Hair & Nails

Some kinds of scarring alopecia may also be related to lipid metabolism, pointing the way to novel therapeutic targets for this class of hair diseases, Dr. Maria Hordinsky said at the Hawaii Dermatology Symposium.

While the scarring alopecias are broadly divided into lymphocytic and neutrophilic alopecias, clinically, they are a heterogeneous group, said Dr. Hordinsky, chair of the department of dermatology at the University of Minnesota, Minneapolis.

Two lymphocytic cicatricial alopecias, lichen planopilaris and frontal fibrosing alopecia, have been associated with peroxisome proliferator-activated receptor gamma (PPARG) deficiency. This finding suggests that they may be a type of lipid metabolism disorder; the theory is bolstered by case reports of improvement with the use of pioglitazone, Dr. Hordinsky said at the meeting provided by Global Academy for Medical Education/Skin Disease Education Foundation.

In both of these cicatricial alopecias, patients may also have significant discomfort including scalp burning, pain, paresthesias, and itching. Patients may even say they feel as though their scalp is on fire.

Dr. Hordinsky and her collaborators are currently conducting a clinical trial of the efficacy of a compounded formulation of 6% topical gabapentin to address the scalp discomfort associated with the cicatricial alopecias. The study is ongoing and recruiting patients. “FFA has been described as an emerging disease, and participation of FFA patients in a national registry focused on improving our understanding of the epidemiology of this disease is highly recommended,” said Dr. Hordinsky.

Currently, stepwise treatment for the lymphocytic cicatricial alopecias can be divided into 3 tiers:

• Tier 1: Topical high potency corticosteroids and/or intralesional steroids, as well as non-steroidal topical anti-inflammatory medications, such as tacrolimus and pemicrolimus.

• Tier 2: Hydroxychloroquine and acetretin, as well as low-dose antibiotics, which are used for anti-inflammatory effect.

• Tier 3: Cyclosporin, mycophenolate mofetil, and prednisone.

Low-level light therapy – approved by the Food and Drug Administration to treat thinning hair in men and women – may also be of benefit for those with inflammatory scalp diseases, Dr. Hordinsky added.

Dr. Hordinsky reported financial relationships with a number of pharmaceutical and consumer product companies in the dermatologic space.

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

[email protected]

On Twitter @karioakes

Some kinds of scarring alopecia may also be related to lipid metabolism, pointing the way to novel therapeutic targets for this class of hair diseases, Dr. Maria Hordinsky said at the Hawaii Dermatology Symposium.

While the scarring alopecias are broadly divided into lymphocytic and neutrophilic alopecias, clinically, they are a heterogeneous group, said Dr. Hordinsky, chair of the department of dermatology at the University of Minnesota, Minneapolis.

Two lymphocytic cicatricial alopecias, lichen planopilaris and frontal fibrosing alopecia, have been associated with peroxisome proliferator-activated receptor gamma (PPARG) deficiency. This finding suggests that they may be a type of lipid metabolism disorder; the theory is bolstered by case reports of improvement with the use of pioglitazone, Dr. Hordinsky said at the meeting provided by Global Academy for Medical Education/Skin Disease Education Foundation.

In both of these cicatricial alopecias, patients may also have significant discomfort including scalp burning, pain, paresthesias, and itching. Patients may even say they feel as though their scalp is on fire.

Dr. Hordinsky and her collaborators are currently conducting a clinical trial of the efficacy of a compounded formulation of 6% topical gabapentin to address the scalp discomfort associated with the cicatricial alopecias. The study is ongoing and recruiting patients. “FFA has been described as an emerging disease, and participation of FFA patients in a national registry focused on improving our understanding of the epidemiology of this disease is highly recommended,” said Dr. Hordinsky.

Currently, stepwise treatment for the lymphocytic cicatricial alopecias can be divided into 3 tiers:

• Tier 1: Topical high potency corticosteroids and/or intralesional steroids, as well as non-steroidal topical anti-inflammatory medications, such as tacrolimus and pemicrolimus.

• Tier 2: Hydroxychloroquine and acetretin, as well as low-dose antibiotics, which are used for anti-inflammatory effect.

• Tier 3: Cyclosporin, mycophenolate mofetil, and prednisone.

Low-level light therapy – approved by the Food and Drug Administration to treat thinning hair in men and women – may also be of benefit for those with inflammatory scalp diseases, Dr. Hordinsky added.

Dr. Hordinsky reported financial relationships with a number of pharmaceutical and consumer product companies in the dermatologic space.

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

[email protected]

On Twitter @karioakes

Some kinds of scarring alopecia may also be related to lipid metabolism, pointing the way to novel therapeutic targets for this class of hair diseases, Dr. Maria Hordinsky said at the Hawaii Dermatology Symposium.

While the scarring alopecias are broadly divided into lymphocytic and neutrophilic alopecias, clinically, they are a heterogeneous group, said Dr. Hordinsky, chair of the department of dermatology at the University of Minnesota, Minneapolis.

Two lymphocytic cicatricial alopecias, lichen planopilaris and frontal fibrosing alopecia, have been associated with peroxisome proliferator-activated receptor gamma (PPARG) deficiency. This finding suggests that they may be a type of lipid metabolism disorder; the theory is bolstered by case reports of improvement with the use of pioglitazone, Dr. Hordinsky said at the meeting provided by Global Academy for Medical Education/Skin Disease Education Foundation.

In both of these cicatricial alopecias, patients may also have significant discomfort including scalp burning, pain, paresthesias, and itching. Patients may even say they feel as though their scalp is on fire.

Dr. Hordinsky and her collaborators are currently conducting a clinical trial of the efficacy of a compounded formulation of 6% topical gabapentin to address the scalp discomfort associated with the cicatricial alopecias. The study is ongoing and recruiting patients. “FFA has been described as an emerging disease, and participation of FFA patients in a national registry focused on improving our understanding of the epidemiology of this disease is highly recommended,” said Dr. Hordinsky.

Currently, stepwise treatment for the lymphocytic cicatricial alopecias can be divided into 3 tiers:

• Tier 1: Topical high potency corticosteroids and/or intralesional steroids, as well as non-steroidal topical anti-inflammatory medications, such as tacrolimus and pemicrolimus.

• Tier 2: Hydroxychloroquine and acetretin, as well as low-dose antibiotics, which are used for anti-inflammatory effect.

• Tier 3: Cyclosporin, mycophenolate mofetil, and prednisone.

Low-level light therapy – approved by the Food and Drug Administration to treat thinning hair in men and women – may also be of benefit for those with inflammatory scalp diseases, Dr. Hordinsky added.

Dr. Hordinsky reported financial relationships with a number of pharmaceutical and consumer product companies in the dermatologic space.

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

[email protected]

On Twitter @karioakes

Bloom syndrome, also called congenital telangiectatic erythema and stunted growth, was first described by David Bloom in 1954.¹ It is a rare autosomal-recessive disorder (Online Mendelian Inheritance in Man 210900) characterized by specific clinical manifestations including photosensitivity, telangiectatic facial erythema, proportionate growth deficiency, hypogonadism, immunodeficiency, and a tendency to develop various malignancies.² Linkage analysis revealed that the Bloom syndrome gene locus resides on chromosome arm 15q26.1,³ and the BLM gene in this region has been identified as being responsible for the development of Bloom syndrome.^4,5 We report the case of a 12-year-old Chinese girl with Bloom syndrome and detected BLM gene. The evaluation was approved by the Institutional Ethical Review Boards of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College (Beijing, China).

Case Report

We evaluated a Bloom syndrome family, which consisted of the patient and her parents. The patient was a 12-year-old Chinese girl who was apparently healthy until 3 months of age when her parents noticed an erythematous eruption with blisters on the face. Exacerbation after exposure to sunlight is usual, which results in the eruption becoming prominent in summer and fainter in winter.² Gradually, the patient’s skin lesions became more progressive, extending to the forehead, nose, and ears, with oozing, crusting, atrophy, and telangiectases developing on the face despite treatment. In the last 3 years, no blisters were present on the patient’s face because of her efforts to avoid sun exposure. She had no history of recurrent infections.

On physical examination, the patient was generally healthy with normal intelligence and short stature. She weighed 26 kg and was approximately 122-cm tall. Telangiectatic erythema and slight scaling were noted on the face, which simulated lupus erythematosus (Figures 1A and 1B). She had additional abnormalities including alopecia areata (Figure 1C), eyebrow hair loss, flat nose, reticular pigmentation on the forehead and trunk, and finger swelling. The distal phalanges on all 10 fingers became short and sharpened and the fingernails became wider than they were long (Figure 1D). Laboratory investigations, including a complete blood cell count, liver and kidney function tests, stool examination, serum complement, and albumin and globulin levels, were within reference range.

After informed consent was obtained, a mutation analysis of the BLM gene was performed in the patient and her parents. We used a genomic DNA purification kit to extract genomic DNA from peripheral blood according to the manufacturer’s protocol. Genomic DNA was used to amplify the exons of the BLM gene with intron flanking sequences by polymerase chain reaction with the primer described elsewhere.⁶ After the amplification, the polymerase chain reaction products were purified and the BLM gene was sequenced. Sequence comparisons and analysis were performed using Phred/Phrap/Consed version 12.0.

The patient was found to carry changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene. The patient’s father was found to carry c.2603C>T and her mother carried c.3961G>A (Figure 2).

Comment

Patients with Bloom syndrome have a characteristic clinical appearance that typically includes photosensitivity, telangiectatic facial erythema, and growth deficiency. Telangiectatic erythema of the face develops during infancy or early childhood as red macules or plaques and may simulate lupus erythematosus. The lesions are described as a butterfly rash affecting the bridge of the nose and cheeks but also may involve the margins of the eyelids, forehead, ears, and sometimes the dorsa of the hands and forearms. Moderate and proportionate growth deficiencies develop both in utero and postnatally. Patients with Bloom syndrome characteristically have narrow, slender, distinct facial features with micrognathism and a relatively prominent nose. They usually may have mild microcephaly, meaning the head is longer and narrower than normal.^2,7-10

German and Takebe¹¹ reported 14 Japanese patients with Bloom syndrome. The phenotype differs somewhat from most cases recognized elsewhere in that dolichocephaly was a less constant feature, the facial skin was less prominent, and life-threatening infections were less common. Our patient had typical telangiectatic facial erythema without microcephaly, dolichocephaly, or any infections. She also had some uncommon manifestations such as alopecia areata, eyebrow hair loss, flat nose, reticular pigmentation, and short sharpened distal phalanges with fingernails that were wider than they were long. Although she had no recurrent infections and laboratory tests were within reference range, the alopecia areata and eyebrow hair loss may be associated with an abnormal immune response. The reasons for the short sharpened distal phalanges and the fingernail findings are unclear. The presence of reticular pigmentation also is unclear but may be associated with photosensitivity. Since the BLM gene was discovered to be the disease-causing gene of Bloom syndrome in 1995,^4,5 approximately 70 mutations were reported. The BLM gene encodes for the Bloom syndrome protein, a DNA helicase of the highly conserved RecQ subfamily of helicases, a group of nuclear proteins important in the maintenance of genomic stability.¹²

Mutation analysis of the BLM gene in our patient showed changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene, which altered proline residue with leucine residue at 868 and valine residue with isoleucine residue at 1321, respectively. According to GenBank,^13,14 c.2603C>T and c.3961G>A are single nucleotide polymorphisms of the BLM gene. The genotypic distribution of International HapMap Project¹⁵ showed that C=602/602 and T=0/602 on c.2603 in 301 unrelated Chinese patients and G=585/602 and A=17/602 on c.3961 in 301 unrelated Chinese patients. Because of the low prevalence of genotypes c.2603T and c.3961A in China, the relationship between clinical features and c.2603C>T and c.3961G>A of the BLM gene in our patient requires further study.

In conclusion, we report a patient with Bloom syndrome with uncommon clinical manifestations. Our findings indicate that c.2603C>T and c.3961G>A of the BLM gene may be the pathogenic nature for Bloom syndrome in China.

Acknowledgments

The authors would like to thank the patient and her family for their participation in the study. The authors also thank Li Qi, BA, Beijing, China, for his contribution to the review of the data in the literature.

Bloom syndrome, also called congenital telangiectatic erythema and stunted growth, was first described by David Bloom in 1954.¹ It is a rare autosomal-recessive disorder (Online Mendelian Inheritance in Man 210900) characterized by specific clinical manifestations including photosensitivity, telangiectatic facial erythema, proportionate growth deficiency, hypogonadism, immunodeficiency, and a tendency to develop various malignancies.² Linkage analysis revealed that the Bloom syndrome gene locus resides on chromosome arm 15q26.1,³ and the BLM gene in this region has been identified as being responsible for the development of Bloom syndrome.^4,5 We report the case of a 12-year-old Chinese girl with Bloom syndrome and detected BLM gene. The evaluation was approved by the Institutional Ethical Review Boards of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College (Beijing, China).

