2006, pregnancies, abortions, and fetal defects associated with isotretinoin exposure continue to be a problem,” Elizabeth Tkachenko, BS, from the University of Massachusetts Medical School, Worcester, and coauthors concluded. “Further research is required to determine the most efficacious system to reduce complications for patients and administrative requirements for physicians while at the same time maintaining access to this important drug.” (iPledge followed other Risk Evaluation and Mitigation Strategy systems for isotretinoin.)

She and her colleagues performed a retrospective evaluation of pregnancy-related adverse events related to isotretinoin that had occurred between January 1997 and December 2017 using the FDA Adverse Event Reporting System (FAERS), which receives reports from prescribers, consumers, and pharmaceutical manufacturers. While there could be many different classification terms for each individual, any number of adverse events reported by an individual was counted as one pregnancy. Ms. Tkachenko and colleagues classified abortions, pregnancies during contraception use, and pregnancy-related defects into separate subgroups for analysis.

From 1997 to 2017, there were 6,740 pregnancies among women (mean age, 24.6 years) during treatment with isotretinoin reported to FAERS, with 7 reports in 1997, and a peak of 768 pregnancies in 2006. Almost 70% (4,647) of the pregnancies were reported after iPledge was introduced. Between 2011 and 2017, there were 218-310 pregnancy reports each year.

Of the total number of pregnancy reports during the study period, 1,896 were abortions (28.1% of the total); 10.9% of the total number of pregnancy reports were spontaneous abortions (733). The number of abortions peaked in 2008, with 291 reports, of which 85% were therapeutic abortions. Also peaking in 2008 was the number of reports of pregnancies while taking a contraceptive (64). After 2008, pregnancies and abortions dropped.

Fetal defects peaked in 2000, with 34 cases reported, and dropped to four or fewer reports annually after 2008.

“Our findings demonstrate that reports of pregnancy among women taking isotretinoin are concentrated among those aged 20 to 29 years, peaked in 2006, and have been consistent since 2011,” the authors wrote.

Limitations of the study, they noted, include limitations of FAERS data and possible reporting fatigue among doctors and patients. The total number of isotretinoin courses prescribed to this patient population is also unknown, which affected their ability to determine the true rate of pregnancy-related adverse events, they noted.

The other authors for this study were from Harvard Medical School and the departments of dermatology at Brigham and Women’s Hospital, both in Boston, as well as the University of Pennsylvania, Philadelphia. One author reported support from an award by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health and salary support from a Pfizer Fellowship in Dermatology Patient Oriented Research grant to the trustees of the University of Pennsylvania. The other authors reported no relevant conflicts of interest.

SOURCE: Tkachenko E et al. JAMA Dermatol. 2019. doi: 10.1001/jamadermatol.2019.1388.

The number of pregnancies among women taking isotretinoin has decreased since the introduction of the iPledge program, but pregnancy, abortions, and fetal defects associated with isotretinoin exposure are still occurring in women of reproductive age, according to a retrospective study published in JAMA Dermatology.

In 2006, the Food and Drug Administration implemented the iPledge program, with requirements that include women of childbearing age having a negative pregnancy test and evidence of using two forms of contraception monthly to use isotretinoin, a teratogen. “Although the number of pregnancy-related adverse events for patients taking isotretinoin has decreased since 2006, pregnancies, abortions, and fetal defects associated with isotretinoin exposure continue to be a problem,” Elizabeth Tkachenko, BS, from the University of Massachusetts Medical School, Worcester, and coauthors concluded. “Further research is required to determine the most efficacious system to reduce complications for patients and administrative requirements for physicians while at the same time maintaining access to this important drug.” (iPledge followed other Risk Evaluation and Mitigation Strategy systems for isotretinoin.)

She and her colleagues performed a retrospective evaluation of pregnancy-related adverse events related to isotretinoin that had occurred between January 1997 and December 2017 using the FDA Adverse Event Reporting System (FAERS), which receives reports from prescribers, consumers, and pharmaceutical manufacturers. While there could be many different classification terms for each individual, any number of adverse events reported by an individual was counted as one pregnancy. Ms. Tkachenko and colleagues classified abortions, pregnancies during contraception use, and pregnancy-related defects into separate subgroups for analysis.

From 1997 to 2017, there were 6,740 pregnancies among women (mean age, 24.6 years) during treatment with isotretinoin reported to FAERS, with 7 reports in 1997, and a peak of 768 pregnancies in 2006. Almost 70% (4,647) of the pregnancies were reported after iPledge was introduced. Between 2011 and 2017, there were 218-310 pregnancy reports each year.

Of the total number of pregnancy reports during the study period, 1,896 were abortions (28.1% of the total); 10.9% of the total number of pregnancy reports were spontaneous abortions (733). The number of abortions peaked in 2008, with 291 reports, of which 85% were therapeutic abortions. Also peaking in 2008 was the number of reports of pregnancies while taking a contraceptive (64). After 2008, pregnancies and abortions dropped.

Fetal defects peaked in 2000, with 34 cases reported, and dropped to four or fewer reports annually after 2008.

“Our findings demonstrate that reports of pregnancy among women taking isotretinoin are concentrated among those aged 20 to 29 years, peaked in 2006, and have been consistent since 2011,” the authors wrote.

Limitations of the study, they noted, include limitations of FAERS data and possible reporting fatigue among doctors and patients. The total number of isotretinoin courses prescribed to this patient population is also unknown, which affected their ability to determine the true rate of pregnancy-related adverse events, they noted.

The other authors for this study were from Harvard Medical School and the departments of dermatology at Brigham and Women’s Hospital, both in Boston, as well as the University of Pennsylvania, Philadelphia. One author reported support from an award by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health and salary support from a Pfizer Fellowship in Dermatology Patient Oriented Research grant to the trustees of the University of Pennsylvania. The other authors reported no relevant conflicts of interest.

SOURCE: Tkachenko E et al. JAMA Dermatol. 2019. doi: 10.1001/jamadermatol.2019.1388.

Since birth, this 5-month-old boy has had a facial rash that comes and goes. At times severe, it is the source of much familial disagreement about its cause: Some say the problem is related to food, while others are sure it represents infection.

Several medications, including triple-antibiotic ointment and nystatin cream, have been tried. None have had much effect.

The child is well in all other respects—gaining weight as expected and experiencing normal growth and development. The rash does not appear to bother him as much as it bothers his family to see.

Further questioning reveals a strong family history of seasonal allergies, eczema, and asthma. Notably, all affected individuals have long since outgrown those problems.

EXAMINATION
The child is in no apparent distress but is noted to have nasal congestion, with continual mouth breathing. Overall, his skin is quite dry and fair.

The rash itself is rather florid, affecting the perioral area and spreading onto the cheeks in a symmetrical configuration. The skin in these areas is focally erythematous, though not swollen. It is also quite scaly in places, giving the appearance of, as his parents note, “chapped” skin. Examination of the diaper area reveals a similar look focally.

What’s the diagnosis?

