Medical Dermatology

NEW YORK – Flaking, itchy, swollen lips represent more than a cosmetic problem. Eczematous cheilitis can interfere with communication and nutrition, but patients may be slow to seek help, Bethanee Schlosser, MD, PhD, said at the American Academy of Dermatology summer meeting.

One of the challenges in helping patients with lip problems is that lips are constantly in motion and constantly interacting with the outside world, said Dr. Schlosser, of the department of dermatology, Northwestern University, Chicago. There’s ongoing low-level trauma with phonation, eating, drinking, and general environmental exposure, she said. Eczematous cheilitis will present with scaling and erythema of the vermilion lips, with lower lip involvement often more pronounced than symptoms on the upper lip. Fissuring and erosion are sometimes, but not always, present as well.

In addition to flaking and redness, Dr. Schlosser noted that patients will complain of dry lips, irritation, itching, and sometimes tingling.

Sorting out the etiology of eczematous cheilitis requires a thorough history. “Ask about habits, such as lip licking, picking, or biting,” she said. Recent dental work, braces, or other appliances for alignment or temporomandibular joint problems can introduce both mechanical irritation and potential allergens, and even musical instruments can be culprits, such as when an oboe reed causes an allergic reaction.

Personal hygiene products, cosmetics, gum chewing, and candy consumption can be the irritant culprits, noted Dr. Schlosser. Careful questioning of patients and examination of the products used can provide clues, since dyes and pigments in cosmetics and gum may provoke reactions.

History taking should also include questions about tobacco in all forms, marijuana, and prescription medication, which can cause lip problems. And it’s important to ask about skin disease in general, to determine if symptoms are present in other anatomic locations, and to ask about any family history of skin disease, she said.

Endogenous contributors can include true atopic dermatitis, psoriasis, and nutritional deficiencies. Psoriatic cheilitis can have prominent crusting and exfoliation. In a Brazilian study that evaluated patents with cutaneous psoriasis and age-, race-, and sex-matched controls with no history of skin disease, psoriasis was associated with geographic tongue, with an odds ratio of 5.0 (95% CI 1.5-16.8). Geographic stomatitis can also be seen, said Dr. Schlosser. Tongue fissures were also more common among those with psoriasis cheilitis (OR 2.7, 95% confidence interval, 1.3-5.6) in the same study (Med Oral Patol Oral Cir Bucal. 2009 Aug 1;14[8]:e371-5).

For psoriatic cheilitis, looking beyond the lips can help refine the diagnosis, she noted. There may be intra-oral signs or signs of extra-oral involvement, especially on the scalp, ears, and genitalia. Koebnerization may be difficult to detect on the lips, but may be present elsewhere. A family history of psoriasis may also tip the scales toward this diagnosis.

Exogenous causes of eczematous cheilitis are much more common and can include contact with irritants and allergens, factitial cheilitis, and cheilitis medicamentosa, Dr Schlosser pointed out.

Allergic contact dermatitis can come from local exposure (to cosmetics and other personal care items, for example) or from incidental exposures. Components of saliva can become concentrated when saliva dries outside the oral cavity, so for chronic lip lickers, saliva alone can be sufficiently irritating to provoke a cheilitis, Dr. Schlosser said.

Transfer of an irritant or allergen is also possible from other body sites, as when a nail-chewer develops allergic cheilitis from an ingredient in nail polish. Transfer from products used on other facial areas and the hair is also possible, as is “connubial transfer,” when an allergen is transferred from an intimate partner.

Cutaneous patch tests can be helpful in pinpointing the offending agent, or agents, according to Dr. Schlosser. She cited a study of 91 patients (77% of whom were female) who underwent patch testing for eczematous cheilitis. The researchers determined that 45% of patients had allergic contact cheilitis (Int J Dermatol. 2016 Jul;55[7]:e386-91).

The patch testing revealed that fragrances, balsam of Peru (Myroxylon pereirae resin), preservatives, and even metals such as nickel and gold were common allergens. The findings echo those in another database review that showed fragrances, M. pereirae, and nickel as the top three allergens on patch testing for lip cheilitis.

Dr. Schlosser said that the most common offending sources are lipsticks, makeup, other cosmetic products, and moisturizer, which are responsible for 10% or more of reactions.

Whatever the etiology, the treatment of eczematous cheilitis can be divided conceptually into two phases. During the induction phase, use of a low- to mid-potency topical corticosteroid ointment quiets inflammation. Examples include alclometasone 0.05%, desonide 0.05%, fluticasone 0.005%, or triamcinolone 0.1%. “Ointment formulations are preferred,” said Dr. Schlosser, since they won’t dissolve so easily with lip licking and will adhere well to the surface of the vermilion lip.

Next, a topical calcineurin inhibitor such as tacrolimus 0.1% can be used for maintenance. Other topical medications, especially topical anesthetics, should be used with caution, she said.

For psoriatic cheilitis, induction with 5% salicylic acid ointment can be followed by the topical calcineurin inhibitor phase, said Dr. Schlosser.

Dr. Schlosser disclosed financial relationships with Beiersdorf, Decision Support in Medicine, and UpToDate.

[email protected]

NEW YORK – Flaking, itchy, swollen lips represent more than a cosmetic problem. Eczematous cheilitis can interfere with communication and nutrition, but patients may be slow to seek help, Bethanee Schlosser, MD, PhD, said at the American Academy of Dermatology summer meeting.

One of the challenges in helping patients with lip problems is that lips are constantly in motion and constantly interacting with the outside world, said Dr. Schlosser, of the department of dermatology, Northwestern University, Chicago. There’s ongoing low-level trauma with phonation, eating, drinking, and general environmental exposure, she said. Eczematous cheilitis will present with scaling and erythema of the vermilion lips, with lower lip involvement often more pronounced than symptoms on the upper lip. Fissuring and erosion are sometimes, but not always, present as well.

In addition to flaking and redness, Dr. Schlosser noted that patients will complain of dry lips, irritation, itching, and sometimes tingling.

Sorting out the etiology of eczematous cheilitis requires a thorough history. “Ask about habits, such as lip licking, picking, or biting,” she said. Recent dental work, braces, or other appliances for alignment or temporomandibular joint problems can introduce both mechanical irritation and potential allergens, and even musical instruments can be culprits, such as when an oboe reed causes an allergic reaction.

Personal hygiene products, cosmetics, gum chewing, and candy consumption can be the irritant culprits, noted Dr. Schlosser. Careful questioning of patients and examination of the products used can provide clues, since dyes and pigments in cosmetics and gum may provoke reactions.

History taking should also include questions about tobacco in all forms, marijuana, and prescription medication, which can cause lip problems. And it’s important to ask about skin disease in general, to determine if symptoms are present in other anatomic locations, and to ask about any family history of skin disease, she said.

Endogenous contributors can include true atopic dermatitis, psoriasis, and nutritional deficiencies. Psoriatic cheilitis can have prominent crusting and exfoliation. In a Brazilian study that evaluated patents with cutaneous psoriasis and age-, race-, and sex-matched controls with no history of skin disease, psoriasis was associated with geographic tongue, with an odds ratio of 5.0 (95% CI 1.5-16.8). Geographic stomatitis can also be seen, said Dr. Schlosser. Tongue fissures were also more common among those with psoriasis cheilitis (OR 2.7, 95% confidence interval, 1.3-5.6) in the same study (Med Oral Patol Oral Cir Bucal. 2009 Aug 1;14[8]:e371-5).

For psoriatic cheilitis, looking beyond the lips can help refine the diagnosis, she noted. There may be intra-oral signs or signs of extra-oral involvement, especially on the scalp, ears, and genitalia. Koebnerization may be difficult to detect on the lips, but may be present elsewhere. A family history of psoriasis may also tip the scales toward this diagnosis.

Exogenous causes of eczematous cheilitis are much more common and can include contact with irritants and allergens, factitial cheilitis, and cheilitis medicamentosa, Dr Schlosser pointed out.

Allergic contact dermatitis can come from local exposure (to cosmetics and other personal care items, for example) or from incidental exposures. Components of saliva can become concentrated when saliva dries outside the oral cavity, so for chronic lip lickers, saliva alone can be sufficiently irritating to provoke a cheilitis, Dr. Schlosser said.

Transfer of an irritant or allergen is also possible from other body sites, as when a nail-chewer develops allergic cheilitis from an ingredient in nail polish. Transfer from products used on other facial areas and the hair is also possible, as is “connubial transfer,” when an allergen is transferred from an intimate partner.

Cutaneous patch tests can be helpful in pinpointing the offending agent, or agents, according to Dr. Schlosser. She cited a study of 91 patients (77% of whom were female) who underwent patch testing for eczematous cheilitis. The researchers determined that 45% of patients had allergic contact cheilitis (Int J Dermatol. 2016 Jul;55[7]:e386-91).

The patch testing revealed that fragrances, balsam of Peru (Myroxylon pereirae resin), preservatives, and even metals such as nickel and gold were common allergens. The findings echo those in another database review that showed fragrances, M. pereirae, and nickel as the top three allergens on patch testing for lip cheilitis.

Dr. Schlosser said that the most common offending sources are lipsticks, makeup, other cosmetic products, and moisturizer, which are responsible for 10% or more of reactions.

Whatever the etiology, the treatment of eczematous cheilitis can be divided conceptually into two phases. During the induction phase, use of a low- to mid-potency topical corticosteroid ointment quiets inflammation. Examples include alclometasone 0.05%, desonide 0.05%, fluticasone 0.005%, or triamcinolone 0.1%. “Ointment formulations are preferred,” said Dr. Schlosser, since they won’t dissolve so easily with lip licking and will adhere well to the surface of the vermilion lip.

Next, a topical calcineurin inhibitor such as tacrolimus 0.1% can be used for maintenance. Other topical medications, especially topical anesthetics, should be used with caution, she said.

For psoriatic cheilitis, induction with 5% salicylic acid ointment can be followed by the topical calcineurin inhibitor phase, said Dr. Schlosser.