Case Report

We evaluated a Bloom syndrome family, which consisted of the patient and her parents. The patient was a 12-year-old Chinese girl who was apparently healthy until 3 months of age when her parents noticed an erythematous eruption with blisters on the face. Exacerbation after exposure to sunlight is usual, which results in the eruption becoming prominent in summer and fainter in winter.² Gradually, the patient’s skin lesions became more progressive, extending to the forehead, nose, and ears, with oozing, crusting, atrophy, and telangiectases developing on the face despite treatment. In the last 3 years, no blisters were present on the patient’s face because of her efforts to avoid sun exposure. She had no history of recurrent infections.

On physical examination, the patient was generally healthy with normal intelligence and short stature. She weighed 26 kg and was approximately 122-cm tall. Telangiectatic erythema and slight scaling were noted on the face, which simulated lupus erythematosus (Figures 1A and 1B). She had additional abnormalities including alopecia areata (Figure 1C), eyebrow hair loss, flat nose, reticular pigmentation on the forehead and trunk, and finger swelling. The distal phalanges on all 10 fingers became short and sharpened and the fingernails became wider than they were long (Figure 1D). Laboratory investigations, including a complete blood cell count, liver and kidney function tests, stool examination, serum complement, and albumin and globulin levels, were within reference range.

After informed consent was obtained, a mutation analysis of the BLM gene was performed in the patient and her parents. We used a genomic DNA purification kit to extract genomic DNA from peripheral blood according to the manufacturer’s protocol. Genomic DNA was used to amplify the exons of the BLM gene with intron flanking sequences by polymerase chain reaction with the primer described elsewhere.⁶ After the amplification, the polymerase chain reaction products were purified and the BLM gene was sequenced. Sequence comparisons and analysis were performed using Phred/Phrap/Consed version 12.0.

The patient was found to carry changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene. The patient’s father was found to carry c.2603C>T and her mother carried c.3961G>A (Figure 2).

Comment

Patients with Bloom syndrome have a characteristic clinical appearance that typically includes photosensitivity, telangiectatic facial erythema, and growth deficiency. Telangiectatic erythema of the face develops during infancy or early childhood as red macules or plaques and may simulate lupus erythematosus. The lesions are described as a butterfly rash affecting the bridge of the nose and cheeks but also may involve the margins of the eyelids, forehead, ears, and sometimes the dorsa of the hands and forearms. Moderate and proportionate growth deficiencies develop both in utero and postnatally. Patients with Bloom syndrome characteristically have narrow, slender, distinct facial features with micrognathism and a relatively prominent nose. They usually may have mild microcephaly, meaning the head is longer and narrower than normal.^2,7-10

German and Takebe¹¹ reported 14 Japanese patients with Bloom syndrome. The phenotype differs somewhat from most cases recognized elsewhere in that dolichocephaly was a less constant feature, the facial skin was less prominent, and life-threatening infections were less common. Our patient had typical telangiectatic facial erythema without microcephaly, dolichocephaly, or any infections. She also had some uncommon manifestations such as alopecia areata, eyebrow hair loss, flat nose, reticular pigmentation, and short sharpened distal phalanges with fingernails that were wider than they were long. Although she had no recurrent infections and laboratory tests were within reference range, the alopecia areata and eyebrow hair loss may be associated with an abnormal immune response. The reasons for the short sharpened distal phalanges and the fingernail findings are unclear. The presence of reticular pigmentation also is unclear but may be associated with photosensitivity. Since the BLM gene was discovered to be the disease-causing gene of Bloom syndrome in 1995,^4,5 approximately 70 mutations were reported. The BLM gene encodes for the Bloom syndrome protein, a DNA helicase of the highly conserved RecQ subfamily of helicases, a group of nuclear proteins important in the maintenance of genomic stability.¹²

Mutation analysis of the BLM gene in our patient showed changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene, which altered proline residue with leucine residue at 868 and valine residue with isoleucine residue at 1321, respectively. According to GenBank,^13,14 c.2603C>T and c.3961G>A are single nucleotide polymorphisms of the BLM gene. The genotypic distribution of International HapMap Project¹⁵ showed that C=602/602 and T=0/602 on c.2603 in 301 unrelated Chinese patients and G=585/602 and A=17/602 on c.3961 in 301 unrelated Chinese patients. Because of the low prevalence of genotypes c.2603T and c.3961A in China, the relationship between clinical features and c.2603C>T and c.3961G>A of the BLM gene in our patient requires further study.

In conclusion, we report a patient with Bloom syndrome with uncommon clinical manifestations. Our findings indicate that c.2603C>T and c.3961G>A of the BLM gene may be the pathogenic nature for Bloom syndrome in China.

Acknowledgments

The authors would like to thank the patient and her family for their participation in the study. The authors also thank Li Qi, BA, Beijing, China, for his contribution to the review of the data in the literature.

Bloom syndrome, also called congenital telangiectatic erythema and stunted growth, was first described by David Bloom in 1954.¹ It is a rare autosomal-recessive disorder (Online Mendelian Inheritance in Man 210900) characterized by specific clinical manifestations including photosensitivity, telangiectatic facial erythema, proportionate growth deficiency, hypogonadism, immunodeficiency, and a tendency to develop various malignancies.² Linkage analysis revealed that the Bloom syndrome gene locus resides on chromosome arm 15q26.1,³ and the BLM gene in this region has been identified as being responsible for the development of Bloom syndrome.^4,5 We report the case of a 12-year-old Chinese girl with Bloom syndrome and detected BLM gene. The evaluation was approved by the Institutional Ethical Review Boards of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College (Beijing, China).

Case Report

We evaluated a Bloom syndrome family, which consisted of the patient and her parents. The patient was a 12-year-old Chinese girl who was apparently healthy until 3 months of age when her parents noticed an erythematous eruption with blisters on the face. Exacerbation after exposure to sunlight is usual, which results in the eruption becoming prominent in summer and fainter in winter.² Gradually, the patient’s skin lesions became more progressive, extending to the forehead, nose, and ears, with oozing, crusting, atrophy, and telangiectases developing on the face despite treatment. In the last 3 years, no blisters were present on the patient’s face because of her efforts to avoid sun exposure. She had no history of recurrent infections.

On physical examination, the patient was generally healthy with normal intelligence and short stature. She weighed 26 kg and was approximately 122-cm tall. Telangiectatic erythema and slight scaling were noted on the face, which simulated lupus erythematosus (Figures 1A and 1B). She had additional abnormalities including alopecia areata (Figure 1C), eyebrow hair loss, flat nose, reticular pigmentation on the forehead and trunk, and finger swelling. The distal phalanges on all 10 fingers became short and sharpened and the fingernails became wider than they were long (Figure 1D). Laboratory investigations, including a complete blood cell count, liver and kidney function tests, stool examination, serum complement, and albumin and globulin levels, were within reference range.

After informed consent was obtained, a mutation analysis of the BLM gene was performed in the patient and her parents. We used a genomic DNA purification kit to extract genomic DNA from peripheral blood according to the manufacturer’s protocol. Genomic DNA was used to amplify the exons of the BLM gene with intron flanking sequences by polymerase chain reaction with the primer described elsewhere.⁶ After the amplification, the polymerase chain reaction products were purified and the BLM gene was sequenced. Sequence comparisons and analysis were performed using Phred/Phrap/Consed version 12.0.

The patient was found to carry changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene. The patient’s father was found to carry c.2603C>T and her mother carried c.3961G>A (Figure 2).

Comment

Patients with Bloom syndrome have a characteristic clinical appearance that typically includes photosensitivity, telangiectatic facial erythema, and growth deficiency. Telangiectatic erythema of the face develops during infancy or early childhood as red macules or plaques and may simulate lupus erythematosus. The lesions are described as a butterfly rash affecting the bridge of the nose and cheeks but also may involve the margins of the eyelids, forehead, ears, and sometimes the dorsa of the hands and forearms. Moderate and proportionate growth deficiencies develop both in utero and postnatally. Patients with Bloom syndrome characteristically have narrow, slender, distinct facial features with micrognathism and a relatively prominent nose. They usually may have mild microcephaly, meaning the head is longer and narrower than normal.^2,7-10

German and Takebe¹¹ reported 14 Japanese patients with Bloom syndrome. The phenotype differs somewhat from most cases recognized elsewhere in that dolichocephaly was a less constant feature, the facial skin was less prominent, and life-threatening infections were less common. Our patient had typical telangiectatic facial erythema without microcephaly, dolichocephaly, or any infections. She also had some uncommon manifestations such as alopecia areata, eyebrow hair loss, flat nose, reticular pigmentation, and short sharpened distal phalanges with fingernails that were wider than they were long. Although she had no recurrent infections and laboratory tests were within reference range, the alopecia areata and eyebrow hair loss may be associated with an abnormal immune response. The reasons for the short sharpened distal phalanges and the fingernail findings are unclear. The presence of reticular pigmentation also is unclear but may be associated with photosensitivity. Since the BLM gene was discovered to be the disease-causing gene of Bloom syndrome in 1995,^4,5 approximately 70 mutations were reported. The BLM gene encodes for the Bloom syndrome protein, a DNA helicase of the highly conserved RecQ subfamily of helicases, a group of nuclear proteins important in the maintenance of genomic stability.¹²

Mutation analysis of the BLM gene in our patient showed changes in 2 heterozygous nucleotide sites, including c.2603C>T in exon 13 and c.3961G>A in exon 21 of the BLM gene, which altered proline residue with leucine residue at 868 and valine residue with isoleucine residue at 1321, respectively. According to GenBank,^13,14 c.2603C>T and c.3961G>A are single nucleotide polymorphisms of the BLM gene. The genotypic distribution of International HapMap Project¹⁵ showed that C=602/602 and T=0/602 on c.2603 in 301 unrelated Chinese patients and G=585/602 and A=17/602 on c.3961 in 301 unrelated Chinese patients. Because of the low prevalence of genotypes c.2603T and c.3961A in China, the relationship between clinical features and c.2603C>T and c.3961G>A of the BLM gene in our patient requires further study.

In conclusion, we report a patient with Bloom syndrome with uncommon clinical manifestations. Our findings indicate that c.2603C>T and c.3961G>A of the BLM gene may be the pathogenic nature for Bloom syndrome in China.

Acknowledgments

The authors would like to thank the patient and her family for their participation in the study. The authors also thank Li Qi, BA, Beijing, China, for his contribution to the review of the data in the literature.

ORLANDO – When it comes to preventing alopecia, it may be best to advise patients against certain trendy hairstyles that can cause early hair loss.

At the Orlando Dermatology Aesthetic and Clinical Conference, Dr. Wendy Roberts, a dermatologist practicing in Rancho Mirage, Calif., spoke about the risks of traction alopecia associated with some hairstyles and why it’s in patients’ best interest to avoid them if they don’t want to experience premature hair loss.

Dr. Roberts brings up the topic of hair loss with patients during the full-body exam. Full-body skin exams are “opportunities for us, as the skin and hair experts, to speak to our patients about hair loss, [but] it’s rarely asked about,” she said. “Typically, what I do is start my full-body skin exam from the head and I always ask the question right away ‘How’s your hair? Are you having any problems with your hair? How’s your scalp?’ And about 50% of the time, there’s a positive answer or an interest in learning more about it.”

To avoid traction alopecia, caused frequently by intense pulling or pressure on the hair follicles, patients should be advised against braiding their hair or, for male patients, styling their hair in a “man bun.” For braids, the tightness of the braid and pulling along the hairlines will cause intense pressure on follicles over time that can lead to hair loss. For the man bun, Dr. Roberts noted that dermatologists will likely see an uptick in male patients with traction alopecia as this hairstyle becomes more popular.

In the evaluation and treatment of traction alopecia – as with any form of alopecia – clinical presentation, ethnicity, and the age of the patient should be considered, Dr. Roberts said. Additionally, collection of evidence – hair pulls, biopsy, dermoscopy, and lab work should be obtained.

Labs will check for iron levels and anemia, thyroid disease, vitamin D deficiency, and perhaps signs of a connective tissue disorder, she noted. “It’s staggering the amount of African-American women who are deficient in vitamin D, [and] there is some soft evidence that perhaps vitamin D deficiency may be a culprit in some of the clinical signs of discoid lupus erythematosus, [so] check the vitamin D and zinc levels.”

After making a diagnosis, it is important to quickly begin rigorous treatment of the alopecia. Aggressive treatment is “the bottom line,” Dr. Roberts emphasized, “because people are losing their hair and when they come to you, they’ve really had enough.”

She did not report any relevant financial disclosures.

[email protected]

ORLANDO – When it comes to preventing alopecia, it may be best to advise patients against certain trendy hairstyles that can cause early hair loss.