DISCUSSION
This case is typical of those seen multiple times daily in primary care and dermatology offices—hardly surprising, since atopic dermatitis (AD) affects about 20% of all newborns in this and other developed countries. In very young children, AD primarily affects the face and diaper area, as well as the trunk. About 50% of affected patients will have cradle cap—as did this child in his first month of life, we subsequently learned.

The tendency to develop AD is inherited. It is not related to food, although children with AD could develop a food allergy. However, it would more likely manifest with gastrointestinal symptoms. Another myth embedded in Western culture is that AD is caused by exposure to a particular laundry detergent.

Rather, this child and others like him have inherited dry, thin, overreactive skin that is bathed early on with nasal secretions, bacteria, and saliva. Later, their eczema will migrate to areas that stay moist, such as the antecubital and popliteal folds, or to the area around the neck, where the itching can be intense—which of course causes the child to scratch, in turn worsening the problem.

Patient/parent education is the key to dealing with AD and can be bolstered by handouts or direction to reliable websites. Besides objectifying the problem, these resources detail its nature and outline the need for daily bathing with mild cleansers, generous application of heavy moisturizers, careful use of topical corticosteroid creams or ointments (eg, 2.5% hydrocortisone), and avoidance of woolen clothing or bedding.

Another important component of patient/parent education is the reassurance that eczema will not scar the patient. It does occasionally become severe enough to require a short course of oral antibiotics (eg, cephalexin) or even the use of oral prednisolone. Since AD is not a histamine-driven process, antihistamines are ineffective for eczema.

TAKE-HOME LEARNING POINTS

• Atopic dermatitis (AD) is extremely common, affecting 20% of all newborns in developed countries.
• Infantile eczema typically centers on the face, particularly the perioral area.
• Later, it begins to involve the antecubital and popliteal areas, which stay moist a good part of the time.
• Most children outgrow the worst of the problem—and go on to have children who develop it.

Since birth, this 5-month-old boy has had a facial rash that comes and goes. At times severe, it is the source of much familial disagreement about its cause: Some say the problem is related to food, while others are sure it represents infection.

Several medications, including triple-antibiotic ointment and nystatin cream, have been tried. None have had much effect.

The child is well in all other respects—gaining weight as expected and experiencing normal growth and development. The rash does not appear to bother him as much as it bothers his family to see.

Further questioning reveals a strong family history of seasonal allergies, eczema, and asthma. Notably, all affected individuals have long since outgrown those problems.

EXAMINATION
The child is in no apparent distress but is noted to have nasal congestion, with continual mouth breathing. Overall, his skin is quite dry and fair.

The rash itself is rather florid, affecting the perioral area and spreading onto the cheeks in a symmetrical configuration. The skin in these areas is focally erythematous, though not swollen. It is also quite scaly in places, giving the appearance of, as his parents note, “chapped” skin. Examination of the diaper area reveals a similar look focally.

What’s the diagnosis?

DISCUSSION
This case is typical of those seen multiple times daily in primary care and dermatology offices—hardly surprising, since atopic dermatitis (AD) affects about 20% of all newborns in this and other developed countries. In very young children, AD primarily affects the face and diaper area, as well as the trunk. About 50% of affected patients will have cradle cap—as did this child in his first month of life, we subsequently learned.

The tendency to develop AD is inherited. It is not related to food, although children with AD could develop a food allergy. However, it would more likely manifest with gastrointestinal symptoms. Another myth embedded in Western culture is that AD is caused by exposure to a particular laundry detergent.

Rather, this child and others like him have inherited dry, thin, overreactive skin that is bathed early on with nasal secretions, bacteria, and saliva. Later, their eczema will migrate to areas that stay moist, such as the antecubital and popliteal folds, or to the area around the neck, where the itching can be intense—which of course causes the child to scratch, in turn worsening the problem.

Patient/parent education is the key to dealing with AD and can be bolstered by handouts or direction to reliable websites. Besides objectifying the problem, these resources detail its nature and outline the need for daily bathing with mild cleansers, generous application of heavy moisturizers, careful use of topical corticosteroid creams or ointments (eg, 2.5% hydrocortisone), and avoidance of woolen clothing or bedding.

Another important component of patient/parent education is the reassurance that eczema will not scar the patient. It does occasionally become severe enough to require a short course of oral antibiotics (eg, cephalexin) or even the use of oral prednisolone. Since AD is not a histamine-driven process, antihistamines are ineffective for eczema.

TAKE-HOME LEARNING POINTS

• Atopic dermatitis (AD) is extremely common, affecting 20% of all newborns in developed countries.
• Infantile eczema typically centers on the face, particularly the perioral area.
• Later, it begins to involve the antecubital and popliteal areas, which stay moist a good part of the time.
• Most children outgrow the worst of the problem—and go on to have children who develop it.

Since birth, this 5-month-old boy has had a facial rash that comes and goes. At times severe, it is the source of much familial disagreement about its cause: Some say the problem is related to food, while others are sure it represents infection.

Several medications, including triple-antibiotic ointment and nystatin cream, have been tried. None have had much effect.

The child is well in all other respects—gaining weight as expected and experiencing normal growth and development. The rash does not appear to bother him as much as it bothers his family to see.

Further questioning reveals a strong family history of seasonal allergies, eczema, and asthma. Notably, all affected individuals have long since outgrown those problems.

EXAMINATION
The child is in no apparent distress but is noted to have nasal congestion, with continual mouth breathing. Overall, his skin is quite dry and fair.

The rash itself is rather florid, affecting the perioral area and spreading onto the cheeks in a symmetrical configuration. The skin in these areas is focally erythematous, though not swollen. It is also quite scaly in places, giving the appearance of, as his parents note, “chapped” skin. Examination of the diaper area reveals a similar look focally.

What’s the diagnosis?

DISCUSSION
This case is typical of those seen multiple times daily in primary care and dermatology offices—hardly surprising, since atopic dermatitis (AD) affects about 20% of all newborns in this and other developed countries. In very young children, AD primarily affects the face and diaper area, as well as the trunk. About 50% of affected patients will have cradle cap—as did this child in his first month of life, we subsequently learned.

The tendency to develop AD is inherited. It is not related to food, although children with AD could develop a food allergy. However, it would more likely manifest with gastrointestinal symptoms. Another myth embedded in Western culture is that AD is caused by exposure to a particular laundry detergent.

Rather, this child and others like him have inherited dry, thin, overreactive skin that is bathed early on with nasal secretions, bacteria, and saliva. Later, their eczema will migrate to areas that stay moist, such as the antecubital and popliteal folds, or to the area around the neck, where the itching can be intense—which of course causes the child to scratch, in turn worsening the problem.

Patient/parent education is the key to dealing with AD and can be bolstered by handouts or direction to reliable websites. Besides objectifying the problem, these resources detail its nature and outline the need for daily bathing with mild cleansers, generous application of heavy moisturizers, careful use of topical corticosteroid creams or ointments (eg, 2.5% hydrocortisone), and avoidance of woolen clothing or bedding.

Another important component of patient/parent education is the reassurance that eczema will not scar the patient. It does occasionally become severe enough to require a short course of oral antibiotics (eg, cephalexin) or even the use of oral prednisolone. Since AD is not a histamine-driven process, antihistamines are ineffective for eczema.