Dr. Schlosser disclosed financial relationships with Beiersdorf, Decision Support in Medicine, and UpToDate.

[email protected]

NEW YORK – Flaking, itchy, swollen lips represent more than a cosmetic problem. Eczematous cheilitis can interfere with communication and nutrition, but patients may be slow to seek help, Bethanee Schlosser, MD, PhD, said at the American Academy of Dermatology summer meeting.

One of the challenges in helping patients with lip problems is that lips are constantly in motion and constantly interacting with the outside world, said Dr. Schlosser, of the department of dermatology, Northwestern University, Chicago. There’s ongoing low-level trauma with phonation, eating, drinking, and general environmental exposure, she said. Eczematous cheilitis will present with scaling and erythema of the vermilion lips, with lower lip involvement often more pronounced than symptoms on the upper lip. Fissuring and erosion are sometimes, but not always, present as well.

In addition to flaking and redness, Dr. Schlosser noted that patients will complain of dry lips, irritation, itching, and sometimes tingling.

Sorting out the etiology of eczematous cheilitis requires a thorough history. “Ask about habits, such as lip licking, picking, or biting,” she said. Recent dental work, braces, or other appliances for alignment or temporomandibular joint problems can introduce both mechanical irritation and potential allergens, and even musical instruments can be culprits, such as when an oboe reed causes an allergic reaction.

Personal hygiene products, cosmetics, gum chewing, and candy consumption can be the irritant culprits, noted Dr. Schlosser. Careful questioning of patients and examination of the products used can provide clues, since dyes and pigments in cosmetics and gum may provoke reactions.

History taking should also include questions about tobacco in all forms, marijuana, and prescription medication, which can cause lip problems. And it’s important to ask about skin disease in general, to determine if symptoms are present in other anatomic locations, and to ask about any family history of skin disease, she said.

Endogenous contributors can include true atopic dermatitis, psoriasis, and nutritional deficiencies. Psoriatic cheilitis can have prominent crusting and exfoliation. In a Brazilian study that evaluated patents with cutaneous psoriasis and age-, race-, and sex-matched controls with no history of skin disease, psoriasis was associated with geographic tongue, with an odds ratio of 5.0 (95% CI 1.5-16.8). Geographic stomatitis can also be seen, said Dr. Schlosser. Tongue fissures were also more common among those with psoriasis cheilitis (OR 2.7, 95% confidence interval, 1.3-5.6) in the same study (Med Oral Patol Oral Cir Bucal. 2009 Aug 1;14[8]:e371-5).

For psoriatic cheilitis, looking beyond the lips can help refine the diagnosis, she noted. There may be intra-oral signs or signs of extra-oral involvement, especially on the scalp, ears, and genitalia. Koebnerization may be difficult to detect on the lips, but may be present elsewhere. A family history of psoriasis may also tip the scales toward this diagnosis.

Exogenous causes of eczematous cheilitis are much more common and can include contact with irritants and allergens, factitial cheilitis, and cheilitis medicamentosa, Dr Schlosser pointed out.

Allergic contact dermatitis can come from local exposure (to cosmetics and other personal care items, for example) or from incidental exposures. Components of saliva can become concentrated when saliva dries outside the oral cavity, so for chronic lip lickers, saliva alone can be sufficiently irritating to provoke a cheilitis, Dr. Schlosser said.

Transfer of an irritant or allergen is also possible from other body sites, as when a nail-chewer develops allergic cheilitis from an ingredient in nail polish. Transfer from products used on other facial areas and the hair is also possible, as is “connubial transfer,” when an allergen is transferred from an intimate partner.

Cutaneous patch tests can be helpful in pinpointing the offending agent, or agents, according to Dr. Schlosser. She cited a study of 91 patients (77% of whom were female) who underwent patch testing for eczematous cheilitis. The researchers determined that 45% of patients had allergic contact cheilitis (Int J Dermatol. 2016 Jul;55[7]:e386-91).

The patch testing revealed that fragrances, balsam of Peru (Myroxylon pereirae resin), preservatives, and even metals such as nickel and gold were common allergens. The findings echo those in another database review that showed fragrances, M. pereirae, and nickel as the top three allergens on patch testing for lip cheilitis.

Dr. Schlosser said that the most common offending sources are lipsticks, makeup, other cosmetic products, and moisturizer, which are responsible for 10% or more of reactions.

Whatever the etiology, the treatment of eczematous cheilitis can be divided conceptually into two phases. During the induction phase, use of a low- to mid-potency topical corticosteroid ointment quiets inflammation. Examples include alclometasone 0.05%, desonide 0.05%, fluticasone 0.005%, or triamcinolone 0.1%. “Ointment formulations are preferred,” said Dr. Schlosser, since they won’t dissolve so easily with lip licking and will adhere well to the surface of the vermilion lip.

Next, a topical calcineurin inhibitor such as tacrolimus 0.1% can be used for maintenance. Other topical medications, especially topical anesthetics, should be used with caution, she said.

For psoriatic cheilitis, induction with 5% salicylic acid ointment can be followed by the topical calcineurin inhibitor phase, said Dr. Schlosser.

Dr. Schlosser disclosed financial relationships with Beiersdorf, Decision Support in Medicine, and UpToDate.

[email protected]

MILAN – A novel synthetic cannabinoid helped reduce the severity of dermatomyositis and improved patient-reported outcomes in early clinical trials, according to Victoria Werth, MD, who presented early-stage findings at the World Congress of Dermatology.

Lenabasum – previously known as anabasum – is a synthetic cannabinoid that binds to the CB2 receptor present on a variety of cells, including lymphocytes, explained Dr. Werth, professor of medicine at the University of Pennsylvania, Philadelphia, and chief of dermatology at the Philadelphia Veterans Administration Hospital. The nonpsychoactive compound’s mechanism of action helps prevent tissue thickening and fibrosis. In addition to its potential for dermatomyositis treatment, it is also being investigated as a treatment for cystic fibrosis, scleroderma, and lupus.

Dr. Werth added that earlier in vitro work with peripheral blood mononuclear cells of patients with dermatomyositis showed that lenabasum markedly suppressed the cells’ secretion of tumor necrosis factor–alpha, interferon-alpha, and interferon-beta (J Invest Dermatol. 2017 Nov;137[11]:2445-7). A randomized, placebo-controlled trial tested lenabasum, known in the trial as JBT-101, in 22 patients with skin-predominant myositis. The study was structured so patients took a half dose of lenabasum for 1 month, followed by 2 months of taking a full dose, and finally 1 month with no lenabasum dosing. Compared with placebo, scores on the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) were significantly improved with full dosing of lenabasum (P = .02), Dr. Werth said.

In this 16-week trial, the mean change in CDASI score dropped for participants in both the lenabasum and placebo groups for the first 4 weeks. After that, however, those taking lenabasum saw an improvement of about 8 points from baseline CDASI score at 8 weeks, while those taking placebo had a decline of 3 points (P = .05). The differences remained significant at trial’s end.

Patient-reported outcomes for pain were significantly better with lenabasum, with patients on lenabasum recording a decrease on the Patient-Reported Outcomes Measurement Information System–29 pain interference scale, while patients on placebo reported an increase in pain by the end of the study period (P = .026). Scores on two other patient-reported dermatomyositis scales were numerically improved for patients taking lenabasum, but the differences from the patients on placebo were not statistically significant, Dr. Werth said.

However, patients in the initial clinical trial were given the opportunity to continue in a long-term extension arm, and that group has seen the clinician-rated CDASI scores continue to fall, with a mean decrease of 22 points from baseline (about 12 further points from the mean for those on lenabasum in the initial trial) at the 68-week mark, she added.

Itch scores continued to drop as well, with a reduction of 3.7 points on the 5-D Itch scale by 68 weeks; at 16 weeks, the reduction for the lenabasum arm had been 1.3 points.

Skin samples taken from trial participants showed many fewer CD4 cells in those taking lenabasum, compared with placebo at week 12 of the initial study. Interferon-beta and -gamma levels also dropped in those taking lenabasum, but not in the placebo arm.

“Lenabasum has effects on cytokine signatures and inflammatory cells correlating with response to therapy,” Dr. Werth said, adding that the findings gave support for a planned global phase 3 clinical trial of lenabasum in dermatomyositis.

Dr. Werth reported receiving grants from Pfizer and Corbus, and consulting fees from Pfizer, Janssen, Neovacs, Idera Pharmaceuticals, Octapharma, CSL Behring, and Corbus Pharmaceuticals. The study was funded by Corbus, the National Institutes of Health, and the University of Pennsylvania.

[email protected]

MILAN – A novel synthetic cannabinoid helped reduce the severity of dermatomyositis and improved patient-reported outcomes in early clinical trials, according to Victoria Werth, MD, who presented early-stage findings at the World Congress of Dermatology.

Lenabasum – previously known as anabasum – is a synthetic cannabinoid that binds to the CB2 receptor present on a variety of cells, including lymphocytes, explained Dr. Werth, professor of medicine at the University of Pennsylvania, Philadelphia, and chief of dermatology at the Philadelphia Veterans Administration Hospital. The nonpsychoactive compound’s mechanism of action helps prevent tissue thickening and fibrosis. In addition to its potential for dermatomyositis treatment, it is also being investigated as a treatment for cystic fibrosis, scleroderma, and lupus.

Dr. Werth added that earlier in vitro work with peripheral blood mononuclear cells of patients with dermatomyositis showed that lenabasum markedly suppressed the cells’ secretion of tumor necrosis factor–alpha, interferon-alpha, and interferon-beta (J Invest Dermatol. 2017 Nov;137[11]:2445-7). A randomized, placebo-controlled trial tested lenabasum, known in the trial as JBT-101, in 22 patients with skin-predominant myositis. The study was structured so patients took a half dose of lenabasum for 1 month, followed by 2 months of taking a full dose, and finally 1 month with no lenabasum dosing. Compared with placebo, scores on the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) were significantly improved with full dosing of lenabasum (P = .02), Dr. Werth said.