At the Orlando Dermatology Aesthetic and Clinical Conference, Dr. Wendy Roberts, a dermatologist practicing in Rancho Mirage, Calif., spoke about the risks of traction alopecia associated with some hairstyles and why it’s in patients’ best interest to avoid them if they don’t want to experience premature hair loss.

Dr. Roberts brings up the topic of hair loss with patients during the full-body exam. Full-body skin exams are “opportunities for us, as the skin and hair experts, to speak to our patients about hair loss, [but] it’s rarely asked about,” she said. “Typically, what I do is start my full-body skin exam from the head and I always ask the question right away ‘How’s your hair? Are you having any problems with your hair? How’s your scalp?’ And about 50% of the time, there’s a positive answer or an interest in learning more about it.”

To avoid traction alopecia, caused frequently by intense pulling or pressure on the hair follicles, patients should be advised against braiding their hair or, for male patients, styling their hair in a “man bun.” For braids, the tightness of the braid and pulling along the hairlines will cause intense pressure on follicles over time that can lead to hair loss. For the man bun, Dr. Roberts noted that dermatologists will likely see an uptick in male patients with traction alopecia as this hairstyle becomes more popular.

In the evaluation and treatment of traction alopecia – as with any form of alopecia – clinical presentation, ethnicity, and the age of the patient should be considered, Dr. Roberts said. Additionally, collection of evidence – hair pulls, biopsy, dermoscopy, and lab work should be obtained.

Labs will check for iron levels and anemia, thyroid disease, vitamin D deficiency, and perhaps signs of a connective tissue disorder, she noted. “It’s staggering the amount of African-American women who are deficient in vitamin D, [and] there is some soft evidence that perhaps vitamin D deficiency may be a culprit in some of the clinical signs of discoid lupus erythematosus, [so] check the vitamin D and zinc levels.”

After making a diagnosis, it is important to quickly begin rigorous treatment of the alopecia. Aggressive treatment is “the bottom line,” Dr. Roberts emphasized, “because people are losing their hair and when they come to you, they’ve really had enough.”

She did not report any relevant financial disclosures.

[email protected]

ORLANDO – When it comes to preventing alopecia, it may be best to advise patients against certain trendy hairstyles that can cause early hair loss.

At the Orlando Dermatology Aesthetic and Clinical Conference, Dr. Wendy Roberts, a dermatologist practicing in Rancho Mirage, Calif., spoke about the risks of traction alopecia associated with some hairstyles and why it’s in patients’ best interest to avoid them if they don’t want to experience premature hair loss.

Dr. Roberts brings up the topic of hair loss with patients during the full-body exam. Full-body skin exams are “opportunities for us, as the skin and hair experts, to speak to our patients about hair loss, [but] it’s rarely asked about,” she said. “Typically, what I do is start my full-body skin exam from the head and I always ask the question right away ‘How’s your hair? Are you having any problems with your hair? How’s your scalp?’ And about 50% of the time, there’s a positive answer or an interest in learning more about it.”

To avoid traction alopecia, caused frequently by intense pulling or pressure on the hair follicles, patients should be advised against braiding their hair or, for male patients, styling their hair in a “man bun.” For braids, the tightness of the braid and pulling along the hairlines will cause intense pressure on follicles over time that can lead to hair loss. For the man bun, Dr. Roberts noted that dermatologists will likely see an uptick in male patients with traction alopecia as this hairstyle becomes more popular.

In the evaluation and treatment of traction alopecia – as with any form of alopecia – clinical presentation, ethnicity, and the age of the patient should be considered, Dr. Roberts said. Additionally, collection of evidence – hair pulls, biopsy, dermoscopy, and lab work should be obtained.

Labs will check for iron levels and anemia, thyroid disease, vitamin D deficiency, and perhaps signs of a connective tissue disorder, she noted. “It’s staggering the amount of African-American women who are deficient in vitamin D, [and] there is some soft evidence that perhaps vitamin D deficiency may be a culprit in some of the clinical signs of discoid lupus erythematosus, [so] check the vitamin D and zinc levels.”

After making a diagnosis, it is important to quickly begin rigorous treatment of the alopecia. Aggressive treatment is “the bottom line,” Dr. Roberts emphasized, “because people are losing their hair and when they come to you, they’ve really had enough.”

She did not report any relevant financial disclosures.

[email protected]

ORLANDO – New diagnostic and treatment options are at the forefront of what’s new and exciting in the area of superficial cutaneous fungal infections, according to Dr. Adam Friedman.

“Although superficial cutaneous mycoses [are] extremely common, they can be quite a challenge for several reasons,” explained Dr. Friedman of the George Washington University in Washington, at the Orlando Dermatology Aesthetic and Clinical annual meeting, adding that “many of the common skin diseases are often confused for tineum, and vice versa.”

In this video interview, Dr. Friedman discusses what dermatologists should look for in terms of diagnosing and treating dermatophytes and onychomycosis, two of most common and increasingly treatable fungal infections patients are likely to present with.

Dr. Friedman did not report any relevant financial disclosures.

[email protected]

ORLANDO – New diagnostic and treatment options are at the forefront of what’s new and exciting in the area of superficial cutaneous fungal infections, according to Dr. Adam Friedman.

“Although superficial cutaneous mycoses [are] extremely common, they can be quite a challenge for several reasons,” explained Dr. Friedman of the George Washington University in Washington, at the Orlando Dermatology Aesthetic and Clinical annual meeting, adding that “many of the common skin diseases are often confused for tineum, and vice versa.”

In this video interview, Dr. Friedman discusses what dermatologists should look for in terms of diagnosing and treating dermatophytes and onychomycosis, two of most common and increasingly treatable fungal infections patients are likely to present with.

Dr. Friedman did not report any relevant financial disclosures.

[email protected]

ORLANDO – New diagnostic and treatment options are at the forefront of what’s new and exciting in the area of superficial cutaneous fungal infections, according to Dr. Adam Friedman.

“Although superficial cutaneous mycoses [are] extremely common, they can be quite a challenge for several reasons,” explained Dr. Friedman of the George Washington University in Washington, at the Orlando Dermatology Aesthetic and Clinical annual meeting, adding that “many of the common skin diseases are often confused for tineum, and vice versa.”

In this video interview, Dr. Friedman discusses what dermatologists should look for in terms of diagnosing and treating dermatophytes and onychomycosis, two of most common and increasingly treatable fungal infections patients are likely to present with.

Dr. Friedman did not report any relevant financial disclosures.

[email protected]

To the Editor:

Sebaceous nevus (SN) is a relatively common hamartoma that presents most often as a single congenital hairless plaque on the scalp. After puberty, histologic features characteristically include papillomatous hyperplasia of the epidermis, a large number of mature or nearly mature sebaceous glands, and a lack of terminally differentiated hair follicles; however, histologic findings can be misleading during childhood when sebaceous glands are still underdeveloped. Bright yellow dots, which are thought to indicate the presence of sebaceous glands, may be seen on dermoscopy and can be useful in differentiating SN from aplasia cutis congenita in newborns.

We report a case of an SN in an 18-year-old woman and discuss how the histology findings correlated with features seen on dermoscopy.

An 18-year-old woman presented to our dermatology clinic with an asymptomatic, hairless plaque on the right parietal scalp that had been present since birth. The patient noted that the plaque had recently become larger in size. On physical examination, an 8×3-cm plaque with a smooth, flesh-colored surface was noted with central comedolike structures and an erythematous, verrucous periphery (Figure 1).

Dermoscopy (handheld dermoscope using polarized light) revealed 3 distinct types of round structures within the lesion: (1) comedolike openings (similar to those seen in seborrheic keratosis) that appeared as brownish-yellow, sharply circumscribed structures; (2) milialike cysts (also found in acanthotic seborrheic keratosis), which appeared as bright yellow structures; and (3) multiple whitish structures that were irregular in shape and size and covered the surface of the lesion where there were no other dermoscopic findings (Figure 2). The affected skin was pale to red in color and the verrucous aspect of the surface was better visualized at the edge of the lesion.

Two 4-mm punch biopsies were performed following dermoscopy: one for horizontal sectioning and one for vertical sectioning. Histologic analysis showed an acanthotic epidermis with an anastomosing network of elongated rete ridges in the superficial dermis. Numerous hyperplasic sebaceous glands were found in the mid dermis, with some also located above this level. Immature hair follicles were present and sebaceous gland ducts communicated directly with the epidermis through dilated hyperkeratinized pathways. Eccrine glands were normal, but no apocrine glands were present. A lymphocytic infiltrate was noted around the sebaceous glands and immature hair follicles and also around dilated capillaries in the superficial dermis. Moderate spongiosis and lymphocytic exocytosis were noted in the glandular epithelium and in the basal layer of the hair follicles and the epidermis. Superficial slides of horizontal sections of the biopsy specimen showed a correlation between the histology findings and dermoscopy images: multiple normal-appearing papilla surrounded by a network of anastomosing rete ridges correlated with multiple whitish structures, keratotic cysts with compact keratin corresponded to bright yellow dots, and larger conglomerates of loose lamelar keratin correlated with comedolike openings. Due to the presence of eczematous changes (eg, epithelial spongiosis, inflammatory cells) observed on histology, a diagnosis of an irritated sebaceous nevus was made, which explained the recent enlargement of the congenital lesion.

Sebaceous nevus is a benign, epidermal appendageal tumor with differentiation towards sebaceous glands that is composed of mature or nearly mature skin structures. Histologically, it is classified as a hamartoma.¹ It commonly arises on the scalp as a yellowish or flesh-colored, hairless plaque of variable size. At birth, its surface is smooth and the differential diagnoses include aplasia cutis congenita, congenital triangular alopecia, and alopecia areata.² As the patient ages, hormones stimulate the proliferation of sebaceous glands and the epidermis, and the lesion gradually acquires a verrucous, waxy surface.³ Benign appendageal tumors often develop inside SN. Basal cell epitheliomas are rarely found.⁴ Surgical excision is recommended for aesthetic purposes or to prevent the development of tumors.

Histology also varies with the patient’s age and can be misleading in childhood because the sebaceous glands are underdeveloped.^5,6 After adrenarche, histology becomes more diagnostic, showing a dermis almost completely filled with sebaceous glands with varying degrees of maturity.² The presence of incompletely differentiated follicles without hair shafts can be found in newborns and children and may be helpful for the correct histological diagnosis before puberty.^1,5 The epidermis presents no abnormalities at birth but develops acanthosis and papillomatosis as the patient ages. Ectopic dilated apocrine glands sometimes can be found deeper in the dermis in the late stage of the lesion.⁵

In a report by Neri et al,⁷ multiple bright yellow dots were noted on dermoscopy in 2 children with SN. The investigators concluded that this characteristic feature, which was thought to represent the sebaceous glands, can be useful in differentiating SN from aplasia cutis congenita in early infancy, but no histologic analyses were performed.⁷ In our patient, we identified 3 different dermoscopic features that correlated with histologic findings. Comedolike openings correlated with the accumulated keratin (ie, keratotic plugs) inside dilated sebaceous gland ducts directly connected to the epidermis. The brownish-yellow color of these openings observed on dermoscopy may be due to the oxidation of kerat-inous material, such as those in seborrheic keratosis lesions (Figure 3). We also noted bright yellow dots similar to those reported by Neri et al⁷; however, histologic analysis in our patient showed these dots more closely correlated with keratotic cysts similar to milialike structures seen in acanthotic seborrheic keratosis. The material remained lightly colored because no oxidation process had occurred (Figure 4). The third structure found on dermoscopy in our patient was multiple whitish structures that were irregular in shape and size. According to our comparison of superficial horizontal histology slides with dermoscopy images, we hypothesized this finding was the result of epidermal papillomatosis over a dermis filled with enlarged sebaceous glands (Figure 5). This finding was likely absent in the cases previously reported by Neri et al⁷ because epidermal and glandular changes occur later in the evolution of SN and the patients in these cases were younger than 4 months old.

Our correlation of dermoscopic features with histology findings in an 18-year-old woman with an irritated SN highlights the need for more studies needed in order to establish the prevalence of certain dermoscopic findings in this setting, particularly considering the important morphological changes that occur in these lesions as patients age as well as the histological variation among different hamartomas. Over the last decade, dermoscopy has proven to be a useful tool in the diagnosis of various hair and scalp diseases.⁸ Histologic correlation of dermoscopy findings is essential for more precise understanding of this new imaging technique and should be conducted whenever possible.

To the Editor:

Sebaceous nevus (SN) is a relatively common hamartoma that presents most often as a single congenital hairless plaque on the scalp. After puberty, histologic features characteristically include papillomatous hyperplasia of the epidermis, a large number of mature or nearly mature sebaceous glands, and a lack of terminally differentiated hair follicles; however, histologic findings can be misleading during childhood when sebaceous glands are still underdeveloped. Bright yellow dots, which are thought to indicate the presence of sebaceous glands, may be seen on dermoscopy and can be useful in differentiating SN from aplasia cutis congenita in newborns.