TAKE-HOME LEARNING POINTS

• Atopic dermatitis (AD) is extremely common, affecting 20% of all newborns in developed countries.
• Infantile eczema typically centers on the face, particularly the perioral area.
• Later, it begins to involve the antecubital and popliteal areas, which stay moist a good part of the time.
• Most children outgrow the worst of the problem—and go on to have children who develop it.

Based on the target lesions with central epithelial disruption, the FP diagnosed erythema multiforme (EM) in this patient. He also diagnosed genital herpes simplex in the crusting stage and suspected that it was the inciting event for the EM.

EM is considered a hypersensitivity reaction that is often secondary to infections or medications. Herpes simplex viruses (HSVI and HSV2) are the most common causative agents and have been implicated in at least 60% of cases.

The patient did not know that she had genital herpes simplex but remembered having sores in the genital area that preceded the similar rash a year earlier. This was a case of recurrent EM responding to recurrent herpes simplex.

The patient suspected that she had genital herpes simplex on and off for the past 10 years but lacked health insurance, so she never visited a doctor for treatment. She recently obtained health insurance and was willing to be tested for other sexually transmitted diseases. She also wanted to have a test done to confirm this was herpes simplex. The FP explained that it was unlikely that an antiviral agent would help the current case of herpes simplex and the associated EM because of the late timing, but antiviral medication could help to prevent further outbreaks and decrease transmission to her husband.

The patient was enthusiastic to start valacyclovir 500 mg/d for prophylaxis. For symptomatic relief, the FP prescribed a 30-g tube of 0.1% triamcinolone appointment and instructed the patient to apply it to the EM twice daily. The patient was sent for blood tests for syphilis and HIV; fortunately, both came back negative. The herpes simplex PCR test was positive for HSV2.

On a 1-week follow-up visit, the skin lesions were resolving, and the patient had no further symptoms. The patient said she understood that she should refrain from sexual intercourse if she developed lesions while on prophylaxis.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Milana C, Smith M. Erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1161-1168.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

Based on the target lesions with central epithelial disruption, the FP diagnosed erythema multiforme (EM) in this patient. He also diagnosed genital herpes simplex in the crusting stage and suspected that it was the inciting event for the EM.

EM is considered a hypersensitivity reaction that is often secondary to infections or medications. Herpes simplex viruses (HSVI and HSV2) are the most common causative agents and have been implicated in at least 60% of cases.

The patient did not know that she had genital herpes simplex but remembered having sores in the genital area that preceded the similar rash a year earlier. This was a case of recurrent EM responding to recurrent herpes simplex.

The patient suspected that she had genital herpes simplex on and off for the past 10 years but lacked health insurance, so she never visited a doctor for treatment. She recently obtained health insurance and was willing to be tested for other sexually transmitted diseases. She also wanted to have a test done to confirm this was herpes simplex. The FP explained that it was unlikely that an antiviral agent would help the current case of herpes simplex and the associated EM because of the late timing, but antiviral medication could help to prevent further outbreaks and decrease transmission to her husband.

The patient was enthusiastic to start valacyclovir 500 mg/d for prophylaxis. For symptomatic relief, the FP prescribed a 30-g tube of 0.1% triamcinolone appointment and instructed the patient to apply it to the EM twice daily. The patient was sent for blood tests for syphilis and HIV; fortunately, both came back negative. The herpes simplex PCR test was positive for HSV2.

On a 1-week follow-up visit, the skin lesions were resolving, and the patient had no further symptoms. The patient said she understood that she should refrain from sexual intercourse if she developed lesions while on prophylaxis.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Milana C, Smith M. Erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1161-1168.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

Based on the target lesions with central epithelial disruption, the FP diagnosed erythema multiforme (EM) in this patient. He also diagnosed genital herpes simplex in the crusting stage and suspected that it was the inciting event for the EM.

EM is considered a hypersensitivity reaction that is often secondary to infections or medications. Herpes simplex viruses (HSVI and HSV2) are the most common causative agents and have been implicated in at least 60% of cases.

The patient did not know that she had genital herpes simplex but remembered having sores in the genital area that preceded the similar rash a year earlier. This was a case of recurrent EM responding to recurrent herpes simplex.

The patient suspected that she had genital herpes simplex on and off for the past 10 years but lacked health insurance, so she never visited a doctor for treatment. She recently obtained health insurance and was willing to be tested for other sexually transmitted diseases. She also wanted to have a test done to confirm this was herpes simplex. The FP explained that it was unlikely that an antiviral agent would help the current case of herpes simplex and the associated EM because of the late timing, but antiviral medication could help to prevent further outbreaks and decrease transmission to her husband.

The patient was enthusiastic to start valacyclovir 500 mg/d for prophylaxis. For symptomatic relief, the FP prescribed a 30-g tube of 0.1% triamcinolone appointment and instructed the patient to apply it to the EM twice daily. The patient was sent for blood tests for syphilis and HIV; fortunately, both came back negative. The herpes simplex PCR test was positive for HSV2.

On a 1-week follow-up visit, the skin lesions were resolving, and the patient had no further symptoms. The patient said she understood that she should refrain from sexual intercourse if she developed lesions while on prophylaxis.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Milana C, Smith M. Erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1161-1168.

To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/

You can get the Color Atlas of Family Medicine app by clicking on this link: usatinemedia.com

NEWPORT BEACH, CALIF. – Acne – which can appear anytime from the neonatal period to puberty – is most worrisome when it appears during the midchildhood years, from ages 1-7 years, according to Sheila Fallon Friedlander, MD.

“This is something you are going to see in your practice,” said Dr. Friedlander, a pediatric dermatologists at Rady Children’s Hospital–San Diego. It’s important to know when it’s time to be concerned and when another condition may be masquerading as acne, she said at the at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Dr. Friedlander, who is professor of dermatology and pediatrics at the University of California, San Diego, talked about treating acne in the following prepubertal age groups:
 

Neonatal acne (ages birth to 4 weeks)

Acne appears in this population up to 20% of the time, according to research, and it is much more common in males than in females, at a ratio of five to one.

The cause is “most likely the relationship between placental androgens and the baby’s adrenal glands,” Dr. Friedlander said. However, something more serious could be going on. “Look at the child and see if he’s sick. If he looks sick, then we need to worry.”

Hormonal abnormalities also could be a cause, she said. Refer a baby to a specialist if there are other signs of hyperandrogenism. However, “the likelihood is very low,” and she’s never needed to refer a neonate with acne for evaluation.

As for treatment, she said, “Mainly, I’m using tincture of time.” However, “many of my mothers have told me that topical yogurt application will work.” Why yogurt? It’s possible that its bacteria could play a role in combating acne, she said.

Masquerader alert! Beware of neonatal cephalic pustulosis, Dr. Friedlander cautioned, which may be an inflammatory response to yeast. Ketoconazole cream may be helpful.
 

Infantile acne (ages 0-12 months)

This form of acne is more common in males and may hint at the future development of severe adolescent acne. It does resolve but it may take months or years, Dr. Friedlander said.