In this 16-week trial, the mean change in CDASI score dropped for participants in both the lenabasum and placebo groups for the first 4 weeks. After that, however, those taking lenabasum saw an improvement of about 8 points from baseline CDASI score at 8 weeks, while those taking placebo had a decline of 3 points (P = .05). The differences remained significant at trial’s end.

Patient-reported outcomes for pain were significantly better with lenabasum, with patients on lenabasum recording a decrease on the Patient-Reported Outcomes Measurement Information System–29 pain interference scale, while patients on placebo reported an increase in pain by the end of the study period (P = .026). Scores on two other patient-reported dermatomyositis scales were numerically improved for patients taking lenabasum, but the differences from the patients on placebo were not statistically significant, Dr. Werth said.

However, patients in the initial clinical trial were given the opportunity to continue in a long-term extension arm, and that group has seen the clinician-rated CDASI scores continue to fall, with a mean decrease of 22 points from baseline (about 12 further points from the mean for those on lenabasum in the initial trial) at the 68-week mark, she added.

Itch scores continued to drop as well, with a reduction of 3.7 points on the 5-D Itch scale by 68 weeks; at 16 weeks, the reduction for the lenabasum arm had been 1.3 points.

Skin samples taken from trial participants showed many fewer CD4 cells in those taking lenabasum, compared with placebo at week 12 of the initial study. Interferon-beta and -gamma levels also dropped in those taking lenabasum, but not in the placebo arm.

“Lenabasum has effects on cytokine signatures and inflammatory cells correlating with response to therapy,” Dr. Werth said, adding that the findings gave support for a planned global phase 3 clinical trial of lenabasum in dermatomyositis.

Dr. Werth reported receiving grants from Pfizer and Corbus, and consulting fees from Pfizer, Janssen, Neovacs, Idera Pharmaceuticals, Octapharma, CSL Behring, and Corbus Pharmaceuticals. The study was funded by Corbus, the National Institutes of Health, and the University of Pennsylvania.

[email protected]

MILAN – A novel synthetic cannabinoid helped reduce the severity of dermatomyositis and improved patient-reported outcomes in early clinical trials, according to Victoria Werth, MD, who presented early-stage findings at the World Congress of Dermatology.

Lenabasum – previously known as anabasum – is a synthetic cannabinoid that binds to the CB2 receptor present on a variety of cells, including lymphocytes, explained Dr. Werth, professor of medicine at the University of Pennsylvania, Philadelphia, and chief of dermatology at the Philadelphia Veterans Administration Hospital. The nonpsychoactive compound’s mechanism of action helps prevent tissue thickening and fibrosis. In addition to its potential for dermatomyositis treatment, it is also being investigated as a treatment for cystic fibrosis, scleroderma, and lupus.

Dr. Werth added that earlier in vitro work with peripheral blood mononuclear cells of patients with dermatomyositis showed that lenabasum markedly suppressed the cells’ secretion of tumor necrosis factor–alpha, interferon-alpha, and interferon-beta (J Invest Dermatol. 2017 Nov;137[11]:2445-7). A randomized, placebo-controlled trial tested lenabasum, known in the trial as JBT-101, in 22 patients with skin-predominant myositis. The study was structured so patients took a half dose of lenabasum for 1 month, followed by 2 months of taking a full dose, and finally 1 month with no lenabasum dosing. Compared with placebo, scores on the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) were significantly improved with full dosing of lenabasum (P = .02), Dr. Werth said.

In this 16-week trial, the mean change in CDASI score dropped for participants in both the lenabasum and placebo groups for the first 4 weeks. After that, however, those taking lenabasum saw an improvement of about 8 points from baseline CDASI score at 8 weeks, while those taking placebo had a decline of 3 points (P = .05). The differences remained significant at trial’s end.

Patient-reported outcomes for pain were significantly better with lenabasum, with patients on lenabasum recording a decrease on the Patient-Reported Outcomes Measurement Information System–29 pain interference scale, while patients on placebo reported an increase in pain by the end of the study period (P = .026). Scores on two other patient-reported dermatomyositis scales were numerically improved for patients taking lenabasum, but the differences from the patients on placebo were not statistically significant, Dr. Werth said.

However, patients in the initial clinical trial were given the opportunity to continue in a long-term extension arm, and that group has seen the clinician-rated CDASI scores continue to fall, with a mean decrease of 22 points from baseline (about 12 further points from the mean for those on lenabasum in the initial trial) at the 68-week mark, she added.

Itch scores continued to drop as well, with a reduction of 3.7 points on the 5-D Itch scale by 68 weeks; at 16 weeks, the reduction for the lenabasum arm had been 1.3 points.

Skin samples taken from trial participants showed many fewer CD4 cells in those taking lenabasum, compared with placebo at week 12 of the initial study. Interferon-beta and -gamma levels also dropped in those taking lenabasum, but not in the placebo arm.

“Lenabasum has effects on cytokine signatures and inflammatory cells correlating with response to therapy,” Dr. Werth said, adding that the findings gave support for a planned global phase 3 clinical trial of lenabasum in dermatomyositis.

Dr. Werth reported receiving grants from Pfizer and Corbus, and consulting fees from Pfizer, Janssen, Neovacs, Idera Pharmaceuticals, Octapharma, CSL Behring, and Corbus Pharmaceuticals. The study was funded by Corbus, the National Institutes of Health, and the University of Pennsylvania.

[email protected]

A patient treated with immune checkpoint inhibitor therapy for thyroid carcinoma presented with lichenoid dermatitis that resembled mycosis fungoides and also showed with monoclonal T-cell receptor gene rearrangement.

A case report published in the Journal of Cutaneous Pathology describes the “unusual” case and highlights another form of lichenoid dermatitis that may occur with immune checkpoint inhibitor therapy.

The patient was a 66-year-old man with BRAF_V600E-mutated anaplastic thyroid carcinoma, who was enrolled in a clinical trial of the checkpoint inhibitor atezolizumab, in combination with the BRAF inhibitor vemurafenib and MEK inhibitor cobimetinib.

Around 11 months after starting treatment, he presented to a dermatology department with a 1.5-cm x 1.2-cm crusted, erythematous plaque on his abdomen that had appeared 3 weeks earlier. He also had several follicular-based erythematous papules on his extremities and a single verrucous papule on his index finger, which the authors wrote were likely associated with the vemurafenib therapy.

The patient had previously had a squamous cell carcinoma removed but had no history of cutaneous lymphoma.

A punch biopsy of the abdominal lesion showed dense lichenoid, lymphohistiocytic infiltrate with papillary dermal fibrosis, and scattered multinucleated giant histiocytes. Immunohistochemical studies showed the lesion had an abnormal immunophenotype in which CD4+ cells were four to five times more common than CD8+ cells, and there was partial loss of CD7 expression.

The lesion was treated with 0.05% clobetasol cream and monitored without interrupting the cancer therapy. The lesion gradually reduced in size, but 4 months later, another lesion appeared on the patient’s right clavicle.

A skin biopsy revealed lichenoid lymphohistiocytic infiltrate with occasional giant cells in the superficial dermis, as well as atypical, hyperchromatic lymphocytes with clear halos. Immunohistochemical studies showed that the new lesion was similar to the earlier abdominal lesion.

T-cell receptor gene rearrangement studies on both lesions showed that the abdominal lesion had both monoclonal TCR-gamma and TCR-beta gene rearrangements. The clavicle lesion showed the same monoclonal TCR-gamma rearrangement as the abdominal lesion, but lacked the TCR-beta gene rearrangement.

The lesions continued to be treated with clobetasol cream (0.05%), and the patient remained on the anticancer treatment regimen.

Michael T. Tetzlaff, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, and coauthors wrote that up to half of all patients treated with immune checkpoint inhibitors develop some kind of cutaneous immune-related adverse event, and lichenoid dermatitis is one of the most common seen in biopsies.

“Clinical and pathological recognition of monoclonal [lichenoid dermatitis associated with immune checkpoint inhibitors] in the context of [immune checkpoint inhibitor] therapy will be important for accurate diagnosis and patient care,” they wrote.

The researchers did not report financial disclosures.

SOURCE: Tetzlaff MT et al. J Cutan Pathol. 2019 Jun 29. doi: 10.1111/cup.13536.

A patient treated with immune checkpoint inhibitor therapy for thyroid carcinoma presented with lichenoid dermatitis that resembled mycosis fungoides and also showed with monoclonal T-cell receptor gene rearrangement.

A case report published in the Journal of Cutaneous Pathology describes the “unusual” case and highlights another form of lichenoid dermatitis that may occur with immune checkpoint inhibitor therapy.

The patient was a 66-year-old man with BRAF_V600E-mutated anaplastic thyroid carcinoma, who was enrolled in a clinical trial of the checkpoint inhibitor atezolizumab, in combination with the BRAF inhibitor vemurafenib and MEK inhibitor cobimetinib.

Around 11 months after starting treatment, he presented to a dermatology department with a 1.5-cm x 1.2-cm crusted, erythematous plaque on his abdomen that had appeared 3 weeks earlier. He also had several follicular-based erythematous papules on his extremities and a single verrucous papule on his index finger, which the authors wrote were likely associated with the vemurafenib therapy.

The patient had previously had a squamous cell carcinoma removed but had no history of cutaneous lymphoma.

A punch biopsy of the abdominal lesion showed dense lichenoid, lymphohistiocytic infiltrate with papillary dermal fibrosis, and scattered multinucleated giant histiocytes. Immunohistochemical studies showed the lesion had an abnormal immunophenotype in which CD4+ cells were four to five times more common than CD8+ cells, and there was partial loss of CD7 expression.

The lesion was treated with 0.05% clobetasol cream and monitored without interrupting the cancer therapy. The lesion gradually reduced in size, but 4 months later, another lesion appeared on the patient’s right clavicle.