We report a case of an SN in an 18-year-old woman and discuss how the histology findings correlated with features seen on dermoscopy.

An 18-year-old woman presented to our dermatology clinic with an asymptomatic, hairless plaque on the right parietal scalp that had been present since birth. The patient noted that the plaque had recently become larger in size. On physical examination, an 8×3-cm plaque with a smooth, flesh-colored surface was noted with central comedolike structures and an erythematous, verrucous periphery (Figure 1).

Dermoscopy (handheld dermoscope using polarized light) revealed 3 distinct types of round structures within the lesion: (1) comedolike openings (similar to those seen in seborrheic keratosis) that appeared as brownish-yellow, sharply circumscribed structures; (2) milialike cysts (also found in acanthotic seborrheic keratosis), which appeared as bright yellow structures; and (3) multiple whitish structures that were irregular in shape and size and covered the surface of the lesion where there were no other dermoscopic findings (Figure 2). The affected skin was pale to red in color and the verrucous aspect of the surface was better visualized at the edge of the lesion.

Two 4-mm punch biopsies were performed following dermoscopy: one for horizontal sectioning and one for vertical sectioning. Histologic analysis showed an acanthotic epidermis with an anastomosing network of elongated rete ridges in the superficial dermis. Numerous hyperplasic sebaceous glands were found in the mid dermis, with some also located above this level. Immature hair follicles were present and sebaceous gland ducts communicated directly with the epidermis through dilated hyperkeratinized pathways. Eccrine glands were normal, but no apocrine glands were present. A lymphocytic infiltrate was noted around the sebaceous glands and immature hair follicles and also around dilated capillaries in the superficial dermis. Moderate spongiosis and lymphocytic exocytosis were noted in the glandular epithelium and in the basal layer of the hair follicles and the epidermis. Superficial slides of horizontal sections of the biopsy specimen showed a correlation between the histology findings and dermoscopy images: multiple normal-appearing papilla surrounded by a network of anastomosing rete ridges correlated with multiple whitish structures, keratotic cysts with compact keratin corresponded to bright yellow dots, and larger conglomerates of loose lamelar keratin correlated with comedolike openings. Due to the presence of eczematous changes (eg, epithelial spongiosis, inflammatory cells) observed on histology, a diagnosis of an irritated sebaceous nevus was made, which explained the recent enlargement of the congenital lesion.

Sebaceous nevus is a benign, epidermal appendageal tumor with differentiation towards sebaceous glands that is composed of mature or nearly mature skin structures. Histologically, it is classified as a hamartoma.¹ It commonly arises on the scalp as a yellowish or flesh-colored, hairless plaque of variable size. At birth, its surface is smooth and the differential diagnoses include aplasia cutis congenita, congenital triangular alopecia, and alopecia areata.² As the patient ages, hormones stimulate the proliferation of sebaceous glands and the epidermis, and the lesion gradually acquires a verrucous, waxy surface.³ Benign appendageal tumors often develop inside SN. Basal cell epitheliomas are rarely found.⁴ Surgical excision is recommended for aesthetic purposes or to prevent the development of tumors.

Histology also varies with the patient’s age and can be misleading in childhood because the sebaceous glands are underdeveloped.^5,6 After adrenarche, histology becomes more diagnostic, showing a dermis almost completely filled with sebaceous glands with varying degrees of maturity.² The presence of incompletely differentiated follicles without hair shafts can be found in newborns and children and may be helpful for the correct histological diagnosis before puberty.^1,5 The epidermis presents no abnormalities at birth but develops acanthosis and papillomatosis as the patient ages. Ectopic dilated apocrine glands sometimes can be found deeper in the dermis in the late stage of the lesion.⁵

In a report by Neri et al,⁷ multiple bright yellow dots were noted on dermoscopy in 2 children with SN. The investigators concluded that this characteristic feature, which was thought to represent the sebaceous glands, can be useful in differentiating SN from aplasia cutis congenita in early infancy, but no histologic analyses were performed.⁷ In our patient, we identified 3 different dermoscopic features that correlated with histologic findings. Comedolike openings correlated with the accumulated keratin (ie, keratotic plugs) inside dilated sebaceous gland ducts directly connected to the epidermis. The brownish-yellow color of these openings observed on dermoscopy may be due to the oxidation of kerat-inous material, such as those in seborrheic keratosis lesions (Figure 3). We also noted bright yellow dots similar to those reported by Neri et al⁷; however, histologic analysis in our patient showed these dots more closely correlated with keratotic cysts similar to milialike structures seen in acanthotic seborrheic keratosis. The material remained lightly colored because no oxidation process had occurred (Figure 4). The third structure found on dermoscopy in our patient was multiple whitish structures that were irregular in shape and size. According to our comparison of superficial horizontal histology slides with dermoscopy images, we hypothesized this finding was the result of epidermal papillomatosis over a dermis filled with enlarged sebaceous glands (Figure 5). This finding was likely absent in the cases previously reported by Neri et al⁷ because epidermal and glandular changes occur later in the evolution of SN and the patients in these cases were younger than 4 months old.

Our correlation of dermoscopic features with histology findings in an 18-year-old woman with an irritated SN highlights the need for more studies needed in order to establish the prevalence of certain dermoscopic findings in this setting, particularly considering the important morphological changes that occur in these lesions as patients age as well as the histological variation among different hamartomas. Over the last decade, dermoscopy has proven to be a useful tool in the diagnosis of various hair and scalp diseases.⁸ Histologic correlation of dermoscopy findings is essential for more precise understanding of this new imaging technique and should be conducted whenever possible.

To the Editor:

Sebaceous nevus (SN) is a relatively common hamartoma that presents most often as a single congenital hairless plaque on the scalp. After puberty, histologic features characteristically include papillomatous hyperplasia of the epidermis, a large number of mature or nearly mature sebaceous glands, and a lack of terminally differentiated hair follicles; however, histologic findings can be misleading during childhood when sebaceous glands are still underdeveloped. Bright yellow dots, which are thought to indicate the presence of sebaceous glands, may be seen on dermoscopy and can be useful in differentiating SN from aplasia cutis congenita in newborns.

We report a case of an SN in an 18-year-old woman and discuss how the histology findings correlated with features seen on dermoscopy.

An 18-year-old woman presented to our dermatology clinic with an asymptomatic, hairless plaque on the right parietal scalp that had been present since birth. The patient noted that the plaque had recently become larger in size. On physical examination, an 8×3-cm plaque with a smooth, flesh-colored surface was noted with central comedolike structures and an erythematous, verrucous periphery (Figure 1).

Dermoscopy (handheld dermoscope using polarized light) revealed 3 distinct types of round structures within the lesion: (1) comedolike openings (similar to those seen in seborrheic keratosis) that appeared as brownish-yellow, sharply circumscribed structures; (2) milialike cysts (also found in acanthotic seborrheic keratosis), which appeared as bright yellow structures; and (3) multiple whitish structures that were irregular in shape and size and covered the surface of the lesion where there were no other dermoscopic findings (Figure 2). The affected skin was pale to red in color and the verrucous aspect of the surface was better visualized at the edge of the lesion.

Two 4-mm punch biopsies were performed following dermoscopy: one for horizontal sectioning and one for vertical sectioning. Histologic analysis showed an acanthotic epidermis with an anastomosing network of elongated rete ridges in the superficial dermis. Numerous hyperplasic sebaceous glands were found in the mid dermis, with some also located above this level. Immature hair follicles were present and sebaceous gland ducts communicated directly with the epidermis through dilated hyperkeratinized pathways. Eccrine glands were normal, but no apocrine glands were present. A lymphocytic infiltrate was noted around the sebaceous glands and immature hair follicles and also around dilated capillaries in the superficial dermis. Moderate spongiosis and lymphocytic exocytosis were noted in the glandular epithelium and in the basal layer of the hair follicles and the epidermis. Superficial slides of horizontal sections of the biopsy specimen showed a correlation between the histology findings and dermoscopy images: multiple normal-appearing papilla surrounded by a network of anastomosing rete ridges correlated with multiple whitish structures, keratotic cysts with compact keratin corresponded to bright yellow dots, and larger conglomerates of loose lamelar keratin correlated with comedolike openings. Due to the presence of eczematous changes (eg, epithelial spongiosis, inflammatory cells) observed on histology, a diagnosis of an irritated sebaceous nevus was made, which explained the recent enlargement of the congenital lesion.

Sebaceous nevus is a benign, epidermal appendageal tumor with differentiation towards sebaceous glands that is composed of mature or nearly mature skin structures. Histologically, it is classified as a hamartoma.¹ It commonly arises on the scalp as a yellowish or flesh-colored, hairless plaque of variable size. At birth, its surface is smooth and the differential diagnoses include aplasia cutis congenita, congenital triangular alopecia, and alopecia areata.² As the patient ages, hormones stimulate the proliferation of sebaceous glands and the epidermis, and the lesion gradually acquires a verrucous, waxy surface.³ Benign appendageal tumors often develop inside SN. Basal cell epitheliomas are rarely found.⁴ Surgical excision is recommended for aesthetic purposes or to prevent the development of tumors.

Histology also varies with the patient’s age and can be misleading in childhood because the sebaceous glands are underdeveloped.^5,6 After adrenarche, histology becomes more diagnostic, showing a dermis almost completely filled with sebaceous glands with varying degrees of maturity.² The presence of incompletely differentiated follicles without hair shafts can be found in newborns and children and may be helpful for the correct histological diagnosis before puberty.^1,5 The epidermis presents no abnormalities at birth but develops acanthosis and papillomatosis as the patient ages. Ectopic dilated apocrine glands sometimes can be found deeper in the dermis in the late stage of the lesion.⁵

In a report by Neri et al,⁷ multiple bright yellow dots were noted on dermoscopy in 2 children with SN. The investigators concluded that this characteristic feature, which was thought to represent the sebaceous glands, can be useful in differentiating SN from aplasia cutis congenita in early infancy, but no histologic analyses were performed.⁷ In our patient, we identified 3 different dermoscopic features that correlated with histologic findings. Comedolike openings correlated with the accumulated keratin (ie, keratotic plugs) inside dilated sebaceous gland ducts directly connected to the epidermis. The brownish-yellow color of these openings observed on dermoscopy may be due to the oxidation of kerat-inous material, such as those in seborrheic keratosis lesions (Figure 3). We also noted bright yellow dots similar to those reported by Neri et al⁷; however, histologic analysis in our patient showed these dots more closely correlated with keratotic cysts similar to milialike structures seen in acanthotic seborrheic keratosis. The material remained lightly colored because no oxidation process had occurred (Figure 4). The third structure found on dermoscopy in our patient was multiple whitish structures that were irregular in shape and size. According to our comparison of superficial horizontal histology slides with dermoscopy images, we hypothesized this finding was the result of epidermal papillomatosis over a dermis filled with enlarged sebaceous glands (Figure 5). This finding was likely absent in the cases previously reported by Neri et al⁷ because epidermal and glandular changes occur later in the evolution of SN and the patients in these cases were younger than 4 months old.

Our correlation of dermoscopic features with histology findings in an 18-year-old woman with an irritated SN highlights the need for more studies needed in order to establish the prevalence of certain dermoscopic findings in this setting, particularly considering the important morphological changes that occur in these lesions as patients age as well as the histological variation among different hamartomas. Over the last decade, dermoscopy has proven to be a useful tool in the diagnosis of various hair and scalp diseases.⁸ Histologic correlation of dermoscopy findings is essential for more precise understanding of this new imaging technique and should be conducted whenever possible.

What does the patient need to know at the first visit?

When I communicate with alopecia patients at the first visit, I make sure they know that I’m there to help them—that I won’t minimize their concerns and that I understand how important their condition is to them. Alopecia can be frustrating for both the patient and the physician, and there often is a confounding background of psychosocial stress and/or a history of physicians who have dismissed the patient’s concerns about his or her hair loss as trivial. Establishing an effective doctor-patient relationship is key in treating alopecia. Physicians sometimes may be left feeling like the patient wants to keep them in the room until his or her hair regrows, but in reality you simply need to reassure the patient that you are comfortable with the evaluation and treatment of alopecia and that several steps will be required but you will get started today.

How do you use punch biopsies to determine the best treatment options?