In general, this acne isn’t a sign of something more serious. “You do not need to go crazy with the work-up,” she said. “With mild to moderate disease, with nothing else suspicious, I don’t do a big work-up.”

However, do consider whether the child is undergoing precocious puberty, Dr. Friedlander said. Signs include axillary hair, pubic hair, and body odor.

As for treatment of infantile acne, “start out topically” and consider options such as Bactrim (sulfamethoxazole/trimethoprim) and erythromycin.

Masquerader alert! Idiopathic facial aseptic granuloma can be mistaken for acne and abscess, and ultrasound is helpful to confirm it. “It’s not so easy to treat,” she said. “Ivermectin may be helpful. Sometimes you do cultures and make sure something else isn’t going on.”
 

Midchildhood (ages 1-7 years)

“It’s not as common to have acne develop in this age group, but when it develops you need to be concerned,” Dr. Friedlander said. “This is the age period when there is more often something really wrong.”

Be on the lookout for a family history of hormonal abnormalities, and check if the child is on medication. “You need to look carefully,” she said, adding that it’s important to check for signs of premature puberty such as giant spikes in growth, abnormally large hands and feet, genital changes, and body odor. Check blood pressure if you’re worried about an adrenal tumor.

It’s possible for children to develop precocious puberty – with acne – because of exposure to testosterone gel used by a father. Dehydroepiandrosterone (DHEA) creams also may cause the condition. “The more creams out there with androgenic effects, the more we may see it,” Dr. Friedlander said. “This is something to ask about because families may not be forthcoming.”

Masquerader alert! Perioral dermatitis may look like acne, and it may be linked to inhaled or topical steroids, she said.

Other masqueraders include demodex folliculitis, angiofibromas (think tuberous sclerosis), and keratosis pilaris (the most common type of bump on a children aged 1-7 years). The latter condition “is not the end of the world,” said Dr. Friedlander, who added that “I’ve never cured anyone of it.”
 

Prepubertal acne (ages 7 years to puberty)

Acne in this group is generally not worrisome, Dr. Friedlander said, but investigate further if there’s significant inflammation and signs of early sexual development or virilization.

Benzoyl peroxide wash may be enough to help the condition initially, and consider topical clindamycin or a combination product. “Start out slow,” she said. Twice a week to start might be appropriate. Moisturizers can be helpful, as can topical adapalene.

Also, keep in mind that even mild acne can be emotionally devastating to a child in this age group and worthy of treatment. “Your assessment may be very different than hers,” she said. It’s possible that “she has a few lesions, but she feels like an outcast.”

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

NEWPORT BEACH, CALIF. – Acne – which can appear anytime from the neonatal period to puberty – is most worrisome when it appears during the midchildhood years, from ages 1-7 years, according to Sheila Fallon Friedlander, MD.

“This is something you are going to see in your practice,” said Dr. Friedlander, a pediatric dermatologists at Rady Children’s Hospital–San Diego. It’s important to know when it’s time to be concerned and when another condition may be masquerading as acne, she said at the at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Dr. Friedlander, who is professor of dermatology and pediatrics at the University of California, San Diego, talked about treating acne in the following prepubertal age groups:
 

Neonatal acne (ages birth to 4 weeks)

Acne appears in this population up to 20% of the time, according to research, and it is much more common in males than in females, at a ratio of five to one.

The cause is “most likely the relationship between placental androgens and the baby’s adrenal glands,” Dr. Friedlander said. However, something more serious could be going on. “Look at the child and see if he’s sick. If he looks sick, then we need to worry.”

Hormonal abnormalities also could be a cause, she said. Refer a baby to a specialist if there are other signs of hyperandrogenism. However, “the likelihood is very low,” and she’s never needed to refer a neonate with acne for evaluation.

As for treatment, she said, “Mainly, I’m using tincture of time.” However, “many of my mothers have told me that topical yogurt application will work.” Why yogurt? It’s possible that its bacteria could play a role in combating acne, she said.

Masquerader alert! Beware of neonatal cephalic pustulosis, Dr. Friedlander cautioned, which may be an inflammatory response to yeast. Ketoconazole cream may be helpful.
 

Infantile acne (ages 0-12 months)

This form of acne is more common in males and may hint at the future development of severe adolescent acne. It does resolve but it may take months or years, Dr. Friedlander said.

In general, this acne isn’t a sign of something more serious. “You do not need to go crazy with the work-up,” she said. “With mild to moderate disease, with nothing else suspicious, I don’t do a big work-up.”

However, do consider whether the child is undergoing precocious puberty, Dr. Friedlander said. Signs include axillary hair, pubic hair, and body odor.

As for treatment of infantile acne, “start out topically” and consider options such as Bactrim (sulfamethoxazole/trimethoprim) and erythromycin.

Masquerader alert! Idiopathic facial aseptic granuloma can be mistaken for acne and abscess, and ultrasound is helpful to confirm it. “It’s not so easy to treat,” she said. “Ivermectin may be helpful. Sometimes you do cultures and make sure something else isn’t going on.”
 

Midchildhood (ages 1-7 years)

“It’s not as common to have acne develop in this age group, but when it develops you need to be concerned,” Dr. Friedlander said. “This is the age period when there is more often something really wrong.”

Be on the lookout for a family history of hormonal abnormalities, and check if the child is on medication. “You need to look carefully,” she said, adding that it’s important to check for signs of premature puberty such as giant spikes in growth, abnormally large hands and feet, genital changes, and body odor. Check blood pressure if you’re worried about an adrenal tumor.

It’s possible for children to develop precocious puberty – with acne – because of exposure to testosterone gel used by a father. Dehydroepiandrosterone (DHEA) creams also may cause the condition. “The more creams out there with androgenic effects, the more we may see it,” Dr. Friedlander said. “This is something to ask about because families may not be forthcoming.”

Masquerader alert! Perioral dermatitis may look like acne, and it may be linked to inhaled or topical steroids, she said.

Other masqueraders include demodex folliculitis, angiofibromas (think tuberous sclerosis), and keratosis pilaris (the most common type of bump on a children aged 1-7 years). The latter condition “is not the end of the world,” said Dr. Friedlander, who added that “I’ve never cured anyone of it.”
 

Prepubertal acne (ages 7 years to puberty)

Acne in this group is generally not worrisome, Dr. Friedlander said, but investigate further if there’s significant inflammation and signs of early sexual development or virilization.

Benzoyl peroxide wash may be enough to help the condition initially, and consider topical clindamycin or a combination product. “Start out slow,” she said. Twice a week to start might be appropriate. Moisturizers can be helpful, as can topical adapalene.

Also, keep in mind that even mild acne can be emotionally devastating to a child in this age group and worthy of treatment. “Your assessment may be very different than hers,” she said. It’s possible that “she has a few lesions, but she feels like an outcast.”

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

NEWPORT BEACH, CALIF. – Acne – which can appear anytime from the neonatal period to puberty – is most worrisome when it appears during the midchildhood years, from ages 1-7 years, according to Sheila Fallon Friedlander, MD.