A skin biopsy revealed lichenoid lymphohistiocytic infiltrate with occasional giant cells in the superficial dermis, as well as atypical, hyperchromatic lymphocytes with clear halos. Immunohistochemical studies showed that the new lesion was similar to the earlier abdominal lesion.

T-cell receptor gene rearrangement studies on both lesions showed that the abdominal lesion had both monoclonal TCR-gamma and TCR-beta gene rearrangements. The clavicle lesion showed the same monoclonal TCR-gamma rearrangement as the abdominal lesion, but lacked the TCR-beta gene rearrangement.

The lesions continued to be treated with clobetasol cream (0.05%), and the patient remained on the anticancer treatment regimen.

Michael T. Tetzlaff, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, and coauthors wrote that up to half of all patients treated with immune checkpoint inhibitors develop some kind of cutaneous immune-related adverse event, and lichenoid dermatitis is one of the most common seen in biopsies.

“Clinical and pathological recognition of monoclonal [lichenoid dermatitis associated with immune checkpoint inhibitors] in the context of [immune checkpoint inhibitor] therapy will be important for accurate diagnosis and patient care,” they wrote.

The researchers did not report financial disclosures.

SOURCE: Tetzlaff MT et al. J Cutan Pathol. 2019 Jun 29. doi: 10.1111/cup.13536.

A patient treated with immune checkpoint inhibitor therapy for thyroid carcinoma presented with lichenoid dermatitis that resembled mycosis fungoides and also showed with monoclonal T-cell receptor gene rearrangement.

A case report published in the Journal of Cutaneous Pathology describes the “unusual” case and highlights another form of lichenoid dermatitis that may occur with immune checkpoint inhibitor therapy.

The patient was a 66-year-old man with BRAF_V600E-mutated anaplastic thyroid carcinoma, who was enrolled in a clinical trial of the checkpoint inhibitor atezolizumab, in combination with the BRAF inhibitor vemurafenib and MEK inhibitor cobimetinib.

Around 11 months after starting treatment, he presented to a dermatology department with a 1.5-cm x 1.2-cm crusted, erythematous plaque on his abdomen that had appeared 3 weeks earlier. He also had several follicular-based erythematous papules on his extremities and a single verrucous papule on his index finger, which the authors wrote were likely associated with the vemurafenib therapy.

The patient had previously had a squamous cell carcinoma removed but had no history of cutaneous lymphoma.

A punch biopsy of the abdominal lesion showed dense lichenoid, lymphohistiocytic infiltrate with papillary dermal fibrosis, and scattered multinucleated giant histiocytes. Immunohistochemical studies showed the lesion had an abnormal immunophenotype in which CD4+ cells were four to five times more common than CD8+ cells, and there was partial loss of CD7 expression.

The lesion was treated with 0.05% clobetasol cream and monitored without interrupting the cancer therapy. The lesion gradually reduced in size, but 4 months later, another lesion appeared on the patient’s right clavicle.

A skin biopsy revealed lichenoid lymphohistiocytic infiltrate with occasional giant cells in the superficial dermis, as well as atypical, hyperchromatic lymphocytes with clear halos. Immunohistochemical studies showed that the new lesion was similar to the earlier abdominal lesion.

T-cell receptor gene rearrangement studies on both lesions showed that the abdominal lesion had both monoclonal TCR-gamma and TCR-beta gene rearrangements. The clavicle lesion showed the same monoclonal TCR-gamma rearrangement as the abdominal lesion, but lacked the TCR-beta gene rearrangement.

The lesions continued to be treated with clobetasol cream (0.05%), and the patient remained on the anticancer treatment regimen.

Michael T. Tetzlaff, MD, PhD, of the University of Texas MD Anderson Cancer Center, Houston, and coauthors wrote that up to half of all patients treated with immune checkpoint inhibitors develop some kind of cutaneous immune-related adverse event, and lichenoid dermatitis is one of the most common seen in biopsies.

“Clinical and pathological recognition of monoclonal [lichenoid dermatitis associated with immune checkpoint inhibitors] in the context of [immune checkpoint inhibitor] therapy will be important for accurate diagnosis and patient care,” they wrote.

The researchers did not report financial disclosures.

SOURCE: Tetzlaff MT et al. J Cutan Pathol. 2019 Jun 29. doi: 10.1111/cup.13536.

Researchers have characterized the clinical presentation, progression, and prognosis of leukemia cutis in a pediatric population, according to findings from a retrospective case series.

“To our knowledge, this is the largest reported case series of pediatric leukemia cutis,” wrote Elena Corina Andriescu of the University of Texas, Houston, and colleagues. The results were published in Pediatric Dermatology.

The study included 31 children with histologically confirmed leukemia cutis at one of two pediatric institutions. The researchers reviewed medical records to distinguish common features among patients.

Various clinical data, including disease subtype, related symptoms, management, and prognosis, were collected from January 1993 to March 2014. The children in the case series ranged in age up to 19 years with a median age at diagnosis of 26.8 months.

After analysis, the researchers reported that the magnitude and morphology of disease lesions differed among pediatric patients, with the most common sites being the lower extremities and head. The most common morphologies were nodules and papules. Additionally, the researchers found that lesions were often erythematous, violaceous, or both colors.

The majority of patients (65%) presented with concomitant systemic leukemia and leukemia cutis. The most common types of leukemia associated with the skin condition were acute myeloid leukemia (in 74% of cases) and acute lymphoblastic leukemia (in 16% of cases). The researchers saw no significant differences in leukemia cutis morphology or distribution based on the leukemia diagnosis.

“Most cases of leukemia cutis arose during initial leukemia episodes, rather than with relapsed leukemia,” they added.

Because of an insufficiency of specific genetic data, investigators were unable to make prognostic inferences in the majority of participants.

Two key limitations of the study were the small sample size and retrospective design. As a result, the investigators were unable to prospectively classify skin findings in a systematic manner. Despite these limitations, the authors noted that these findings add to the present knowledge of leukemia cutis in pediatric patients.

“Importantly, the presence of [leukemia cutis] changed the management of systemic leukemia in one‐third of patients,” the researchers wrote. “The potential for major changes in treatment plans such as adding radiation therapy and deferring hematopoietic stem cell transplantation underscores the importance of diagnosing [leukemia cutis].”

No funding sources were reported. The authors did not report conflicts of interest.

SOURCE: Andriescu EC et al. Pediatr Dermatol. 2019 Jul 5. doi: 10.1111/pde.13864.

Researchers have characterized the clinical presentation, progression, and prognosis of leukemia cutis in a pediatric population, according to findings from a retrospective case series.

“To our knowledge, this is the largest reported case series of pediatric leukemia cutis,” wrote Elena Corina Andriescu of the University of Texas, Houston, and colleagues. The results were published in Pediatric Dermatology.

The study included 31 children with histologically confirmed leukemia cutis at one of two pediatric institutions. The researchers reviewed medical records to distinguish common features among patients.

Various clinical data, including disease subtype, related symptoms, management, and prognosis, were collected from January 1993 to March 2014. The children in the case series ranged in age up to 19 years with a median age at diagnosis of 26.8 months.

After analysis, the researchers reported that the magnitude and morphology of disease lesions differed among pediatric patients, with the most common sites being the lower extremities and head. The most common morphologies were nodules and papules. Additionally, the researchers found that lesions were often erythematous, violaceous, or both colors.

The majority of patients (65%) presented with concomitant systemic leukemia and leukemia cutis. The most common types of leukemia associated with the skin condition were acute myeloid leukemia (in 74% of cases) and acute lymphoblastic leukemia (in 16% of cases). The researchers saw no significant differences in leukemia cutis morphology or distribution based on the leukemia diagnosis.

“Most cases of leukemia cutis arose during initial leukemia episodes, rather than with relapsed leukemia,” they added.

Because of an insufficiency of specific genetic data, investigators were unable to make prognostic inferences in the majority of participants.

Two key limitations of the study were the small sample size and retrospective design. As a result, the investigators were unable to prospectively classify skin findings in a systematic manner. Despite these limitations, the authors noted that these findings add to the present knowledge of leukemia cutis in pediatric patients.

“Importantly, the presence of [leukemia cutis] changed the management of systemic leukemia in one‐third of patients,” the researchers wrote. “The potential for major changes in treatment plans such as adding radiation therapy and deferring hematopoietic stem cell transplantation underscores the importance of diagnosing [leukemia cutis].”

No funding sources were reported. The authors did not report conflicts of interest.

SOURCE: Andriescu EC et al. Pediatr Dermatol. 2019 Jul 5. doi: 10.1111/pde.13864.

Researchers have characterized the clinical presentation, progression, and prognosis of leukemia cutis in a pediatric population, according to findings from a retrospective case series.

“To our knowledge, this is the largest reported case series of pediatric leukemia cutis,” wrote Elena Corina Andriescu of the University of Texas, Houston, and colleagues. The results were published in Pediatric Dermatology.

The study included 31 children with histologically confirmed leukemia cutis at one of two pediatric institutions. The researchers reviewed medical records to distinguish common features among patients.

Various clinical data, including disease subtype, related symptoms, management, and prognosis, were collected from January 1993 to March 2014. The children in the case series ranged in age up to 19 years with a median age at diagnosis of 26.8 months.

After analysis, the researchers reported that the magnitude and morphology of disease lesions differed among pediatric patients, with the most common sites being the lower extremities and head. The most common morphologies were nodules and papules. Additionally, the researchers found that lesions were often erythematous, violaceous, or both colors.

The majority of patients (65%) presented with concomitant systemic leukemia and leukemia cutis. The most common types of leukemia associated with the skin condition were acute myeloid leukemia (in 74% of cases) and acute lymphoblastic leukemia (in 16% of cases). The researchers saw no significant differences in leukemia cutis morphology or distribution based on the leukemia diagnosis.

“Most cases of leukemia cutis arose during initial leukemia episodes, rather than with relapsed leukemia,” they added.

Because of an insufficiency of specific genetic data, investigators were unable to make prognostic inferences in the majority of participants.