My most important tips regarding alopecia diagnosis relate to scalp biopsies, which usually are required in distinguishing chronic cutaneous lupus erythematosus from other scarring alopecias. First, an absorbable gelatin compressed sponge is your best friend. A small strip inserted into the punch biopsy wound results in prompt hemostasis without the need for sutures, and the resulting scar often looks as good or better than that produced by suturing. Next, don’t biopsy the active advancing borders of an alopecia patch, as the findings usually are nonspecific. Instead, biopsy a well-established portion that has been present for at least 4 to 6 months but is still active. In inconclusive cases, a biopsy of a scarred area stained with Verhoeff elastic stain can demonstrate characteristic patterns of elastic tissue loss and often establish a diagnosis. It is important to distinguish chronic cutaneous lupus erythematosus from other forms of scarring alopecia, as it is more likely to respond to antimalarials.

What are your go-to treatments? Are your recommendations anecdotal or evidence based?

There isn’t an extensive arsenal of evidence-based therapy for refractory scarring alopecia, but that doesn’t mean we don’t have effective therapies; it simply means that our treatments are based on experience without accompanying randomized controlled trials. We need to produce more evidence, but patients with severe disease still need to be treated in the meantime. It’s important to remember that therapeutic complacency can result in permanent irreversible scarring. The presence of easily extractable anagen hairs is a sign of active disease. This simple test is helpful to monitor therapeutic progress.

Topical and intralesional corticosteroids can be extremely useful and often are underused. In general, the risk of scarring and atrophy from untreated disease is much greater than that from the corticosteroid. On the scalp, atrophy often presents as erythema, which should not be confused with erythema related to active disease. Dermoscopy is useful to demonstrate that the redness represents dermal atrophy with prominence of the subpapillary plexus of vessels.

When systemic therapy is required, antimalarials, retinoids, dapsone, thalidomide, sulfasalazine, mycophenolate mofetil, and methotrexate have all been used successfully in the setting of cutaneous lupus erythematosus, while topical tazarotene and topical calcineurin inhibitors are generally disappointing.

For the treatment of lichen planopilaris, intralesional corticosteroids, oral retinoids, and excimer laser can be effective. In contrast, antimalarials usually are not effective in preventing disease progression. The peroxisome proliferator-activated receptor-γ agonist pioglitazone can be effective, but reported results vary widely. In my experience, mycophenolate mofetil is generally reliable in patients with refractory disease. Dutasteride can be effective as a first-line therapy in the setting of frontal fibrosing alopecia, although some of the noted improvement may relate to the nonscarring portion of the disease in patients with a background of pattern alopecia.

How do you keep patients compliant with treatment?  

Again, the key to treatment compliance is to establish an effective doctor-patient relationship. Whenever possible, begin with adequately potent therapy to give patients an early response. Don’t hesitate to use prednisone initially for inflammatory scarring alopecia. Patients need to see signs of progress in order to stay compliant with treatment, and long trials of ineffective therapies destroy trust. Adequate doses of intralesional or oral corticosteroids often are appropriate to ensure an early response with subsequent transition to steroid-sparing agents.

What do you do if they refuse treatment? 

Try to find out why—often it’s simply fear of side effects. Patient education is key, and it can help tremendously to share with them the number of patients you have treated safely with the medication in question and assure them that you know how to monitor for the important side effects.

What resources do you recommend to patients for more information? 

It is helpful to keep a handy list of patient advocacy Web sites. Well-established support groups such as the National Alopecia Areata Foundation (https://www.naaf.org) and the Cicatricial Alopecia Research Foundation (http://www.carfintl.org) provide excellent information for patients and help to support research to improve outcomes for these difficult disorders.

What does the patient need to know at the first visit?

When I communicate with alopecia patients at the first visit, I make sure they know that I’m there to help them—that I won’t minimize their concerns and that I understand how important their condition is to them. Alopecia can be frustrating for both the patient and the physician, and there often is a confounding background of psychosocial stress and/or a history of physicians who have dismissed the patient’s concerns about his or her hair loss as trivial. Establishing an effective doctor-patient relationship is key in treating alopecia. Physicians sometimes may be left feeling like the patient wants to keep them in the room until his or her hair regrows, but in reality you simply need to reassure the patient that you are comfortable with the evaluation and treatment of alopecia and that several steps will be required but you will get started today.

How do you use punch biopsies to determine the best treatment options?

My most important tips regarding alopecia diagnosis relate to scalp biopsies, which usually are required in distinguishing chronic cutaneous lupus erythematosus from other scarring alopecias. First, an absorbable gelatin compressed sponge is your best friend. A small strip inserted into the punch biopsy wound results in prompt hemostasis without the need for sutures, and the resulting scar often looks as good or better than that produced by suturing. Next, don’t biopsy the active advancing borders of an alopecia patch, as the findings usually are nonspecific. Instead, biopsy a well-established portion that has been present for at least 4 to 6 months but is still active. In inconclusive cases, a biopsy of a scarred area stained with Verhoeff elastic stain can demonstrate characteristic patterns of elastic tissue loss and often establish a diagnosis. It is important to distinguish chronic cutaneous lupus erythematosus from other forms of scarring alopecia, as it is more likely to respond to antimalarials.

What are your go-to treatments? Are your recommendations anecdotal or evidence based?

There isn’t an extensive arsenal of evidence-based therapy for refractory scarring alopecia, but that doesn’t mean we don’t have effective therapies; it simply means that our treatments are based on experience without accompanying randomized controlled trials. We need to produce more evidence, but patients with severe disease still need to be treated in the meantime. It’s important to remember that therapeutic complacency can result in permanent irreversible scarring. The presence of easily extractable anagen hairs is a sign of active disease. This simple test is helpful to monitor therapeutic progress.

Topical and intralesional corticosteroids can be extremely useful and often are underused. In general, the risk of scarring and atrophy from untreated disease is much greater than that from the corticosteroid. On the scalp, atrophy often presents as erythema, which should not be confused with erythema related to active disease. Dermoscopy is useful to demonstrate that the redness represents dermal atrophy with prominence of the subpapillary plexus of vessels.

When systemic therapy is required, antimalarials, retinoids, dapsone, thalidomide, sulfasalazine, mycophenolate mofetil, and methotrexate have all been used successfully in the setting of cutaneous lupus erythematosus, while topical tazarotene and topical calcineurin inhibitors are generally disappointing.

For the treatment of lichen planopilaris, intralesional corticosteroids, oral retinoids, and excimer laser can be effective. In contrast, antimalarials usually are not effective in preventing disease progression. The peroxisome proliferator-activated receptor-γ agonist pioglitazone can be effective, but reported results vary widely. In my experience, mycophenolate mofetil is generally reliable in patients with refractory disease. Dutasteride can be effective as a first-line therapy in the setting of frontal fibrosing alopecia, although some of the noted improvement may relate to the nonscarring portion of the disease in patients with a background of pattern alopecia.

How do you keep patients compliant with treatment?  

Again, the key to treatment compliance is to establish an effective doctor-patient relationship. Whenever possible, begin with adequately potent therapy to give patients an early response. Don’t hesitate to use prednisone initially for inflammatory scarring alopecia. Patients need to see signs of progress in order to stay compliant with treatment, and long trials of ineffective therapies destroy trust. Adequate doses of intralesional or oral corticosteroids often are appropriate to ensure an early response with subsequent transition to steroid-sparing agents.

What do you do if they refuse treatment? 

Try to find out why—often it’s simply fear of side effects. Patient education is key, and it can help tremendously to share with them the number of patients you have treated safely with the medication in question and assure them that you know how to monitor for the important side effects.

What resources do you recommend to patients for more information? 

It is helpful to keep a handy list of patient advocacy Web sites. Well-established support groups such as the National Alopecia Areata Foundation (https://www.naaf.org) and the Cicatricial Alopecia Research Foundation (http://www.carfintl.org) provide excellent information for patients and help to support research to improve outcomes for these difficult disorders.

What does the patient need to know at the first visit?

When I communicate with alopecia patients at the first visit, I make sure they know that I’m there to help them—that I won’t minimize their concerns and that I understand how important their condition is to them. Alopecia can be frustrating for both the patient and the physician, and there often is a confounding background of psychosocial stress and/or a history of physicians who have dismissed the patient’s concerns about his or her hair loss as trivial. Establishing an effective doctor-patient relationship is key in treating alopecia. Physicians sometimes may be left feeling like the patient wants to keep them in the room until his or her hair regrows, but in reality you simply need to reassure the patient that you are comfortable with the evaluation and treatment of alopecia and that several steps will be required but you will get started today.

How do you use punch biopsies to determine the best treatment options?

My most important tips regarding alopecia diagnosis relate to scalp biopsies, which usually are required in distinguishing chronic cutaneous lupus erythematosus from other scarring alopecias. First, an absorbable gelatin compressed sponge is your best friend. A small strip inserted into the punch biopsy wound results in prompt hemostasis without the need for sutures, and the resulting scar often looks as good or better than that produced by suturing. Next, don’t biopsy the active advancing borders of an alopecia patch, as the findings usually are nonspecific. Instead, biopsy a well-established portion that has been present for at least 4 to 6 months but is still active. In inconclusive cases, a biopsy of a scarred area stained with Verhoeff elastic stain can demonstrate characteristic patterns of elastic tissue loss and often establish a diagnosis. It is important to distinguish chronic cutaneous lupus erythematosus from other forms of scarring alopecia, as it is more likely to respond to antimalarials.

What are your go-to treatments? Are your recommendations anecdotal or evidence based?

There isn’t an extensive arsenal of evidence-based therapy for refractory scarring alopecia, but that doesn’t mean we don’t have effective therapies; it simply means that our treatments are based on experience without accompanying randomized controlled trials. We need to produce more evidence, but patients with severe disease still need to be treated in the meantime. It’s important to remember that therapeutic complacency can result in permanent irreversible scarring. The presence of easily extractable anagen hairs is a sign of active disease. This simple test is helpful to monitor therapeutic progress.

Topical and intralesional corticosteroids can be extremely useful and often are underused. In general, the risk of scarring and atrophy from untreated disease is much greater than that from the corticosteroid. On the scalp, atrophy often presents as erythema, which should not be confused with erythema related to active disease. Dermoscopy is useful to demonstrate that the redness represents dermal atrophy with prominence of the subpapillary plexus of vessels.

When systemic therapy is required, antimalarials, retinoids, dapsone, thalidomide, sulfasalazine, mycophenolate mofetil, and methotrexate have all been used successfully in the setting of cutaneous lupus erythematosus, while topical tazarotene and topical calcineurin inhibitors are generally disappointing.

For the treatment of lichen planopilaris, intralesional corticosteroids, oral retinoids, and excimer laser can be effective. In contrast, antimalarials usually are not effective in preventing disease progression. The peroxisome proliferator-activated receptor-γ agonist pioglitazone can be effective, but reported results vary widely. In my experience, mycophenolate mofetil is generally reliable in patients with refractory disease. Dutasteride can be effective as a first-line therapy in the setting of frontal fibrosing alopecia, although some of the noted improvement may relate to the nonscarring portion of the disease in patients with a background of pattern alopecia.

How do you keep patients compliant with treatment?  

Again, the key to treatment compliance is to establish an effective doctor-patient relationship. Whenever possible, begin with adequately potent therapy to give patients an early response. Don’t hesitate to use prednisone initially for inflammatory scarring alopecia. Patients need to see signs of progress in order to stay compliant with treatment, and long trials of ineffective therapies destroy trust. Adequate doses of intralesional or oral corticosteroids often are appropriate to ensure an early response with subsequent transition to steroid-sparing agents.

What do you do if they refuse treatment? 

Try to find out why—often it’s simply fear of side effects. Patient education is key, and it can help tremendously to share with them the number of patients you have treated safely with the medication in question and assure them that you know how to monitor for the important side effects.

What resources do you recommend to patients for more information? 

It is helpful to keep a handy list of patient advocacy Web sites. Well-established support groups such as the National Alopecia Areata Foundation (https://www.naaf.org) and the Cicatricial Alopecia Research Foundation (http://www.carfintl.org) provide excellent information for patients and help to support research to improve outcomes for these difficult disorders.

LAS VEGAS – Tinea pedis plagues millions of patients yearly, and treatment is lengthy, cumbersome, and often ineffective.

But two potent new antifungals promise an easier treatment regimen and a higher rate of successful treatment outcomes, according to Dr. David M. Pariser, who shared data about luliconazole and a new formulation of naftifine as topical treatments for tinea infections, at the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar.

Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, pointed out that most antifungals currently approved for tinea pedis require at least daily – and sometimes twice daily – application for at least 4 weeks. Terbinafine and tolnaftate are the exceptions, with treatment periods ranging from 1-6 weeks for the two products, depending on clinical response.

A new formulation of naftifine hydrochloride 2%, (Naftin), a potent prescription topical allylamine antifungal available as a cream or a gel, has shown equivalent efficacy with just two weeks of treatment. Naftifine has lipophilic and keratinophilic properties; further, it has clinically significant anti-inflammatory and antibacterial effects, in addition to its potent fungicidal and fungistatic effects against dermatophytes, Dr. Pariser said at the meeting. The preparations are currently approved for topical treatment of tinea pedis, tinea cruris, and tinea corporis.