“This is something you are going to see in your practice,” said Dr. Friedlander, a pediatric dermatologists at Rady Children’s Hospital–San Diego. It’s important to know when it’s time to be concerned and when another condition may be masquerading as acne, she said at the at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Dr. Friedlander, who is professor of dermatology and pediatrics at the University of California, San Diego, talked about treating acne in the following prepubertal age groups:
 

Neonatal acne (ages birth to 4 weeks)

Acne appears in this population up to 20% of the time, according to research, and it is much more common in males than in females, at a ratio of five to one.

The cause is “most likely the relationship between placental androgens and the baby’s adrenal glands,” Dr. Friedlander said. However, something more serious could be going on. “Look at the child and see if he’s sick. If he looks sick, then we need to worry.”

Hormonal abnormalities also could be a cause, she said. Refer a baby to a specialist if there are other signs of hyperandrogenism. However, “the likelihood is very low,” and she’s never needed to refer a neonate with acne for evaluation.

As for treatment, she said, “Mainly, I’m using tincture of time.” However, “many of my mothers have told me that topical yogurt application will work.” Why yogurt? It’s possible that its bacteria could play a role in combating acne, she said.

Masquerader alert! Beware of neonatal cephalic pustulosis, Dr. Friedlander cautioned, which may be an inflammatory response to yeast. Ketoconazole cream may be helpful.
 

Infantile acne (ages 0-12 months)

This form of acne is more common in males and may hint at the future development of severe adolescent acne. It does resolve but it may take months or years, Dr. Friedlander said.

In general, this acne isn’t a sign of something more serious. “You do not need to go crazy with the work-up,” she said. “With mild to moderate disease, with nothing else suspicious, I don’t do a big work-up.”

However, do consider whether the child is undergoing precocious puberty, Dr. Friedlander said. Signs include axillary hair, pubic hair, and body odor.

As for treatment of infantile acne, “start out topically” and consider options such as Bactrim (sulfamethoxazole/trimethoprim) and erythromycin.

Masquerader alert! Idiopathic facial aseptic granuloma can be mistaken for acne and abscess, and ultrasound is helpful to confirm it. “It’s not so easy to treat,” she said. “Ivermectin may be helpful. Sometimes you do cultures and make sure something else isn’t going on.”
 

Midchildhood (ages 1-7 years)

“It’s not as common to have acne develop in this age group, but when it develops you need to be concerned,” Dr. Friedlander said. “This is the age period when there is more often something really wrong.”

Be on the lookout for a family history of hormonal abnormalities, and check if the child is on medication. “You need to look carefully,” she said, adding that it’s important to check for signs of premature puberty such as giant spikes in growth, abnormally large hands and feet, genital changes, and body odor. Check blood pressure if you’re worried about an adrenal tumor.

It’s possible for children to develop precocious puberty – with acne – because of exposure to testosterone gel used by a father. Dehydroepiandrosterone (DHEA) creams also may cause the condition. “The more creams out there with androgenic effects, the more we may see it,” Dr. Friedlander said. “This is something to ask about because families may not be forthcoming.”

Masquerader alert! Perioral dermatitis may look like acne, and it may be linked to inhaled or topical steroids, she said.

Other masqueraders include demodex folliculitis, angiofibromas (think tuberous sclerosis), and keratosis pilaris (the most common type of bump on a children aged 1-7 years). The latter condition “is not the end of the world,” said Dr. Friedlander, who added that “I’ve never cured anyone of it.”
 

Prepubertal acne (ages 7 years to puberty)

Acne in this group is generally not worrisome, Dr. Friedlander said, but investigate further if there’s significant inflammation and signs of early sexual development or virilization.

Benzoyl peroxide wash may be enough to help the condition initially, and consider topical clindamycin or a combination product. “Start out slow,” she said. Twice a week to start might be appropriate. Moisturizers can be helpful, as can topical adapalene.

Also, keep in mind that even mild acne can be emotionally devastating to a child in this age group and worthy of treatment. “Your assessment may be very different than hers,” she said. It’s possible that “she has a few lesions, but she feels like an outcast.”

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

Alopecia areata is more common among African Americans but less common among Asians, compared with whites, according to a new study involving registry data for more than 11,000 individuals.

These new findings “raise a different perspective from the conventional view that AA does not differ by race/ethnicity,” said Hemin Lee, MD, MPH, of the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital, Boston, and associates.

Multivariate-adjusted odds ratios for ever-diagnosis of AA were 1.77 for African Americans and 0.4 for Asians when whites were the referent group. Hispanics/Latinos were similar to whites, with an odds ratio of 0.9, and the group of other races/ethnicities (including American Indians and Pacific Islanders) was higher at 1.27, the investigators noted. The report is in the Journal of the American Academy of Dermatology.

The odds played out in a similar fashion when broken down by AA subtype. With whites as the referent at 1.0, blacks were most likely to have been diagnosed with AA transient/persistent at 1.93 and Asians were lowest at 0.46. For AA totalis/universalis, odds ratios were 1.57 for blacks and 0.32 for Asians, they said, based on 2000-2016 data from the National Alopecia Areata Registry.

“An intricate interplay between genetic and environmental factors may account for the racial differences. Pathogenesis of AA is at times linked with autoimmunity by its strong association with HLA class II alleles,” Dr. Lee and associates wrote.

The study involved 11,404 participants from the registry: 9,340 had reported at least one episode of AA and 2,064 had no history of lifetime alopecia. The multivariate analysis was based on the same group of noncases but a subgroup of 1,970 AA patients who had been enrolled in the registry “through academic institutions after dermatologist-confirmed diagnosis,” they said.

There was no funding source to report. One of Dr. Lee’s associates has received honoraria from Abbvie, Amgen, the Centers for Disease Control and Prevention, Janssen, Merck, Novartis, Pfizer, and Amgen, which have been donated to charity, and is an investigator for Sanofi/Regeneron with no financial compensation. All other authors have no conflicts of interest.

[email protected]

SOURCE: Lee H et al. J Am Acad Dermatol. 2019 Jul 3. doi: 10.1016/j.jaad.2019.06.1300.

Alopecia areata is more common among African Americans but less common among Asians, compared with whites, according to a new study involving registry data for more than 11,000 individuals.

These new findings “raise a different perspective from the conventional view that AA does not differ by race/ethnicity,” said Hemin Lee, MD, MPH, of the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital, Boston, and associates.

Multivariate-adjusted odds ratios for ever-diagnosis of AA were 1.77 for African Americans and 0.4 for Asians when whites were the referent group. Hispanics/Latinos were similar to whites, with an odds ratio of 0.9, and the group of other races/ethnicities (including American Indians and Pacific Islanders) was higher at 1.27, the investigators noted. The report is in the Journal of the American Academy of Dermatology.

The odds played out in a similar fashion when broken down by AA subtype. With whites as the referent at 1.0, blacks were most likely to have been diagnosed with AA transient/persistent at 1.93 and Asians were lowest at 0.46. For AA totalis/universalis, odds ratios were 1.57 for blacks and 0.32 for Asians, they said, based on 2000-2016 data from the National Alopecia Areata Registry.