Two key limitations of the study were the small sample size and retrospective design. As a result, the investigators were unable to prospectively classify skin findings in a systematic manner. Despite these limitations, the authors noted that these findings add to the present knowledge of leukemia cutis in pediatric patients.

“Importantly, the presence of [leukemia cutis] changed the management of systemic leukemia in one‐third of patients,” the researchers wrote. “The potential for major changes in treatment plans such as adding radiation therapy and deferring hematopoietic stem cell transplantation underscores the importance of diagnosing [leukemia cutis].”

No funding sources were reported. The authors did not report conflicts of interest.

SOURCE: Andriescu EC et al. Pediatr Dermatol. 2019 Jul 5. doi: 10.1111/pde.13864.

BANGKOK – Cutaneous reactions to antiepileptic drugs in patients with chronic epilepsy suggest increased likelihood of an autoimmune element to their seizure disorder, Fernando Cendes, MD, PhD, reported at the International Epilepsy Congress.

Bruce Jancin/MDedge News

“My recommendation based on our findings is that if you have a patient who has a history of skin reactions to AEDs [antiepileptic drugs], or who has psychosis, or who has a very strange response to antiepileptic medication – meaning that at some points they are refractory and at other points they are very well controlled – I think those patients are probably at risk for having an autoantibody,” he said at the congress sponsored by the International League Against Epilepsy.

Screening for autoantibodies in such patients is appropriate. However, there’s a caveat: “The thing is, we don’t have evidence that treating these autoantibodies with immunotherapy will have any benefit on seizure control in these patients. We don’t have that data yet, but we are looking into it,” according to Dr. Cendes, professor of neurology at the State University of Campinas (Brazil).

He presented a study of 221 consecutive adults with severe chronic refractory epilepsy as evidenced by a mean disease duration of nearly 29 years, with an average of 5.93 seizures per month. A total of 77% had a structural etiology for their epilepsy, in most cases hippocampal sclerosis. In 19% of patients, the etiology was unknown. Overall, 95% of subjects had focal epilepsy, and the remainder had generalized epilepsy. All underwent serum testing for a variety of antibodies against neuronal surface antigens that have been implicated in encephalitis, seizures, and/or psychosis. Those who tested positive then underwent confirmatory testing of their cerebrospinal fluid.

The impetus for this study, the neurologist explained, is that although it’s now well established that seizures are a common clinical expression of acute- and subacute-phase autoimmune encephalitis marked by neuronal autoantibodies, little is known about the relationship between chronic epilepsy and such antibodies.


Only five Brazilian patients with chronic epilepsy, or 2.2%, tested positive for autoantibodies, all of whom had mesial temporal lobe epilepsy with hippocampal sclerosis. This suggests a possible autoimmune etiology for hippocampal sclerosis. Three of the five patients had anti-N-methyl-D-aspartate receptor antibodies (anti-NMDA) and two had antiglutamic acid decarboxylate antibodies (anti-GAD). No one was positive for anti–leucine-rich glioma-inactivated 1 antibodies (anti-LGI1), anti–contactin-associated proteinlike 2 (anti-caspr2), anti-glutamate receptor antibodies (anti-AMPAr), or anti–gamma-aminobutyric acid receptor antibodies (anti-GABAr).

The autoantibody-negative and the much smaller autoantibody-positive groups didn’t differ significantly in terms of demographics, seizure frequency, disease duration, drug resistance, cognitive impairment, comorbid autoimmune conditions, or history of status epilepticus. Indeed, only two between-group differences were found: fluctuation in seizure control was an issue in 10.6% of autoantibody-negative and 40% of autoantibody-positive patients, and cutaneous adverse reactions to antiepileptic drugs were noted in 10.6% of antibody-negative and 60% of antibody-positive patients. Psychiatric comorbidities were present in 49.5% of autoantibody-negative patients as compared with 80% – that is, four of five – who were autoantibody-positive, a trend that didn’t achieve statistical significance.

Asked if he thinks the autoantibodies found in a small subset of patients with chronic epilepsy were a cause or an effect of repeated seizures for so long, Dr. Cendes replied, “That’s a very interesting question, and I don’t have an answer, actually. But if seizures trigger development of these antibodies – and remember, this population we’re talking about had many, many seizures over the years – I would expect antibodies to be more frequent than the figure we found.”

He reported having no financial conflicts regarding his study.

[email protected]

SOURCE: Watanabe N et al. IEC 2019, Abstract P004.

BANGKOK – Cutaneous reactions to antiepileptic drugs in patients with chronic epilepsy suggest increased likelihood of an autoimmune element to their seizure disorder, Fernando Cendes, MD, PhD, reported at the International Epilepsy Congress.

Bruce Jancin/MDedge News

“My recommendation based on our findings is that if you have a patient who has a history of skin reactions to AEDs [antiepileptic drugs], or who has psychosis, or who has a very strange response to antiepileptic medication – meaning that at some points they are refractory and at other points they are very well controlled – I think those patients are probably at risk for having an autoantibody,” he said at the congress sponsored by the International League Against Epilepsy.

Screening for autoantibodies in such patients is appropriate. However, there’s a caveat: “The thing is, we don’t have evidence that treating these autoantibodies with immunotherapy will have any benefit on seizure control in these patients. We don’t have that data yet, but we are looking into it,” according to Dr. Cendes, professor of neurology at the State University of Campinas (Brazil).

He presented a study of 221 consecutive adults with severe chronic refractory epilepsy as evidenced by a mean disease duration of nearly 29 years, with an average of 5.93 seizures per month. A total of 77% had a structural etiology for their epilepsy, in most cases hippocampal sclerosis. In 19% of patients, the etiology was unknown. Overall, 95% of subjects had focal epilepsy, and the remainder had generalized epilepsy. All underwent serum testing for a variety of antibodies against neuronal surface antigens that have been implicated in encephalitis, seizures, and/or psychosis. Those who tested positive then underwent confirmatory testing of their cerebrospinal fluid.

The impetus for this study, the neurologist explained, is that although it’s now well established that seizures are a common clinical expression of acute- and subacute-phase autoimmune encephalitis marked by neuronal autoantibodies, little is known about the relationship between chronic epilepsy and such antibodies.


Only five Brazilian patients with chronic epilepsy, or 2.2%, tested positive for autoantibodies, all of whom had mesial temporal lobe epilepsy with hippocampal sclerosis. This suggests a possible autoimmune etiology for hippocampal sclerosis. Three of the five patients had anti-N-methyl-D-aspartate receptor antibodies (anti-NMDA) and two had antiglutamic acid decarboxylate antibodies (anti-GAD). No one was positive for anti–leucine-rich glioma-inactivated 1 antibodies (anti-LGI1), anti–contactin-associated proteinlike 2 (anti-caspr2), anti-glutamate receptor antibodies (anti-AMPAr), or anti–gamma-aminobutyric acid receptor antibodies (anti-GABAr).

The autoantibody-negative and the much smaller autoantibody-positive groups didn’t differ significantly in terms of demographics, seizure frequency, disease duration, drug resistance, cognitive impairment, comorbid autoimmune conditions, or history of status epilepticus. Indeed, only two between-group differences were found: fluctuation in seizure control was an issue in 10.6% of autoantibody-negative and 40% of autoantibody-positive patients, and cutaneous adverse reactions to antiepileptic drugs were noted in 10.6% of antibody-negative and 60% of antibody-positive patients. Psychiatric comorbidities were present in 49.5% of autoantibody-negative patients as compared with 80% – that is, four of five – who were autoantibody-positive, a trend that didn’t achieve statistical significance.

Asked if he thinks the autoantibodies found in a small subset of patients with chronic epilepsy were a cause or an effect of repeated seizures for so long, Dr. Cendes replied, “That’s a very interesting question, and I don’t have an answer, actually. But if seizures trigger development of these antibodies – and remember, this population we’re talking about had many, many seizures over the years – I would expect antibodies to be more frequent than the figure we found.”

He reported having no financial conflicts regarding his study.

[email protected]

SOURCE: Watanabe N et al. IEC 2019, Abstract P004.

BANGKOK – Cutaneous reactions to antiepileptic drugs in patients with chronic epilepsy suggest increased likelihood of an autoimmune element to their seizure disorder, Fernando Cendes, MD, PhD, reported at the International Epilepsy Congress.

Bruce Jancin/MDedge News

“My recommendation based on our findings is that if you have a patient who has a history of skin reactions to AEDs [antiepileptic drugs], or who has psychosis, or who has a very strange response to antiepileptic medication – meaning that at some points they are refractory and at other points they are very well controlled – I think those patients are probably at risk for having an autoantibody,” he said at the congress sponsored by the International League Against Epilepsy.

Screening for autoantibodies in such patients is appropriate. However, there’s a caveat: “The thing is, we don’t have evidence that treating these autoantibodies with immunotherapy will have any benefit on seizure control in these patients. We don’t have that data yet, but we are looking into it,” according to Dr. Cendes, professor of neurology at the State University of Campinas (Brazil).

He presented a study of 221 consecutive adults with severe chronic refractory epilepsy as evidenced by a mean disease duration of nearly 29 years, with an average of 5.93 seizures per month. A total of 77% had a structural etiology for their epilepsy, in most cases hippocampal sclerosis. In 19% of patients, the etiology was unknown. Overall, 95% of subjects had focal epilepsy, and the remainder had generalized epilepsy. All underwent serum testing for a variety of antibodies against neuronal surface antigens that have been implicated in encephalitis, seizures, and/or psychosis. Those who tested positive then underwent confirmatory testing of their cerebrospinal fluid.

The impetus for this study, the neurologist explained, is that although it’s now well established that seizures are a common clinical expression of acute- and subacute-phase autoimmune encephalitis marked by neuronal autoantibodies, little is known about the relationship between chronic epilepsy and such antibodies.