Notably, naftifine maintains a “clinically relevant therapeutic reservoir effect after treatment completion, with naftifine detected in the stratum corneum for up to 4 weeks posttreatment,” he said. This reservoir effect permits a significantly easier treatment regimen, with topical application of either formulation daily for just 2 weeks.

The clinical trials of naftifine HCl 2% with daily administration for 2 weeks showed equivalence with the 1% formulation administered for 4 weeks; the higher concentration was well tolerated and was effective in both the moccasin and interdigital distributions of tinea pedis involvement. Trials also showed the mycologic and clinical cure rates of naftifine 2% to be equivalent or superior to those of terbinafine, econazole, clotrimazole, miconazole, and tolnaftate.

Clinical trials showed treatment effectiveness – defined as 90% improvement over baseline and achieving “essentially normal skin” – in 52% of patients receiving naftifine 2%, compared with 20% of patients receiving vehicle only. Overall clinical success – defined as mycologic cure and either clinical cure of effective clinical treatment – was seen in 78% of the naftifine 2% patients, compared with 49% of the vehicle patients.

The second antifungal Dr. Pariser discussed is luliconazole (Luzu), a prescription topical imidazole that is available as a 1% cream. Luliconazole is also a broad-spectrum, potent antifungal with effects that persist several weeks after treatment. The preparation is at least as effective as bifonazole, terbinafine, and lanoconazole, both in vitro and in vivo, Dr. Pariser said.

In two parallel clinical trials comparing luliconazole 1% cream to its vehicle, treatment was effective (at least 90% clearing and with normal-appearing skin) in 48% and 33% of patients receiving luliconazole, compared with 10% and 15% of patients receiving vehicle alone.

An advantage of the topical agents is that there are generally no major systemic side effects, since there is minimal systemic absorption, Dr. Pariser noted. Allergic contact dermatitis may be a local reaction, but tends to be mild and transient, he said.

Clinicians should always be alert for tinea pedis when treating onychomycosis, said Dr. Pariser, and untreated tinea can contribute to recurrence of nail fungus. “If you don’t look for tinea, you might not find it, and you’ve missed a treatment opportunity,” he said.

Dr. Pariser disclosed that he is an investigator and consultant for Valeant and an investigator for Anacor Pharmaceuticals.

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

[email protected]

On Twitter @karioakes

LAS VEGAS – Tinea pedis plagues millions of patients yearly, and treatment is lengthy, cumbersome, and often ineffective.

But two potent new antifungals promise an easier treatment regimen and a higher rate of successful treatment outcomes, according to Dr. David M. Pariser, who shared data about luliconazole and a new formulation of naftifine as topical treatments for tinea infections, at the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar.

Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, pointed out that most antifungals currently approved for tinea pedis require at least daily – and sometimes twice daily – application for at least 4 weeks. Terbinafine and tolnaftate are the exceptions, with treatment periods ranging from 1-6 weeks for the two products, depending on clinical response.

A new formulation of naftifine hydrochloride 2%, (Naftin), a potent prescription topical allylamine antifungal available as a cream or a gel, has shown equivalent efficacy with just two weeks of treatment. Naftifine has lipophilic and keratinophilic properties; further, it has clinically significant anti-inflammatory and antibacterial effects, in addition to its potent fungicidal and fungistatic effects against dermatophytes, Dr. Pariser said at the meeting. The preparations are currently approved for topical treatment of tinea pedis, tinea cruris, and tinea corporis.

Notably, naftifine maintains a “clinically relevant therapeutic reservoir effect after treatment completion, with naftifine detected in the stratum corneum for up to 4 weeks posttreatment,” he said. This reservoir effect permits a significantly easier treatment regimen, with topical application of either formulation daily for just 2 weeks.

The clinical trials of naftifine HCl 2% with daily administration for 2 weeks showed equivalence with the 1% formulation administered for 4 weeks; the higher concentration was well tolerated and was effective in both the moccasin and interdigital distributions of tinea pedis involvement. Trials also showed the mycologic and clinical cure rates of naftifine 2% to be equivalent or superior to those of terbinafine, econazole, clotrimazole, miconazole, and tolnaftate.

Clinical trials showed treatment effectiveness – defined as 90% improvement over baseline and achieving “essentially normal skin” – in 52% of patients receiving naftifine 2%, compared with 20% of patients receiving vehicle only. Overall clinical success – defined as mycologic cure and either clinical cure of effective clinical treatment – was seen in 78% of the naftifine 2% patients, compared with 49% of the vehicle patients.

The second antifungal Dr. Pariser discussed is luliconazole (Luzu), a prescription topical imidazole that is available as a 1% cream. Luliconazole is also a broad-spectrum, potent antifungal with effects that persist several weeks after treatment. The preparation is at least as effective as bifonazole, terbinafine, and lanoconazole, both in vitro and in vivo, Dr. Pariser said.

In two parallel clinical trials comparing luliconazole 1% cream to its vehicle, treatment was effective (at least 90% clearing and with normal-appearing skin) in 48% and 33% of patients receiving luliconazole, compared with 10% and 15% of patients receiving vehicle alone.

An advantage of the topical agents is that there are generally no major systemic side effects, since there is minimal systemic absorption, Dr. Pariser noted. Allergic contact dermatitis may be a local reaction, but tends to be mild and transient, he said.

Clinicians should always be alert for tinea pedis when treating onychomycosis, said Dr. Pariser, and untreated tinea can contribute to recurrence of nail fungus. “If you don’t look for tinea, you might not find it, and you’ve missed a treatment opportunity,” he said.

Dr. Pariser disclosed that he is an investigator and consultant for Valeant and an investigator for Anacor Pharmaceuticals.

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

[email protected]

On Twitter @karioakes

LAS VEGAS – Tinea pedis plagues millions of patients yearly, and treatment is lengthy, cumbersome, and often ineffective.

But two potent new antifungals promise an easier treatment regimen and a higher rate of successful treatment outcomes, according to Dr. David M. Pariser, who shared data about luliconazole and a new formulation of naftifine as topical treatments for tinea infections, at the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar.

Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, pointed out that most antifungals currently approved for tinea pedis require at least daily – and sometimes twice daily – application for at least 4 weeks. Terbinafine and tolnaftate are the exceptions, with treatment periods ranging from 1-6 weeks for the two products, depending on clinical response.

A new formulation of naftifine hydrochloride 2%, (Naftin), a potent prescription topical allylamine antifungal available as a cream or a gel, has shown equivalent efficacy with just two weeks of treatment. Naftifine has lipophilic and keratinophilic properties; further, it has clinically significant anti-inflammatory and antibacterial effects, in addition to its potent fungicidal and fungistatic effects against dermatophytes, Dr. Pariser said at the meeting. The preparations are currently approved for topical treatment of tinea pedis, tinea cruris, and tinea corporis.

Notably, naftifine maintains a “clinically relevant therapeutic reservoir effect after treatment completion, with naftifine detected in the stratum corneum for up to 4 weeks posttreatment,” he said. This reservoir effect permits a significantly easier treatment regimen, with topical application of either formulation daily for just 2 weeks.

The clinical trials of naftifine HCl 2% with daily administration for 2 weeks showed equivalence with the 1% formulation administered for 4 weeks; the higher concentration was well tolerated and was effective in both the moccasin and interdigital distributions of tinea pedis involvement. Trials also showed the mycologic and clinical cure rates of naftifine 2% to be equivalent or superior to those of terbinafine, econazole, clotrimazole, miconazole, and tolnaftate.

Clinical trials showed treatment effectiveness – defined as 90% improvement over baseline and achieving “essentially normal skin” – in 52% of patients receiving naftifine 2%, compared with 20% of patients receiving vehicle only. Overall clinical success – defined as mycologic cure and either clinical cure of effective clinical treatment – was seen in 78% of the naftifine 2% patients, compared with 49% of the vehicle patients.

The second antifungal Dr. Pariser discussed is luliconazole (Luzu), a prescription topical imidazole that is available as a 1% cream. Luliconazole is also a broad-spectrum, potent antifungal with effects that persist several weeks after treatment. The preparation is at least as effective as bifonazole, terbinafine, and lanoconazole, both in vitro and in vivo, Dr. Pariser said.

In two parallel clinical trials comparing luliconazole 1% cream to its vehicle, treatment was effective (at least 90% clearing and with normal-appearing skin) in 48% and 33% of patients receiving luliconazole, compared with 10% and 15% of patients receiving vehicle alone.

An advantage of the topical agents is that there are generally no major systemic side effects, since there is minimal systemic absorption, Dr. Pariser noted. Allergic contact dermatitis may be a local reaction, but tends to be mild and transient, he said.

Clinicians should always be alert for tinea pedis when treating onychomycosis, said Dr. Pariser, and untreated tinea can contribute to recurrence of nail fungus. “If you don’t look for tinea, you might not find it, and you’ve missed a treatment opportunity,” he said.

Dr. Pariser disclosed that he is an investigator and consultant for Valeant and an investigator for Anacor Pharmaceuticals.

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

[email protected]

On Twitter @karioakes

LAS VEGAS – Better penetration through the nail is a key driver behind the increased efficacy of newer topical treatments for onychomycosis, affording a better chance for a clinical and mycologic cure without the potential for toxicity that comes with systemic treatments, according to Dr. David M. Pariser.

At the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar, Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, reviewed clinical trial data for 10% topical efinaconazole solution and 5% tavaborole topical solution, newer treatment options for the old problem of nail fungus. “New topical antifungals have improved the challenge of nail penetration,” which had been a key obstacle to efficacy with earlier topical treatments, he said.

Though topical treatments for onychomycosis avoid the risk of systemic side effects and the need for periodic blood tests to check liver function, historically, these treatments have not been very effective, he commented.

Ciclopirox (Penlac), one of the more efficacious treatments, achieves a cure rate of 5.5%-8.5%, and the buildup of the lacquer vehicle requires frequent nail debridement. Because of real or perceived risks, patients may be reluctant to take oral antifungals for onychomycosis, he said, noting that in addition to the potential for liver injury, use of these medications may also be limited by multiple drug-drug interactions.

The two new topical formulations he reviewed have a low molecular weight to allow better penetration through the dense, keratin-rich nail plate, Dr. Pariser said.

One of the topicals, 10% topical efinaconazole solution (Jublia), uses a formulation with low surface tension for good penetration with no surface buildup of vehicle material, achieving better nail penetration than do lacquer-based products, he noted.

A key efinaconazole study assessed clinical improvement in nail appearance in combination with mycologic cure, defined as negative findings on KOH prep exam and negative fungal culture. A complete cure was defined as a “totally clear target toenail and negative KOH/negative fungal culture,” and an “almost complete cure” was defined as mycologic cure, combined with no more than 5% clinically apparent involvement of the target toenail.

©Metin Cengiz Bar/Thinkstock

After double-blinded randomization into two parallel studies, patients applied either efinaconazole or the vehicle alone once daily at bedtime to the target toenail for 48 weeks. In the studies, 18% and 15% of those in the efinaconazole arm had achieved complete cure 52 weeks after beginning treatment, compared with 3% and 6% of the vehicle arm patients, respectively. However, for a pooled intent-to-treat population, the treatment arm saw a 28% cured or almost-cured rate, compared with 7% of the pooled vehicle-treated patients (P less than .001). Mycologic cure was achieved by 55% and 53% of the patients in the two efinaconazole arms, compared with 17% of the vehicle-only patients in each arm, according to Dr. Pariser.

Adverse events, similar between treatment arms, were mostly mild to moderate and localized, with dermatitis, vesicles, pain, and ingrown toenails the most commonly reported effects.

Tavaborole topical solution, 5% (Kerydin), is a boron-based compound that is highly water soluble, with broad antifungal activity that persists in the presence of keratin. As with efinaconazole, there is no product buildup, so nail debridement is not needed during treatment, Dr. Pariser said.

Two multicenter tavaborole trials compared the active tavaborole solution with a vehicle-only arm in a randomized, double-blind fashion, with product application daily for 48 weeks. The primary efficacy outcome for the trials was complete cure of the target great toenail at week 52. Secondary endpoints were a completely clear or almost clear (10% or less involvement of the target nail) target great toenail, as well as mycologic cure of the nail. Safety was measured by tracking adverse events, and local tolerability, as well as monitoring labs and ECG parameters.

A complete cure for the tavaborole trials required a completely clear nail on clinical exam, as well as negative mycology (negative KOH and negative fungal culture). At 52 weeks, 6.5% and 9.1% of the tavaborole-treated patients saw a complete cure, compared with 0.5% and 1.5% of vehicle-only patients in the two studies. Of those treated with tavaborole, 31.1% and 35.9% achieved mycologic cure, compared with 7.2% and 12.2% of those in the vehicle arm.