“An intricate interplay between genetic and environmental factors may account for the racial differences. Pathogenesis of AA is at times linked with autoimmunity by its strong association with HLA class II alleles,” Dr. Lee and associates wrote.

The study involved 11,404 participants from the registry: 9,340 had reported at least one episode of AA and 2,064 had no history of lifetime alopecia. The multivariate analysis was based on the same group of noncases but a subgroup of 1,970 AA patients who had been enrolled in the registry “through academic institutions after dermatologist-confirmed diagnosis,” they said.

There was no funding source to report. One of Dr. Lee’s associates has received honoraria from Abbvie, Amgen, the Centers for Disease Control and Prevention, Janssen, Merck, Novartis, Pfizer, and Amgen, which have been donated to charity, and is an investigator for Sanofi/Regeneron with no financial compensation. All other authors have no conflicts of interest.

[email protected]

SOURCE: Lee H et al. J Am Acad Dermatol. 2019 Jul 3. doi: 10.1016/j.jaad.2019.06.1300.

Alopecia areata is more common among African Americans but less common among Asians, compared with whites, according to a new study involving registry data for more than 11,000 individuals.

These new findings “raise a different perspective from the conventional view that AA does not differ by race/ethnicity,” said Hemin Lee, MD, MPH, of the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women’s Hospital, Boston, and associates.

Multivariate-adjusted odds ratios for ever-diagnosis of AA were 1.77 for African Americans and 0.4 for Asians when whites were the referent group. Hispanics/Latinos were similar to whites, with an odds ratio of 0.9, and the group of other races/ethnicities (including American Indians and Pacific Islanders) was higher at 1.27, the investigators noted. The report is in the Journal of the American Academy of Dermatology.

The odds played out in a similar fashion when broken down by AA subtype. With whites as the referent at 1.0, blacks were most likely to have been diagnosed with AA transient/persistent at 1.93 and Asians were lowest at 0.46. For AA totalis/universalis, odds ratios were 1.57 for blacks and 0.32 for Asians, they said, based on 2000-2016 data from the National Alopecia Areata Registry.

“An intricate interplay between genetic and environmental factors may account for the racial differences. Pathogenesis of AA is at times linked with autoimmunity by its strong association with HLA class II alleles,” Dr. Lee and associates wrote.

The study involved 11,404 participants from the registry: 9,340 had reported at least one episode of AA and 2,064 had no history of lifetime alopecia. The multivariate analysis was based on the same group of noncases but a subgroup of 1,970 AA patients who had been enrolled in the registry “through academic institutions after dermatologist-confirmed diagnosis,” they said.

There was no funding source to report. One of Dr. Lee’s associates has received honoraria from Abbvie, Amgen, the Centers for Disease Control and Prevention, Janssen, Merck, Novartis, Pfizer, and Amgen, which have been donated to charity, and is an investigator for Sanofi/Regeneron with no financial compensation. All other authors have no conflicts of interest.

[email protected]

SOURCE: Lee H et al. J Am Acad Dermatol. 2019 Jul 3. doi: 10.1016/j.jaad.2019.06.1300.

Despite higher rates of skin cancer morbidity and mortality among racial and ethnic minorities, affected adults often are not recognizing their risks or taking preventive measures, said Costner McKenzie, BA, and Roopal V. Kundu, MD of Northwestern University, Chicago.

RuslanDashinsky/Getty Images

In a multivariable logistic regression analysis, Mr. Costner and Dr. Kundu sampled data of 33,672 adults included in the 2015 National Health Interview Survey. Data from the 2010 U.S. Census Bureau also were used to develop sample weights representative of the U.S. population. There was a survey of a smaller sample of adults who were determined to have sun-sensitive skin. The findings were published in the Journal of the American Academy of Dermatology.

Sun sensitivity was determined by skin reaction to 1 hour of unprotected sun exposure. Those who self-reported severe sunburn with blisters or moderate sunburn with peeling were determined to be sun sensitive.

The sample surveyed comprised 3,665 women (41%) and 5,287 men (59%). Of these, 82% were white non-Hispanic, 3% black non-Hispanic, 3% Asian non-Hispanic, 11% Hispanic, and 1% other non-Hispanic.

Mr. McKenzie and Dr. Kundu found that non-Hispanic black, non-Hispanic Asian, and Hispanic adults were less likely to use sunscreen than were non-Hispanic white adults (adjusted odds ratio [aOR], 0.43, 0.54, and 0.70, respectively). Non-Hispanic blacks and Hispanics also were less likely to use sunscreen greater than SPF 15 (a0R, 0.39 and 0.64, respectively). Non-Hispanic blacks, non-Hispanic Asians, and Hispanics were less likely to have ever had a total body skin examination (aOR, 0.29, 0.21, and 0.39, respectively).

Yet these same three groups were more likely to wear long sleeves outside (non-Hispanic blacks aOR, 1.96, non-Hispanic Asians aOR, 2.09, and Hispanics aOR, 2.29). In addition, non-Hispanic Asians and Hispanics were more likely to shelter in the shade on warm, sunny days (aOR, 1.63 and 1.85, respectively).

Citing recent literature, the authors noted that although skin cancer is the most commonly diagnosed cancer, it is not typically thought of as a disease that afflicts minority populations, especially among minorities themselves, who do not generally recognize their own risk (Arch Dermatol. 2009;145[2]:207-8). In fact, morbidity and mortality from skin cancer actually are greater in racial and ethnic minorities (J Am Acad Dermatol. 2016;75[5]:983-91; J Am Acad Dermatol. 2006;55[5]:741-60), despite greater incidence of skin cancer among white adults.

“This study highlights the impact of race and ethnicity on sun protective behaviors,” said Mr. McKenzie and Dr. Kundu. Cultural beliefs, stigma, personal preferences, as well as a lack of “knowledge-based interventions” specifically intended for minorities could be responsible for the observed differences between population groups, they speculated.

The primary limitations of the study were its cross-sectional design and the use of self-reported data, the authors noted.

Additional research is needed to fully examine the reasons behind these differences as well as to identify appropriate interventions that promote sun protection, they added.

There was no external funding and the authors had no conflicts of interest to disclose.

SOURCE: McKenzie C and Kundu RV. J Am Acad Dermatol. 2019 Jun 19. doi: 10.1016/j.jaad.2019.06.1306.

Despite higher rates of skin cancer morbidity and mortality among racial and ethnic minorities, affected adults often are not recognizing their risks or taking preventive measures, said Costner McKenzie, BA, and Roopal V. Kundu, MD of Northwestern University, Chicago.

RuslanDashinsky/Getty Images

In a multivariable logistic regression analysis, Mr. Costner and Dr. Kundu sampled data of 33,672 adults included in the 2015 National Health Interview Survey. Data from the 2010 U.S. Census Bureau also were used to develop sample weights representative of the U.S. population. There was a survey of a smaller sample of adults who were determined to have sun-sensitive skin. The findings were published in the Journal of the American Academy of Dermatology.