Only five Brazilian patients with chronic epilepsy, or 2.2%, tested positive for autoantibodies, all of whom had mesial temporal lobe epilepsy with hippocampal sclerosis. This suggests a possible autoimmune etiology for hippocampal sclerosis. Three of the five patients had anti-N-methyl-D-aspartate receptor antibodies (anti-NMDA) and two had antiglutamic acid decarboxylate antibodies (anti-GAD). No one was positive for anti–leucine-rich glioma-inactivated 1 antibodies (anti-LGI1), anti–contactin-associated proteinlike 2 (anti-caspr2), anti-glutamate receptor antibodies (anti-AMPAr), or anti–gamma-aminobutyric acid receptor antibodies (anti-GABAr).

The autoantibody-negative and the much smaller autoantibody-positive groups didn’t differ significantly in terms of demographics, seizure frequency, disease duration, drug resistance, cognitive impairment, comorbid autoimmune conditions, or history of status epilepticus. Indeed, only two between-group differences were found: fluctuation in seizure control was an issue in 10.6% of autoantibody-negative and 40% of autoantibody-positive patients, and cutaneous adverse reactions to antiepileptic drugs were noted in 10.6% of antibody-negative and 60% of antibody-positive patients. Psychiatric comorbidities were present in 49.5% of autoantibody-negative patients as compared with 80% – that is, four of five – who were autoantibody-positive, a trend that didn’t achieve statistical significance.

Asked if he thinks the autoantibodies found in a small subset of patients with chronic epilepsy were a cause or an effect of repeated seizures for so long, Dr. Cendes replied, “That’s a very interesting question, and I don’t have an answer, actually. But if seizures trigger development of these antibodies – and remember, this population we’re talking about had many, many seizures over the years – I would expect antibodies to be more frequent than the figure we found.”

He reported having no financial conflicts regarding his study.

[email protected]

SOURCE: Watanabe N et al. IEC 2019, Abstract P004.

NEWPORT BEACH, CALIF. – What can set off an allergic skin reaction? Some unusual suspects are wrinkle-free clothing, spinach salads, plywood, tires, and Italian food, according to dermatologist Jennifer H. Perryman, MD.

Here’s a closer look at the allergens highlighted by Dr. Perryman in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar:

Formaldehyde: It’s everywhere

“In general, formaldehyde is found on everyone in this room in two different places: preservatives in skin care products and in a lot of our clothing,” said Dr. Perryman, who practices in Greeley and Fort Collins, Colo.

The preservative is used in an even wider variety of products, including fluids used in industry (such as metalworking) and topical medications. But people are especially likely to encounter it in clothing – via formaldehyde textile resins – as well as in cosmetics, soaps, and lotions.

On the clothing front, Dr. Perryman said, formaldehyde textile resins have been used since the 1930s. They’re used to treat blends of synthetic and cotton fibers and bed sheets. Beware of “wrinkle resistant” and “permanent press” clothing (although not all have been treated with this resin). “Newer formaldehyde textile resins have less formaldehyde release, but they may be more expensive, and some industries may not use them,” she said.


Avoiding formaldehyde textile resins isn’t a simple matter.” You have to go out of your way to stay away from a polyester-cotton blend,” she said. “And don’t forget bedsheets,” she added, noting that the packaging on some sheets include information about cotton count, “but when you flip over the label it says it’s ‘50% cotton and 50% polyester or other.’ ”

Some patients will bring their own bedsheets to hotels so they don’t experience flares from hotel bedsheets, she added.

Other products can trigger this skin allergy. Beware, Dr. Perryman said, of formaldehyde exposure from paper, cardboard, cigarette smoke, processed wood products like plywood, foam housing and industrial insulation, embalming fluid and tissue fixatives, and some paints and adhesives.

What are the signs that someone may have a case of formaldehyde allergy? It may cause patchy generalized dermatitis, erythroderma, and nummular dermatitis. It may spare the hands, feet, and face because those parts of the body have less exposure to clothing, and it’s likely to especially affect body areas where clothing is tight. And for unknown reasons, this allergy is more common in the elderly, Dr. Perryman said.

Textile dye: Beware polyester

This allergy is mainly triggered by synthetic fabrics like polyester, rayon, and acetate, she noted. Darker colors are more allergenic. Clothes made of natural fibers such as cotton, silk, linen, and wool are alternatives. These are not dyed with these dyes, she said, adding that a reaction to wool will be from irritation, not from the dye.

Paraphenylenediamine: Keep an eye out for this dye ingredient

Paraphenylenediamine, which can trigger allergic reactions, is found in leather dye, fur dye, and some (but not all) hair dyes. Be aware that it can cross-react with other allergens like sulfonamide medications.

If a patch test turns up a reaction to “Black-Rubber Mix,” which includes paraphenylenediamine, consider whether the patient has exposure to the rubber in tires. Car mechanics may be affected by this allergy, Dr. Perryman said.

Neomycin: A drop of trouble

Allergy to the antibiotic neomycin can be triggered by exposure to gentamicin and tobramycin eye drops. Patients may believe they have an infection, Dr. Perryman said, so consider getting a culture. In some cases, an allergic reaction to neomycin may be incorrectly diagnosed as cellulitis.

Nickel: Not just a jewelry hazard

Jewelry and coins can trigger nickel allergies, but be aware that systemic nickel allergy can also trigger skin problems from a patient’s diet. It may be necessary to put patients on a low-nickel diet that avoids foods such as healthy grains, greens (especially spinach), nuts, legumes, and chocolate. “I always feel bad” putting patients on a restrictive diet, Dr. Perryman said, but it can be helpful to take 500 mg of vitamin C three times a day since it binds to nickel.

Cobalt: Watch the chocolate and coffee

Jewelry with cobalt can cause an allergic reaction. Dr. Perryman tells patients to buy an inexpensive “spot test” product online that detects whether jewelry has nickel or cobalt. Cobalt allergy can also trigger symptoms in patients exposed to “hard metal” industrial tools, cement, and masonry. Workers in the plastics and dye industries may be exposed too.

Like nickel, Dr. Perryman said, systemic cobalt allergy related to diet is also possible. The list of foods that contain higher levels of cobalt is long, and includes apricots, beans, beer, chocolate, coffee, nuts, tea, and whole-grain flour.

Dr. Perryman also mentioned several other allergens to keep in mind:

• Chromate can trigger reactions in people who wear leather shoes (the metal can be used in tanning). It can also cause problems in workers exposed to it via cement, bricks, drywall, and metal plating.
• Chromium picolinate, an over-the-counter supplement, can cause systemic dermatitis.
• Gold in jewelry can trigger an allergic reaction. Talk to patients about replating their jewelry, Dr. Perryman said.
• Rubber can trigger reactions due to exposure to rubber bands, makeup sponges, and rubber gloves (even nitrile ones). Be aware that both rubber and latex allergies may coexist and consider a blood test for latex allergy.
• Systemic balsam allergy related to an individual’s diet is possible. Tomato is an especially big villain on this front, along with citrus fruits, spices, cola, chili, and chocolate.

Dr. Perryman disclosed consulting work for IntraDerm. SDEF and this news organization are owned by the same parent company.

NEWPORT BEACH, CALIF. – What can set off an allergic skin reaction? Some unusual suspects are wrinkle-free clothing, spinach salads, plywood, tires, and Italian food, according to dermatologist Jennifer H. Perryman, MD.

Here’s a closer look at the allergens highlighted by Dr. Perryman in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar:

Formaldehyde: It’s everywhere

“In general, formaldehyde is found on everyone in this room in two different places: preservatives in skin care products and in a lot of our clothing,” said Dr. Perryman, who practices in Greeley and Fort Collins, Colo.

The preservative is used in an even wider variety of products, including fluids used in industry (such as metalworking) and topical medications. But people are especially likely to encounter it in clothing – via formaldehyde textile resins – as well as in cosmetics, soaps, and lotions.

On the clothing front, Dr. Perryman said, formaldehyde textile resins have been used since the 1930s. They’re used to treat blends of synthetic and cotton fibers and bed sheets. Beware of “wrinkle resistant” and “permanent press” clothing (although not all have been treated with this resin). “Newer formaldehyde textile resins have less formaldehyde release, but they may be more expensive, and some industries may not use them,” she said.


Avoiding formaldehyde textile resins isn’t a simple matter.” You have to go out of your way to stay away from a polyester-cotton blend,” she said. “And don’t forget bedsheets,” she added, noting that the packaging on some sheets include information about cotton count, “but when you flip over the label it says it’s ‘50% cotton and 50% polyester or other.’ ”

Some patients will bring their own bedsheets to hotels so they don’t experience flares from hotel bedsheets, she added.

Other products can trigger this skin allergy. Beware, Dr. Perryman said, of formaldehyde exposure from paper, cardboard, cigarette smoke, processed wood products like plywood, foam housing and industrial insulation, embalming fluid and tissue fixatives, and some paints and adhesives.

What are the signs that someone may have a case of formaldehyde allergy? It may cause patchy generalized dermatitis, erythroderma, and nummular dermatitis. It may spare the hands, feet, and face because those parts of the body have less exposure to clothing, and it’s likely to especially affect body areas where clothing is tight. And for unknown reasons, this allergy is more common in the elderly, Dr. Perryman said.

Textile dye: Beware polyester

This allergy is mainly triggered by synthetic fabrics like polyester, rayon, and acetate, she noted. Darker colors are more allergenic. Clothes made of natural fibers such as cotton, silk, linen, and wool are alternatives. These are not dyed with these dyes, she said, adding that a reaction to wool will be from irritation, not from the dye.

Paraphenylenediamine: Keep an eye out for this dye ingredient

Paraphenylenediamine, which can trigger allergic reactions, is found in leather dye, fur dye, and some (but not all) hair dyes. Be aware that it can cross-react with other allergens like sulfonamide medications.

If a patch test turns up a reaction to “Black-Rubber Mix,” which includes paraphenylenediamine, consider whether the patient has exposure to the rubber in tires. Car mechanics may be affected by this allergy, Dr. Perryman said.