The rates of complete or almost complete clearing of the target great toenail for those in the tavaborole arms were 26.1% and 27.5%, compared with 9.3% and 14.6% in the vehicle arms. Predefined treatment success – a combination of mycologic cure and clear or almost clear target great toenail – was seen in 15.3% and 17.9% of the tavaborole-treated patients, compared with 1.5% and 3.9% of the vehicle-only patients (P less than or equal to .001 for all endpoints in both studies).

Treatment-related adverse events were generally mild and similar between the vehicle and treatment arms, with application site exfoliation, erythema, dermatitis, as well as ingrown toenails, the most commonly reported events for both arms.

Dr. Pariser noted that comparing efficacy of the newer agents directly is difficult, since the pivotal clinical trials for each had different designs, entry criteria, clinical assessments, and endpoints.

He disclosed that he is an investigator and consultant for Valeant, which manufactures the 10% topical efinaconazole solution, and an investigator for Anacor Pharmaceuticals, which markets tavaborole.

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

[email protected]

On Twitter @karioakes

LAS VEGAS – Better penetration through the nail is a key driver behind the increased efficacy of newer topical treatments for onychomycosis, affording a better chance for a clinical and mycologic cure without the potential for toxicity that comes with systemic treatments, according to Dr. David M. Pariser.

At the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar, Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, reviewed clinical trial data for 10% topical efinaconazole solution and 5% tavaborole topical solution, newer treatment options for the old problem of nail fungus. “New topical antifungals have improved the challenge of nail penetration,” which had been a key obstacle to efficacy with earlier topical treatments, he said.

Though topical treatments for onychomycosis avoid the risk of systemic side effects and the need for periodic blood tests to check liver function, historically, these treatments have not been very effective, he commented.

Ciclopirox (Penlac), one of the more efficacious treatments, achieves a cure rate of 5.5%-8.5%, and the buildup of the lacquer vehicle requires frequent nail debridement. Because of real or perceived risks, patients may be reluctant to take oral antifungals for onychomycosis, he said, noting that in addition to the potential for liver injury, use of these medications may also be limited by multiple drug-drug interactions.

The two new topical formulations he reviewed have a low molecular weight to allow better penetration through the dense, keratin-rich nail plate, Dr. Pariser said.

One of the topicals, 10% topical efinaconazole solution (Jublia), uses a formulation with low surface tension for good penetration with no surface buildup of vehicle material, achieving better nail penetration than do lacquer-based products, he noted.

A key efinaconazole study assessed clinical improvement in nail appearance in combination with mycologic cure, defined as negative findings on KOH prep exam and negative fungal culture. A complete cure was defined as a “totally clear target toenail and negative KOH/negative fungal culture,” and an “almost complete cure” was defined as mycologic cure, combined with no more than 5% clinically apparent involvement of the target toenail.

©Metin Cengiz Bar/Thinkstock

After double-blinded randomization into two parallel studies, patients applied either efinaconazole or the vehicle alone once daily at bedtime to the target toenail for 48 weeks. In the studies, 18% and 15% of those in the efinaconazole arm had achieved complete cure 52 weeks after beginning treatment, compared with 3% and 6% of the vehicle arm patients, respectively. However, for a pooled intent-to-treat population, the treatment arm saw a 28% cured or almost-cured rate, compared with 7% of the pooled vehicle-treated patients (P less than .001). Mycologic cure was achieved by 55% and 53% of the patients in the two efinaconazole arms, compared with 17% of the vehicle-only patients in each arm, according to Dr. Pariser.

Adverse events, similar between treatment arms, were mostly mild to moderate and localized, with dermatitis, vesicles, pain, and ingrown toenails the most commonly reported effects.

Tavaborole topical solution, 5% (Kerydin), is a boron-based compound that is highly water soluble, with broad antifungal activity that persists in the presence of keratin. As with efinaconazole, there is no product buildup, so nail debridement is not needed during treatment, Dr. Pariser said.

Two multicenter tavaborole trials compared the active tavaborole solution with a vehicle-only arm in a randomized, double-blind fashion, with product application daily for 48 weeks. The primary efficacy outcome for the trials was complete cure of the target great toenail at week 52. Secondary endpoints were a completely clear or almost clear (10% or less involvement of the target nail) target great toenail, as well as mycologic cure of the nail. Safety was measured by tracking adverse events, and local tolerability, as well as monitoring labs and ECG parameters.

A complete cure for the tavaborole trials required a completely clear nail on clinical exam, as well as negative mycology (negative KOH and negative fungal culture). At 52 weeks, 6.5% and 9.1% of the tavaborole-treated patients saw a complete cure, compared with 0.5% and 1.5% of vehicle-only patients in the two studies. Of those treated with tavaborole, 31.1% and 35.9% achieved mycologic cure, compared with 7.2% and 12.2% of those in the vehicle arm.

The rates of complete or almost complete clearing of the target great toenail for those in the tavaborole arms were 26.1% and 27.5%, compared with 9.3% and 14.6% in the vehicle arms. Predefined treatment success – a combination of mycologic cure and clear or almost clear target great toenail – was seen in 15.3% and 17.9% of the tavaborole-treated patients, compared with 1.5% and 3.9% of the vehicle-only patients (P less than or equal to .001 for all endpoints in both studies).

Treatment-related adverse events were generally mild and similar between the vehicle and treatment arms, with application site exfoliation, erythema, dermatitis, as well as ingrown toenails, the most commonly reported events for both arms.

Dr. Pariser noted that comparing efficacy of the newer agents directly is difficult, since the pivotal clinical trials for each had different designs, entry criteria, clinical assessments, and endpoints.

He disclosed that he is an investigator and consultant for Valeant, which manufactures the 10% topical efinaconazole solution, and an investigator for Anacor Pharmaceuticals, which markets tavaborole.

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

[email protected]

On Twitter @karioakes

LAS VEGAS – Better penetration through the nail is a key driver behind the increased efficacy of newer topical treatments for onychomycosis, affording a better chance for a clinical and mycologic cure without the potential for toxicity that comes with systemic treatments, according to Dr. David M. Pariser.

At the Skin Disease Education Foundation’s annual Las Vegas dermatology seminar, Dr. Pariser, professor in the department of dermatology at Eastern Virginia Medical School, Norfolk, reviewed clinical trial data for 10% topical efinaconazole solution and 5% tavaborole topical solution, newer treatment options for the old problem of nail fungus. “New topical antifungals have improved the challenge of nail penetration,” which had been a key obstacle to efficacy with earlier topical treatments, he said.

Though topical treatments for onychomycosis avoid the risk of systemic side effects and the need for periodic blood tests to check liver function, historically, these treatments have not been very effective, he commented.

Ciclopirox (Penlac), one of the more efficacious treatments, achieves a cure rate of 5.5%-8.5%, and the buildup of the lacquer vehicle requires frequent nail debridement. Because of real or perceived risks, patients may be reluctant to take oral antifungals for onychomycosis, he said, noting that in addition to the potential for liver injury, use of these medications may also be limited by multiple drug-drug interactions.

The two new topical formulations he reviewed have a low molecular weight to allow better penetration through the dense, keratin-rich nail plate, Dr. Pariser said.

One of the topicals, 10% topical efinaconazole solution (Jublia), uses a formulation with low surface tension for good penetration with no surface buildup of vehicle material, achieving better nail penetration than do lacquer-based products, he noted.

A key efinaconazole study assessed clinical improvement in nail appearance in combination with mycologic cure, defined as negative findings on KOH prep exam and negative fungal culture. A complete cure was defined as a “totally clear target toenail and negative KOH/negative fungal culture,” and an “almost complete cure” was defined as mycologic cure, combined with no more than 5% clinically apparent involvement of the target toenail.

©Metin Cengiz Bar/Thinkstock

After double-blinded randomization into two parallel studies, patients applied either efinaconazole or the vehicle alone once daily at bedtime to the target toenail for 48 weeks. In the studies, 18% and 15% of those in the efinaconazole arm had achieved complete cure 52 weeks after beginning treatment, compared with 3% and 6% of the vehicle arm patients, respectively. However, for a pooled intent-to-treat population, the treatment arm saw a 28% cured or almost-cured rate, compared with 7% of the pooled vehicle-treated patients (P less than .001). Mycologic cure was achieved by 55% and 53% of the patients in the two efinaconazole arms, compared with 17% of the vehicle-only patients in each arm, according to Dr. Pariser.

Adverse events, similar between treatment arms, were mostly mild to moderate and localized, with dermatitis, vesicles, pain, and ingrown toenails the most commonly reported effects.

Tavaborole topical solution, 5% (Kerydin), is a boron-based compound that is highly water soluble, with broad antifungal activity that persists in the presence of keratin. As with efinaconazole, there is no product buildup, so nail debridement is not needed during treatment, Dr. Pariser said.

Two multicenter tavaborole trials compared the active tavaborole solution with a vehicle-only arm in a randomized, double-blind fashion, with product application daily for 48 weeks. The primary efficacy outcome for the trials was complete cure of the target great toenail at week 52. Secondary endpoints were a completely clear or almost clear (10% or less involvement of the target nail) target great toenail, as well as mycologic cure of the nail. Safety was measured by tracking adverse events, and local tolerability, as well as monitoring labs and ECG parameters.

A complete cure for the tavaborole trials required a completely clear nail on clinical exam, as well as negative mycology (negative KOH and negative fungal culture). At 52 weeks, 6.5% and 9.1% of the tavaborole-treated patients saw a complete cure, compared with 0.5% and 1.5% of vehicle-only patients in the two studies. Of those treated with tavaborole, 31.1% and 35.9% achieved mycologic cure, compared with 7.2% and 12.2% of those in the vehicle arm.

The rates of complete or almost complete clearing of the target great toenail for those in the tavaborole arms were 26.1% and 27.5%, compared with 9.3% and 14.6% in the vehicle arms. Predefined treatment success – a combination of mycologic cure and clear or almost clear target great toenail – was seen in 15.3% and 17.9% of the tavaborole-treated patients, compared with 1.5% and 3.9% of the vehicle-only patients (P less than or equal to .001 for all endpoints in both studies).

Treatment-related adverse events were generally mild and similar between the vehicle and treatment arms, with application site exfoliation, erythema, dermatitis, as well as ingrown toenails, the most commonly reported events for both arms.

Dr. Pariser noted that comparing efficacy of the newer agents directly is difficult, since the pivotal clinical trials for each had different designs, entry criteria, clinical assessments, and endpoints.

He disclosed that he is an investigator and consultant for Valeant, which manufactures the 10% topical efinaconazole solution, and an investigator for Anacor Pharmaceuticals, which markets tavaborole.

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

[email protected]

On Twitter @karioakes

To the Editor:

We read with great interest the article, 
“Omphalith-Associated Relapsing Umbilical Cellulitis: Recurrent Omphalitis Secondary to a 
Hair-Containing Belly Button Bezoar” (Cutis. 2010;86:199-202), which introduced the terms omphalotrich and tricomphalith to describe the pilar composition of a hair-containing umbilical foreign body in an 18-year-old man. We report a similar case.

A 38-year-old man presented with a 10-year history of an unusual odor in the umbilical region with recurrent discharge. He diligently maintained proper hygiene of the umbilicus using cotton swabs and had received recurrent cycles of oral antibiotics prescribed by his general practitioner with temporary improvement of the odor and amount of discharge. Physical examination revealed a normal umbilicus with a deep and tight umbilical cleft that required the use of curved mosquito forceps for further examination (Figure 1). A bezoar comprised of a compact collection of terminal hair shafts was noted deep in the umbilicus (Figure 2). A considerable amount of terminal hairs also were noted on the skin of the abdominal area. Following removal of the bezoar, no umbilical fistula was observed, and the presence of embryologic abnormalities (eg, omphalomesenteric duct remnants) was ruled out on magnetic resonance imaging. A diagnosis of recurrent omphalitis secondary to a hair-containing bezoar was made. Following extraction of the bezoar, the odor and discharge promptly resolved, thereby avoiding the need for oral antibiotics; however, a smaller bezoar comprised of a collection of terminal hair shafts was removed 
4 months later.

Figure 1. Deep and narrow umbilical cleft with serous exudate in the umbilicus after removal of the foreign body.		Figure 2. A section of the umbilical foreign body composed of a collection of terminal hair shafts.