Sun sensitivity was determined by skin reaction to 1 hour of unprotected sun exposure. Those who self-reported severe sunburn with blisters or moderate sunburn with peeling were determined to be sun sensitive.

The sample surveyed comprised 3,665 women (41%) and 5,287 men (59%). Of these, 82% were white non-Hispanic, 3% black non-Hispanic, 3% Asian non-Hispanic, 11% Hispanic, and 1% other non-Hispanic.

Mr. McKenzie and Dr. Kundu found that non-Hispanic black, non-Hispanic Asian, and Hispanic adults were less likely to use sunscreen than were non-Hispanic white adults (adjusted odds ratio [aOR], 0.43, 0.54, and 0.70, respectively). Non-Hispanic blacks and Hispanics also were less likely to use sunscreen greater than SPF 15 (a0R, 0.39 and 0.64, respectively). Non-Hispanic blacks, non-Hispanic Asians, and Hispanics were less likely to have ever had a total body skin examination (aOR, 0.29, 0.21, and 0.39, respectively).

Yet these same three groups were more likely to wear long sleeves outside (non-Hispanic blacks aOR, 1.96, non-Hispanic Asians aOR, 2.09, and Hispanics aOR, 2.29). In addition, non-Hispanic Asians and Hispanics were more likely to shelter in the shade on warm, sunny days (aOR, 1.63 and 1.85, respectively).

Citing recent literature, the authors noted that although skin cancer is the most commonly diagnosed cancer, it is not typically thought of as a disease that afflicts minority populations, especially among minorities themselves, who do not generally recognize their own risk (Arch Dermatol. 2009;145[2]:207-8). In fact, morbidity and mortality from skin cancer actually are greater in racial and ethnic minorities (J Am Acad Dermatol. 2016;75[5]:983-91; J Am Acad Dermatol. 2006;55[5]:741-60), despite greater incidence of skin cancer among white adults.

“This study highlights the impact of race and ethnicity on sun protective behaviors,” said Mr. McKenzie and Dr. Kundu. Cultural beliefs, stigma, personal preferences, as well as a lack of “knowledge-based interventions” specifically intended for minorities could be responsible for the observed differences between population groups, they speculated.

The primary limitations of the study were its cross-sectional design and the use of self-reported data, the authors noted.

Additional research is needed to fully examine the reasons behind these differences as well as to identify appropriate interventions that promote sun protection, they added.

There was no external funding and the authors had no conflicts of interest to disclose.

SOURCE: McKenzie C and Kundu RV. J Am Acad Dermatol. 2019 Jun 19. doi: 10.1016/j.jaad.2019.06.1306.

Despite higher rates of skin cancer morbidity and mortality among racial and ethnic minorities, affected adults often are not recognizing their risks or taking preventive measures, said Costner McKenzie, BA, and Roopal V. Kundu, MD of Northwestern University, Chicago.

RuslanDashinsky/Getty Images

In a multivariable logistic regression analysis, Mr. Costner and Dr. Kundu sampled data of 33,672 adults included in the 2015 National Health Interview Survey. Data from the 2010 U.S. Census Bureau also were used to develop sample weights representative of the U.S. population. There was a survey of a smaller sample of adults who were determined to have sun-sensitive skin. The findings were published in the Journal of the American Academy of Dermatology.

Sun sensitivity was determined by skin reaction to 1 hour of unprotected sun exposure. Those who self-reported severe sunburn with blisters or moderate sunburn with peeling were determined to be sun sensitive.

The sample surveyed comprised 3,665 women (41%) and 5,287 men (59%). Of these, 82% were white non-Hispanic, 3% black non-Hispanic, 3% Asian non-Hispanic, 11% Hispanic, and 1% other non-Hispanic.

Mr. McKenzie and Dr. Kundu found that non-Hispanic black, non-Hispanic Asian, and Hispanic adults were less likely to use sunscreen than were non-Hispanic white adults (adjusted odds ratio [aOR], 0.43, 0.54, and 0.70, respectively). Non-Hispanic blacks and Hispanics also were less likely to use sunscreen greater than SPF 15 (a0R, 0.39 and 0.64, respectively). Non-Hispanic blacks, non-Hispanic Asians, and Hispanics were less likely to have ever had a total body skin examination (aOR, 0.29, 0.21, and 0.39, respectively).

Yet these same three groups were more likely to wear long sleeves outside (non-Hispanic blacks aOR, 1.96, non-Hispanic Asians aOR, 2.09, and Hispanics aOR, 2.29). In addition, non-Hispanic Asians and Hispanics were more likely to shelter in the shade on warm, sunny days (aOR, 1.63 and 1.85, respectively).

Citing recent literature, the authors noted that although skin cancer is the most commonly diagnosed cancer, it is not typically thought of as a disease that afflicts minority populations, especially among minorities themselves, who do not generally recognize their own risk (Arch Dermatol. 2009;145[2]:207-8). In fact, morbidity and mortality from skin cancer actually are greater in racial and ethnic minorities (J Am Acad Dermatol. 2016;75[5]:983-91; J Am Acad Dermatol. 2006;55[5]:741-60), despite greater incidence of skin cancer among white adults.

“This study highlights the impact of race and ethnicity on sun protective behaviors,” said Mr. McKenzie and Dr. Kundu. Cultural beliefs, stigma, personal preferences, as well as a lack of “knowledge-based interventions” specifically intended for minorities could be responsible for the observed differences between population groups, they speculated.

The primary limitations of the study were its cross-sectional design and the use of self-reported data, the authors noted.

Additional research is needed to fully examine the reasons behind these differences as well as to identify appropriate interventions that promote sun protection, they added.

There was no external funding and the authors had no conflicts of interest to disclose.

SOURCE: McKenzie C and Kundu RV. J Am Acad Dermatol. 2019 Jun 19. doi: 10.1016/j.jaad.2019.06.1306.

NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But there still are plenty of reasons to pay close attention to psoriasis drugs in any women who is or could become pregnant.

Bruce Jancin/Frontline Medical News

Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.

In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:

Counsel patients before pregnancy

There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).

Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.

Make adjustments to timing as needed

In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.

Adjust steroids as necessary

There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.

Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.

Some topical drugs appear to be OK

Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”

There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.

Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”

Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.

Phototherapy is OK in pregnancy

Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.

Avoid certain systemic drugs

Dr. Wu offered these recommendations:

• Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
• Acitretin (Soriatane): Avoid all use in women who may become pregnant.
• Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
• Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.

Avoid monoclonal antibodies

These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”

Nix the PUVA

While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.

Watch for waxing and waning

Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).

Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.

NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But there still are plenty of reasons to pay close attention to psoriasis drugs in any women who is or could become pregnant.

Bruce Jancin/Frontline Medical News

Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.

In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:

Counsel patients before pregnancy

There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).

Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.

Make adjustments to timing as needed

In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.

Adjust steroids as necessary

There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.

Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.

Some topical drugs appear to be OK

Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”

There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.

Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”

Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.

Phototherapy is OK in pregnancy

Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.

Avoid certain systemic drugs

Dr. Wu offered these recommendations:

• Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
• Acitretin (Soriatane): Avoid all use in women who may become pregnant.
• Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
• Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.