Neomycin: A drop of trouble

Allergy to the antibiotic neomycin can be triggered by exposure to gentamicin and tobramycin eye drops. Patients may believe they have an infection, Dr. Perryman said, so consider getting a culture. In some cases, an allergic reaction to neomycin may be incorrectly diagnosed as cellulitis.

Nickel: Not just a jewelry hazard

Jewelry and coins can trigger nickel allergies, but be aware that systemic nickel allergy can also trigger skin problems from a patient’s diet. It may be necessary to put patients on a low-nickel diet that avoids foods such as healthy grains, greens (especially spinach), nuts, legumes, and chocolate. “I always feel bad” putting patients on a restrictive diet, Dr. Perryman said, but it can be helpful to take 500 mg of vitamin C three times a day since it binds to nickel.

Cobalt: Watch the chocolate and coffee

Jewelry with cobalt can cause an allergic reaction. Dr. Perryman tells patients to buy an inexpensive “spot test” product online that detects whether jewelry has nickel or cobalt. Cobalt allergy can also trigger symptoms in patients exposed to “hard metal” industrial tools, cement, and masonry. Workers in the plastics and dye industries may be exposed too.

Like nickel, Dr. Perryman said, systemic cobalt allergy related to diet is also possible. The list of foods that contain higher levels of cobalt is long, and includes apricots, beans, beer, chocolate, coffee, nuts, tea, and whole-grain flour.

Dr. Perryman also mentioned several other allergens to keep in mind:

• Chromate can trigger reactions in people who wear leather shoes (the metal can be used in tanning). It can also cause problems in workers exposed to it via cement, bricks, drywall, and metal plating.
• Chromium picolinate, an over-the-counter supplement, can cause systemic dermatitis.
• Gold in jewelry can trigger an allergic reaction. Talk to patients about replating their jewelry, Dr. Perryman said.
• Rubber can trigger reactions due to exposure to rubber bands, makeup sponges, and rubber gloves (even nitrile ones). Be aware that both rubber and latex allergies may coexist and consider a blood test for latex allergy.
• Systemic balsam allergy related to an individual’s diet is possible. Tomato is an especially big villain on this front, along with citrus fruits, spices, cola, chili, and chocolate.

Dr. Perryman disclosed consulting work for IntraDerm. SDEF and this news organization are owned by the same parent company.

NEWPORT BEACH, CALIF. – What can set off an allergic skin reaction? Some unusual suspects are wrinkle-free clothing, spinach salads, plywood, tires, and Italian food, according to dermatologist Jennifer H. Perryman, MD.

Here’s a closer look at the allergens highlighted by Dr. Perryman in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar:

Formaldehyde: It’s everywhere

“In general, formaldehyde is found on everyone in this room in two different places: preservatives in skin care products and in a lot of our clothing,” said Dr. Perryman, who practices in Greeley and Fort Collins, Colo.

The preservative is used in an even wider variety of products, including fluids used in industry (such as metalworking) and topical medications. But people are especially likely to encounter it in clothing – via formaldehyde textile resins – as well as in cosmetics, soaps, and lotions.

On the clothing front, Dr. Perryman said, formaldehyde textile resins have been used since the 1930s. They’re used to treat blends of synthetic and cotton fibers and bed sheets. Beware of “wrinkle resistant” and “permanent press” clothing (although not all have been treated with this resin). “Newer formaldehyde textile resins have less formaldehyde release, but they may be more expensive, and some industries may not use them,” she said.


Avoiding formaldehyde textile resins isn’t a simple matter.” You have to go out of your way to stay away from a polyester-cotton blend,” she said. “And don’t forget bedsheets,” she added, noting that the packaging on some sheets include information about cotton count, “but when you flip over the label it says it’s ‘50% cotton and 50% polyester or other.’ ”

Some patients will bring their own bedsheets to hotels so they don’t experience flares from hotel bedsheets, she added.

Other products can trigger this skin allergy. Beware, Dr. Perryman said, of formaldehyde exposure from paper, cardboard, cigarette smoke, processed wood products like plywood, foam housing and industrial insulation, embalming fluid and tissue fixatives, and some paints and adhesives.

What are the signs that someone may have a case of formaldehyde allergy? It may cause patchy generalized dermatitis, erythroderma, and nummular dermatitis. It may spare the hands, feet, and face because those parts of the body have less exposure to clothing, and it’s likely to especially affect body areas where clothing is tight. And for unknown reasons, this allergy is more common in the elderly, Dr. Perryman said.

Textile dye: Beware polyester

This allergy is mainly triggered by synthetic fabrics like polyester, rayon, and acetate, she noted. Darker colors are more allergenic. Clothes made of natural fibers such as cotton, silk, linen, and wool are alternatives. These are not dyed with these dyes, she said, adding that a reaction to wool will be from irritation, not from the dye.

Paraphenylenediamine: Keep an eye out for this dye ingredient

Paraphenylenediamine, which can trigger allergic reactions, is found in leather dye, fur dye, and some (but not all) hair dyes. Be aware that it can cross-react with other allergens like sulfonamide medications.

If a patch test turns up a reaction to “Black-Rubber Mix,” which includes paraphenylenediamine, consider whether the patient has exposure to the rubber in tires. Car mechanics may be affected by this allergy, Dr. Perryman said.

Neomycin: A drop of trouble

Allergy to the antibiotic neomycin can be triggered by exposure to gentamicin and tobramycin eye drops. Patients may believe they have an infection, Dr. Perryman said, so consider getting a culture. In some cases, an allergic reaction to neomycin may be incorrectly diagnosed as cellulitis.

Nickel: Not just a jewelry hazard

Jewelry and coins can trigger nickel allergies, but be aware that systemic nickel allergy can also trigger skin problems from a patient’s diet. It may be necessary to put patients on a low-nickel diet that avoids foods such as healthy grains, greens (especially spinach), nuts, legumes, and chocolate. “I always feel bad” putting patients on a restrictive diet, Dr. Perryman said, but it can be helpful to take 500 mg of vitamin C three times a day since it binds to nickel.

Cobalt: Watch the chocolate and coffee

Jewelry with cobalt can cause an allergic reaction. Dr. Perryman tells patients to buy an inexpensive “spot test” product online that detects whether jewelry has nickel or cobalt. Cobalt allergy can also trigger symptoms in patients exposed to “hard metal” industrial tools, cement, and masonry. Workers in the plastics and dye industries may be exposed too.

Like nickel, Dr. Perryman said, systemic cobalt allergy related to diet is also possible. The list of foods that contain higher levels of cobalt is long, and includes apricots, beans, beer, chocolate, coffee, nuts, tea, and whole-grain flour.

Dr. Perryman also mentioned several other allergens to keep in mind:

• Chromate can trigger reactions in people who wear leather shoes (the metal can be used in tanning). It can also cause problems in workers exposed to it via cement, bricks, drywall, and metal plating.
• Chromium picolinate, an over-the-counter supplement, can cause systemic dermatitis.
• Gold in jewelry can trigger an allergic reaction. Talk to patients about replating their jewelry, Dr. Perryman said.
• Rubber can trigger reactions due to exposure to rubber bands, makeup sponges, and rubber gloves (even nitrile ones). Be aware that both rubber and latex allergies may coexist and consider a blood test for latex allergy.
• Systemic balsam allergy related to an individual’s diet is possible. Tomato is an especially big villain on this front, along with citrus fruits, spices, cola, chili, and chocolate.

Dr. Perryman disclosed consulting work for IntraDerm. SDEF and this news organization are owned by the same parent company.

Cutaneous endometriosis should be considered as a diagnosis when umbilical lesions are present, especially if there is a history of pain flares during menses, according to Liza Raffi of the University of Southern California, Los Angeles, and associates.

KatarzynaBialasiewicz/Thinkstock

The report, published in the International Journal of Women’s Dermatology, detailed a case of a woman aged 41 years who presented with a 5-month history of a painful firm subcutaneous nodule in the umbilicus and flares of pain during menstrual periods. Her past history indicated a missed miscarriage (removed by dilation and curettage) and laparoscopic left salpingectomy for a ruptured ectopic pregnancy.

At presentation, the woman reported undergoing fertility treatments including subcutaneous injections of follitropin beta and choriogonadotropin alfa.

Because of the patient’s history of salpingectomy and painful menstrual periods, her physicians suspected cutaneous endometriosis. An ultrasound was performed to rule out fistula, and then a punch biopsy of the nodule was performed. The biopsy showed endometrial glands with encompassing fibrotic stroma, which was consistent with cutaneous endometriosis, likely transplanted during the laparoscopic port site entry during salpingectomy.

The patient chose to undergo surgery for excision of the nodule, declining hormonal therapy because she was undergoing fertility treatment.

“The differential diagnosis of umbilical lesions with similar presentation includes keloid, dermatofibroma, dermatofibrosarcoma protuberans, and cutaneous metastasis of cancer,” the investigators wrote. “Ultimately, patients should be referred to obstetrics & gynecology if they describe classic symptoms including pain with menses, dyspareunia, and infertility and wish to explore diagnostic and therapeutic options.”

Ms. Raffi and associates reported they had no conflicts of interest. There was no external funding.

[email protected]

SOURCE: Raffi L et al. Int J Womens Dermatol. 2019 Jul 2. doi: 10.1016/j.ijwd.2019.06.025.

Cutaneous endometriosis should be considered as a diagnosis when umbilical lesions are present, especially if there is a history of pain flares during menses, according to Liza Raffi of the University of Southern California, Los Angeles, and associates.

KatarzynaBialasiewicz/Thinkstock

The report, published in the International Journal of Women’s Dermatology, detailed a case of a woman aged 41 years who presented with a 5-month history of a painful firm subcutaneous nodule in the umbilicus and flares of pain during menstrual periods. Her past history indicated a missed miscarriage (removed by dilation and curettage) and laparoscopic left salpingectomy for a ruptured ectopic pregnancy.