An omphalith is an umbilical foreign body that results from the accumulation of keratinous and amorphous sebaceous material.² Several predisposing factors have been proposed for its pathogenesis, such as the anatomical disposition of the umbilicus and the patient’s hygiene. We hypothesize that a deep umbilicus and a large amount of terminal hairs in the abdominal area were predisposing factors in our patient. Cohen et al¹ proposed the terms omphalotrich and trichomphalith to describe the pilar composition of a hair-containing umbilical foreign body that did not have the characteristic stonelike presentation of a traditional omphalith. The authors also referred to the umbilical foreign body in their patient as a trichobezoar, a term used to describe exogenous foreign bodies composed of ingested hair in the gastrointestinal tract, given the embryologic origin of the umbilicus and epithelium of the 
gastrointestinal tract. We agree that the terms omphalotrich and trichomphalith appropriately describe the current presentation; we also propose the terms omphalitrichia or thricomphalia to describe the findings seen in our patient, which should always be ruled 
out in patients with recurrent omphalitis that is unresponsive to antibiotics.

To the Editor:

We read with great interest the article, 
“Omphalith-Associated Relapsing Umbilical Cellulitis: Recurrent Omphalitis Secondary to a 
Hair-Containing Belly Button Bezoar” (Cutis. 2010;86:199-202), which introduced the terms omphalotrich and tricomphalith to describe the pilar composition of a hair-containing umbilical foreign body in an 18-year-old man. We report a similar case.

A 38-year-old man presented with a 10-year history of an unusual odor in the umbilical region with recurrent discharge. He diligently maintained proper hygiene of the umbilicus using cotton swabs and had received recurrent cycles of oral antibiotics prescribed by his general practitioner with temporary improvement of the odor and amount of discharge. Physical examination revealed a normal umbilicus with a deep and tight umbilical cleft that required the use of curved mosquito forceps for further examination (Figure 1). A bezoar comprised of a compact collection of terminal hair shafts was noted deep in the umbilicus (Figure 2). A considerable amount of terminal hairs also were noted on the skin of the abdominal area. Following removal of the bezoar, no umbilical fistula was observed, and the presence of embryologic abnormalities (eg, omphalomesenteric duct remnants) was ruled out on magnetic resonance imaging. A diagnosis of recurrent omphalitis secondary to a hair-containing bezoar was made. Following extraction of the bezoar, the odor and discharge promptly resolved, thereby avoiding the need for oral antibiotics; however, a smaller bezoar comprised of a collection of terminal hair shafts was removed 
4 months later.

Figure 1. Deep and narrow umbilical cleft with serous exudate in the umbilicus after removal of the foreign body.		Figure 2. A section of the umbilical foreign body composed of a collection of terminal hair shafts.

An omphalith is an umbilical foreign body that results from the accumulation of keratinous and amorphous sebaceous material.² Several predisposing factors have been proposed for its pathogenesis, such as the anatomical disposition of the umbilicus and the patient’s hygiene. We hypothesize that a deep umbilicus and a large amount of terminal hairs in the abdominal area were predisposing factors in our patient. Cohen et al¹ proposed the terms omphalotrich and trichomphalith to describe the pilar composition of a hair-containing umbilical foreign body that did not have the characteristic stonelike presentation of a traditional omphalith. The authors also referred to the umbilical foreign body in their patient as a trichobezoar, a term used to describe exogenous foreign bodies composed of ingested hair in the gastrointestinal tract, given the embryologic origin of the umbilicus and epithelium of the 
gastrointestinal tract. We agree that the terms omphalotrich and trichomphalith appropriately describe the current presentation; we also propose the terms omphalitrichia or thricomphalia to describe the findings seen in our patient, which should always be ruled 
out in patients with recurrent omphalitis that is unresponsive to antibiotics.

To the Editor:

We read with great interest the article, 
“Omphalith-Associated Relapsing Umbilical Cellulitis: Recurrent Omphalitis Secondary to a 
Hair-Containing Belly Button Bezoar” (Cutis. 2010;86:199-202), which introduced the terms omphalotrich and tricomphalith to describe the pilar composition of a hair-containing umbilical foreign body in an 18-year-old man. We report a similar case.

A 38-year-old man presented with a 10-year history of an unusual odor in the umbilical region with recurrent discharge. He diligently maintained proper hygiene of the umbilicus using cotton swabs and had received recurrent cycles of oral antibiotics prescribed by his general practitioner with temporary improvement of the odor and amount of discharge. Physical examination revealed a normal umbilicus with a deep and tight umbilical cleft that required the use of curved mosquito forceps for further examination (Figure 1). A bezoar comprised of a compact collection of terminal hair shafts was noted deep in the umbilicus (Figure 2). A considerable amount of terminal hairs also were noted on the skin of the abdominal area. Following removal of the bezoar, no umbilical fistula was observed, and the presence of embryologic abnormalities (eg, omphalomesenteric duct remnants) was ruled out on magnetic resonance imaging. A diagnosis of recurrent omphalitis secondary to a hair-containing bezoar was made. Following extraction of the bezoar, the odor and discharge promptly resolved, thereby avoiding the need for oral antibiotics; however, a smaller bezoar comprised of a collection of terminal hair shafts was removed 
4 months later.

Figure 1. Deep and narrow umbilical cleft with serous exudate in the umbilicus after removal of the foreign body.		Figure 2. A section of the umbilical foreign body composed of a collection of terminal hair shafts.

An omphalith is an umbilical foreign body that results from the accumulation of keratinous and amorphous sebaceous material.² Several predisposing factors have been proposed for its pathogenesis, such as the anatomical disposition of the umbilicus and the patient’s hygiene. We hypothesize that a deep umbilicus and a large amount of terminal hairs in the abdominal area were predisposing factors in our patient. Cohen et al¹ proposed the terms omphalotrich and trichomphalith to describe the pilar composition of a hair-containing umbilical foreign body that did not have the characteristic stonelike presentation of a traditional omphalith. The authors also referred to the umbilical foreign body in their patient as a trichobezoar, a term used to describe exogenous foreign bodies composed of ingested hair in the gastrointestinal tract, given the embryologic origin of the umbilicus and epithelium of the 
gastrointestinal tract. We agree that the terms omphalotrich and trichomphalith appropriately describe the current presentation; we also propose the terms omphalitrichia or thricomphalia to describe the findings seen in our patient, which should always be ruled 
out in patients with recurrent omphalitis that is unresponsive to antibiotics.

COPENHAGEN – Hidradenitis suppurativa, a common, chronic, inflammatory scarring skin disease of the hair follicles, is a red flag signaling elevated levels of multiple cardiovascular risk factors, according to a systematic review and meta-analysis.

“The need for screening of hidradenitis suppurativa patients for modifiable cardiovascular risk is emphasized,” Dr. Thrasyvoulos Tzellos said in presenting the findings at the annual congress of the European Academy of Dermatology and Venereology.

For such a common and dramatically destructive disease, hidradenitis suppurativa (HS) was underresearched until recently. Investigative interest grew as the tumor necrosis factor inhibitor adalimumab (Humira) underwent development as a novel therapy for what has been traditionally a notoriously difficult to treat disease. The biologic agent received Food and Drug Administration marketing approval in October as the first and only approved treatment for HS.

Dr. Tzellos’s meta-analysis included nine published studies totaling 6,174 HS patients and 24,993 controls. Five studies were case control, and the other four were cross sectional. An indicator of the recent explosive research interest in HS can be seen in the fact that 80% of all the HS patients included in the meta-analysis come from two studies published within just the last year, one from Massachusetts General Hospital (J Am Acad Dermatol. 2014 Dec;71[6]:1144-50) and the other from Israel (Br J Dermatol. 2015 Aug;173[2]:464-70).

Not all the studies examined the same cardiovascular risk factors. For example, only six of nine studies looked at diabetes mellitus as an endpoint. Of those studies that did, diabetes occurred in 856 of 5,685 HS patients, a rate 2.85-fold higher than in controls, according to Dr. Tzellos of University Hospital of North Norway in Troms.

The only cardiovascular risk factor examined that was not significantly more common among patients with HS than controls was hypertension. The 1.57-fold increased likelihood of hypertension among HS patients didn’t achieve statistical significance.

Although patients whose HS was treated exclusively in outpatient settings had significantly higher levels of cardiovascular risk factors than did controls, risk levels were consistently higher still in patients who had been hospitalized for HS.

A meta-analysis such as this cannot address causality, leaving open the question of whether increased cardiovascular risk factors are intrinsic to HS, or the debilitating recurrent skin disease causes affected patients to take a defeatest attitude toward maintenance of a healthy lifestyle.

Dr. Tzellos reported having no financial conflicts regarding this meta-analysis, carried out with academic funding.

COPENHAGEN – Hidradenitis suppurativa, a common, chronic, inflammatory scarring skin disease of the hair follicles, is a red flag signaling elevated levels of multiple cardiovascular risk factors, according to a systematic review and meta-analysis.

“The need for screening of hidradenitis suppurativa patients for modifiable cardiovascular risk is emphasized,” Dr. Thrasyvoulos Tzellos said in presenting the findings at the annual congress of the European Academy of Dermatology and Venereology.

For such a common and dramatically destructive disease, hidradenitis suppurativa (HS) was underresearched until recently. Investigative interest grew as the tumor necrosis factor inhibitor adalimumab (Humira) underwent development as a novel therapy for what has been traditionally a notoriously difficult to treat disease. The biologic agent received Food and Drug Administration marketing approval in October as the first and only approved treatment for HS.

Dr. Tzellos’s meta-analysis included nine published studies totaling 6,174 HS patients and 24,993 controls. Five studies were case control, and the other four were cross sectional. An indicator of the recent explosive research interest in HS can be seen in the fact that 80% of all the HS patients included in the meta-analysis come from two studies published within just the last year, one from Massachusetts General Hospital (J Am Acad Dermatol. 2014 Dec;71[6]:1144-50) and the other from Israel (Br J Dermatol. 2015 Aug;173[2]:464-70).

Not all the studies examined the same cardiovascular risk factors. For example, only six of nine studies looked at diabetes mellitus as an endpoint. Of those studies that did, diabetes occurred in 856 of 5,685 HS patients, a rate 2.85-fold higher than in controls, according to Dr. Tzellos of University Hospital of North Norway in Troms.

The only cardiovascular risk factor examined that was not significantly more common among patients with HS than controls was hypertension. The 1.57-fold increased likelihood of hypertension among HS patients didn’t achieve statistical significance.

Although patients whose HS was treated exclusively in outpatient settings had significantly higher levels of cardiovascular risk factors than did controls, risk levels were consistently higher still in patients who had been hospitalized for HS.

A meta-analysis such as this cannot address causality, leaving open the question of whether increased cardiovascular risk factors are intrinsic to HS, or the debilitating recurrent skin disease causes affected patients to take a defeatest attitude toward maintenance of a healthy lifestyle.

Dr. Tzellos reported having no financial conflicts regarding this meta-analysis, carried out with academic funding.

COPENHAGEN – Hidradenitis suppurativa, a common, chronic, inflammatory scarring skin disease of the hair follicles, is a red flag signaling elevated levels of multiple cardiovascular risk factors, according to a systematic review and meta-analysis.

“The need for screening of hidradenitis suppurativa patients for modifiable cardiovascular risk is emphasized,” Dr. Thrasyvoulos Tzellos said in presenting the findings at the annual congress of the European Academy of Dermatology and Venereology.

For such a common and dramatically destructive disease, hidradenitis suppurativa (HS) was underresearched until recently. Investigative interest grew as the tumor necrosis factor inhibitor adalimumab (Humira) underwent development as a novel therapy for what has been traditionally a notoriously difficult to treat disease. The biologic agent received Food and Drug Administration marketing approval in October as the first and only approved treatment for HS.

Dr. Tzellos’s meta-analysis included nine published studies totaling 6,174 HS patients and 24,993 controls. Five studies were case control, and the other four were cross sectional. An indicator of the recent explosive research interest in HS can be seen in the fact that 80% of all the HS patients included in the meta-analysis come from two studies published within just the last year, one from Massachusetts General Hospital (J Am Acad Dermatol. 2014 Dec;71[6]:1144-50) and the other from Israel (Br J Dermatol. 2015 Aug;173[2]:464-70).

Not all the studies examined the same cardiovascular risk factors. For example, only six of nine studies looked at diabetes mellitus as an endpoint. Of those studies that did, diabetes occurred in 856 of 5,685 HS patients, a rate 2.85-fold higher than in controls, according to Dr. Tzellos of University Hospital of North Norway in Troms.

The only cardiovascular risk factor examined that was not significantly more common among patients with HS than controls was hypertension. The 1.57-fold increased likelihood of hypertension among HS patients didn’t achieve statistical significance.

Although patients whose HS was treated exclusively in outpatient settings had significantly higher levels of cardiovascular risk factors than did controls, risk levels were consistently higher still in patients who had been hospitalized for HS.

A meta-analysis such as this cannot address causality, leaving open the question of whether increased cardiovascular risk factors are intrinsic to HS, or the debilitating recurrent skin disease causes affected patients to take a defeatest attitude toward maintenance of a healthy lifestyle.

Dr. Tzellos reported having no financial conflicts regarding this meta-analysis, carried out with academic funding.