Avoid monoclonal antibodies

These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”

Nix the PUVA

While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.

Watch for waxing and waning

Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).

Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.

NEWPORT BEACH, CALIF. – Psoriasis often clears in pregnant women, giving them a rare break from the skin disease. But there still are plenty of reasons to pay close attention to psoriasis drugs in any women who is or could become pregnant.

Bruce Jancin/Frontline Medical News

Data from 2011 found 45% of pregnancies in U.S. women aged 15-44 years were unintended (N Engl J Med. 2016 Mar 3;374[9]:843-52), cautioned Jashin J. Wu, MD, of Dermatology Research and Education Foundation, Irvine, Calif.

In a presentation at the Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar, Dr. Wu offered these tips about pregnancy and psoriasis:

Counsel patients before pregnancy

There’s conflicting data about the risks of psoriasis in pregnancy, Dr. Wu said. One 23-year-old study suggests a link to adverse outcomes such as preterm and low-birth-weight babies. But another more recent study found no sign of increased risk (Int J Dermatol. 1996;35:169-72; J Am Acad Dermatol. 2011;64:71-7).

Counseling can include information about risks such as hospitalization during pregnancy because of undertreatment of psoriasis, he said. Discuss lowering medication doses to the lowest effective dose, he recommended, and talk about alternatives to systemic medications.

Make adjustments to timing as needed

In patients with severe cases, it may be appropriate to recommend that they postpone pregnancy until their psoriasis is under better control. As for treatment of psoriasis, “you may want to consider timing medication to end around the first trimester to get the medication out of them during the greatest risk period for the baby,” Dr. Wu said.

Adjust steroids as necessary

There are no “good” studies about the use of steroids in pregnant women with psoriasis, Dr. Wu said. “We can probably assume they are safe overall. Weaker steroids may have less risk,” and some of the stronger steroids may raise concerns.

Dr. Wu made these recommendations: Limit mild-potency topical corticosteroids to less than 100 g/week, potent topical corticosteroids to less than 50 g/week, and superpotent topical corticosteroids to less than 30 g/week.

Some topical drugs appear to be OK

Vitamin D analogues have not been well-studied in pregnancy, he said, but “we consider topical use to be fairly safe.”

There’s no data on calcineurin inhibitors in pregnancy, he said, but topical use is considered to be safe because there’s limited systemic absorption.

Beware of certain drugs in pregnancyTazarotene is considered to be dangerous in pregnancy, Dr. Wu said, and females of childbearing age who take it should use effective contraception, and have a recent negative pregnancy test (within 2 weeks before treatment begins). “In general, I’d probably not use this,” he said. “We have so many other options.”

Data about pregnancy safety for three topical drugs – coal tar, anthralin, and salicylic acid – is limited or nonexistent, Dr. Wu said, and he recommends against their use in pregnancy.

Phototherapy is OK in pregnancy

Phototherapy is considered safe because UVB doesn’t penetrate the superficial layer of the skin, he said. But phototherapy brings a potential risk of lowered folic acid levels, and he urges folic acid supplementation in women undergoing the treatment who are considering pregnancy or who are in the first trimester.

Avoid certain systemic drugs

Dr. Wu offered these recommendations:

• Methotrexate: Do not take during pregnancy, or 3 months prior to conception.
• Acitretin (Soriatane): Avoid all use in women who may become pregnant.
• Cyclosporine: Be aware of reports of prematurity and low birth weight linked to the drug.
• Apremilast (Otezla): Animal studies have shown a risk in pregnancy. Stop the drug at least 2 days before conception.

Avoid monoclonal antibodies

These drugs “result in therapeutic levels in the fetus, which is not a good thing,” Dr. Wu said. “You obviously don’t want to have monoclonal antibodies in the baby.”

Nix the PUVA

While one study found no link between psoralen plus UVA (PUVA) and birth defects (Arch Dermatol. 1993 Mar;129[3]:320-3), there’s still a theoretical risk, Dr. Wu said. He recommended that the treatment be avoided during pregnancy.

Watch for waxing and waning

Dr. Wu pointed to a small 2005 study that suggested that psoriasis activity declines during pregnancy. The study used different measures, finding that psoriasis improved by 30% (based on at least a 3% change in body surface area) or 55% (based on patient self-reporting). But it flares after pregnancy as reported by 65% of women surveyed; a body surface area analysis found that psoriasis worsened in 41% (Arch Dermatol. 2005 May;141[5]:601-6).

Dr. Wu reports various relationships (research, consultation and speaking) with 15 pharmaceutical companies. SDEF and this news organization are owned by the same parent company.

In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .

In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .

In a phase 3, active comparator controlled trial, treatment with risankizumab led to better skin clearance than treatment with adalimumab in patients with moderate-to-severe plaque psoriasis. Results of the IMMvent trial were published online ahead of print July 4 in the Lancet.

Risankizumab targets the p19 subunit of the cytokine IL-23. Selectivity for p19 has the potential to be safer than some other approaches that target the p40 subunit, because p19 is specific to IL-23, and many immune defense processes can function without IL-23. The p40 subunit is shared with IL-12, and blocking it can therefore lead to off-target effects.

Risankizumab was previously shown to have superior safety and efficacy over ustekinumab, which inhibits a subunit shared by IL-23 and IL-12 (Gordon KB et al. Lancet. 2018;392[10148]:650-61). Adalimumab is a TNF-alpha inhibitor that is frequently used to treat psoriasis, and which became available in biosimilar form in Europe in 2018.

The researchers randomized 605 adult patients from 66 sites in 11 countries to receive either risankizumab or adalimumab. The first phase (Part A) of the trial lasted up to 16 weeks, and tested the general superiority of risankizumab over adalimumab. The second phase (Part B), from week 16 to 44, evaluated the efficacy of risankizumab in participants who experienced an intermediate response, defined as Psoriasis Area and Severity Index (PASI) score of 50-90.

At the start of Part B, subjects initially receiving adalimumab who had at least a 90% improvement in PASI stayed on adalimumab (PASI 90), while those who had less than 50% improvement in PASI were switched to risankizumab. The remaining intermediate responders (PASI 50-90) were re-randomized to continue adalimumab or switch to risankizumab. All subjects initially randomized to risankizumab continued risankizumab during part B.

At the end of Part A, 72% of the risankizumab group achieved PASI 90, compared with 47% in the adalimumab group (p < 0.0001). A total of 84% in the risankizumab group had a static Physician’s Global Assessment (sPGA) score of 0 or 1 at the end of Part A, compared with 60% in the adalimumab group (p < 0.0001).

During Part B, among intermediate adalimumab responders, 66% of those switched to risankizumab achieved PASI 90, compared with 21% of continued on adalimumab (p < 0.0001).

In Part A, 56% of patients taking risankizumab experienced an adverse event, as did 57% of those taking adalimumab. Among adalimumab intermediate responders, 75% of those who switched to risankizumab during Part B had an adverse event, compared with 66% of those who continued adalimumab.

SOURCE: Reich K, et al. Lancet 2019, July 4 .