At presentation, the woman reported undergoing fertility treatments including subcutaneous injections of follitropin beta and choriogonadotropin alfa.

Because of the patient’s history of salpingectomy and painful menstrual periods, her physicians suspected cutaneous endometriosis. An ultrasound was performed to rule out fistula, and then a punch biopsy of the nodule was performed. The biopsy showed endometrial glands with encompassing fibrotic stroma, which was consistent with cutaneous endometriosis, likely transplanted during the laparoscopic port site entry during salpingectomy.

The patient chose to undergo surgery for excision of the nodule, declining hormonal therapy because she was undergoing fertility treatment.

“The differential diagnosis of umbilical lesions with similar presentation includes keloid, dermatofibroma, dermatofibrosarcoma protuberans, and cutaneous metastasis of cancer,” the investigators wrote. “Ultimately, patients should be referred to obstetrics & gynecology if they describe classic symptoms including pain with menses, dyspareunia, and infertility and wish to explore diagnostic and therapeutic options.”

Ms. Raffi and associates reported they had no conflicts of interest. There was no external funding.

[email protected]

SOURCE: Raffi L et al. Int J Womens Dermatol. 2019 Jul 2. doi: 10.1016/j.ijwd.2019.06.025.

Cutaneous endometriosis should be considered as a diagnosis when umbilical lesions are present, especially if there is a history of pain flares during menses, according to Liza Raffi of the University of Southern California, Los Angeles, and associates.

KatarzynaBialasiewicz/Thinkstock

The report, published in the International Journal of Women’s Dermatology, detailed a case of a woman aged 41 years who presented with a 5-month history of a painful firm subcutaneous nodule in the umbilicus and flares of pain during menstrual periods. Her past history indicated a missed miscarriage (removed by dilation and curettage) and laparoscopic left salpingectomy for a ruptured ectopic pregnancy.

At presentation, the woman reported undergoing fertility treatments including subcutaneous injections of follitropin beta and choriogonadotropin alfa.

Because of the patient’s history of salpingectomy and painful menstrual periods, her physicians suspected cutaneous endometriosis. An ultrasound was performed to rule out fistula, and then a punch biopsy of the nodule was performed. The biopsy showed endometrial glands with encompassing fibrotic stroma, which was consistent with cutaneous endometriosis, likely transplanted during the laparoscopic port site entry during salpingectomy.

The patient chose to undergo surgery for excision of the nodule, declining hormonal therapy because she was undergoing fertility treatment.

“The differential diagnosis of umbilical lesions with similar presentation includes keloid, dermatofibroma, dermatofibrosarcoma protuberans, and cutaneous metastasis of cancer,” the investigators wrote. “Ultimately, patients should be referred to obstetrics & gynecology if they describe classic symptoms including pain with menses, dyspareunia, and infertility and wish to explore diagnostic and therapeutic options.”

Ms. Raffi and associates reported they had no conflicts of interest. There was no external funding.

[email protected]

SOURCE: Raffi L et al. Int J Womens Dermatol. 2019 Jul 2. doi: 10.1016/j.ijwd.2019.06.025.

MILAN – Among the dermatologic adverse effects of immune checkpoint inhibitor therapy, bullous disorders are relatively infrequent but associated with a high likelihood of treatment interruption, according to results of a single-center study described at the World Congress of Dermatology.

Bullous disorders were seen in about 1% of patients receiving anti-PD-1 or anti-PD-L1 therapy in the single-center retrospective review, and nearly all required systemic steroids and were associated with interruptions and discontinuations of the anti-cancer treatment, reported Jonathan Leventhal, MD, director of the oncodermatology clinic at Yale University, New Haven, Conn.

“This series highlights a very important, clinically relevant, cutaneous immune-related adverse event,” Dr. Leventhal said in an oral presentation at the congress. “These disorders manifested in most patients as bullous pemphigoid, occurred several months after starting therapy, and at a frequency rate of 1%” among all patients treated with these agents, “at least in our institution.”

The retrospective review presented by Dr. Leventhal was based on medical records of patients evaluated at Yale New Haven Hospital between 2016 and 2018. This included a total of 853 patients who received anti-PD-1/PD-L1 therapy, of whom 98 (11.5%) were evaluated at the oncodermatology clinic or inpatient consultative service.

Nine patients – five men, four women – developed bullous disorders, representing about 1% of patients treated with PD-1/PD-L1 blocking therapy, according to Dr. Leventhal. The mean age of the patients was 67.4 years. Seven of the nine patients had received PD-1 inhibitors, while two received PD-L1 inhibitors, for tumors of the lung in four cases, melanoma in two, genitourinary tumors in two, and acute myeloid leukemia in one.

“The time from rash onset to first administration of the drug was over 6 months, which is quite long compared to a lot of the other (checkpoint inhibitor–associated) toxicities that we see more commonly, which often occur in several weeks to just a few months,” Dr. Leventhal said.

Of the 853 patients in this retrospective study, 463 (54.3%) were treated with nivolumab (Opdivo) and 242 (28.4%) were treated with pembrolizumab (Keytruda), both PD-1 blockers. Of the remainder, 112 (13.1%) received the PD-L1 blockers atezolizumab (Tecentriq), 29 (3.4%) received durvalumab (Imfinzi), and 7 (0.8%) received avelumab (Bavencio), Dr. Leventhal reported.

All these patients presented with both pruritus and vesiculobullous eruptions seen mainly on the trunk and extremities, while two patients had oral ulcerations. Other presentations included urticarial-predominant bullous pemphigoid, dyshidrosiform pemphigoid, and lichenoid papules and vesicles. The diagnosis was bullous pemphigoid in seven of nine cases, Dr. Leventhal said.

The best management approach for immune-related bullous disorders would be use of high-potency topical steroids to avoid systemic steroids and avoid interruptions in checkpoint inhibitor therapy, he pointed out. However, eight of the nine patients in this retrospective series required systemic steroids due to progression of the bullae, he added.

Several notable cases were described, including one patient refractory to prednisone and omalizumab who eventually achieved control with methotrexate, a second patient who was well controlled with omalizumab monotherapy and able to resume treatment with an anti PD-1 inhibitor, and another patient who responded to prednisone and dapsone maintenance therapy.

The immunotherapy treatment for cancer was interrupted in four of nine patients due to the bullous disorders, and was permanently discontinued in another four, Dr. Leventhal said.

It’s not clear why patients receiving cancer immunotherapy treatment develop bullous pemphigoid. However, the 180-kd bullous pemphigoid antigen (BP180) is expressed in melanoma and non-small cell lung cancer, which may lead to production of antibodies against tumor cell antigens that also impact the skin, according to Dr. Leventhal.

Further studies are needed to evaluate whether immune-related bullous disorders have any prognostic significance in cancer patients, he added.

Dr. Leventhal reported that he had no relevant disclosures.

MILAN – Among the dermatologic adverse effects of immune checkpoint inhibitor therapy, bullous disorders are relatively infrequent but associated with a high likelihood of treatment interruption, according to results of a single-center study described at the World Congress of Dermatology.

Bullous disorders were seen in about 1% of patients receiving anti-PD-1 or anti-PD-L1 therapy in the single-center retrospective review, and nearly all required systemic steroids and were associated with interruptions and discontinuations of the anti-cancer treatment, reported Jonathan Leventhal, MD, director of the oncodermatology clinic at Yale University, New Haven, Conn.

“This series highlights a very important, clinically relevant, cutaneous immune-related adverse event,” Dr. Leventhal said in an oral presentation at the congress. “These disorders manifested in most patients as bullous pemphigoid, occurred several months after starting therapy, and at a frequency rate of 1%” among all patients treated with these agents, “at least in our institution.”

The retrospective review presented by Dr. Leventhal was based on medical records of patients evaluated at Yale New Haven Hospital between 2016 and 2018. This included a total of 853 patients who received anti-PD-1/PD-L1 therapy, of whom 98 (11.5%) were evaluated at the oncodermatology clinic or inpatient consultative service.

Nine patients – five men, four women – developed bullous disorders, representing about 1% of patients treated with PD-1/PD-L1 blocking therapy, according to Dr. Leventhal. The mean age of the patients was 67.4 years. Seven of the nine patients had received PD-1 inhibitors, while two received PD-L1 inhibitors, for tumors of the lung in four cases, melanoma in two, genitourinary tumors in two, and acute myeloid leukemia in one.

“The time from rash onset to first administration of the drug was over 6 months, which is quite long compared to a lot of the other (checkpoint inhibitor–associated) toxicities that we see more commonly, which often occur in several weeks to just a few months,” Dr. Leventhal said.

Of the 853 patients in this retrospective study, 463 (54.3%) were treated with nivolumab (Opdivo) and 242 (28.4%) were treated with pembrolizumab (Keytruda), both PD-1 blockers. Of the remainder, 112 (13.1%) received the PD-L1 blockers atezolizumab (Tecentriq), 29 (3.4%) received durvalumab (Imfinzi), and 7 (0.8%) received avelumab (Bavencio), Dr. Leventhal reported.

All these patients presented with both pruritus and vesiculobullous eruptions seen mainly on the trunk and extremities, while two patients had oral ulcerations. Other presentations included urticarial-predominant bullous pemphigoid, dyshidrosiform pemphigoid, and lichenoid papules and vesicles. The diagnosis was bullous pemphigoid in seven of nine cases, Dr. Leventhal said.

The best management approach for immune-related bullous disorders would be use of high-potency topical steroids to avoid systemic steroids and avoid interruptions in checkpoint inhibitor therapy, he pointed out. However, eight of the nine patients in this retrospective series required systemic steroids due to progression of the bullae, he added.

Several notable cases were described, including one patient refractory to prednisone and omalizumab who eventually achieved control with methotrexate, a second patient who was well controlled with omalizumab monotherapy and able to resume treatment with an anti PD-1 inhibitor, and another patient who responded to prednisone and dapsone maintenance therapy.

The immunotherapy treatment for cancer was interrupted in four of nine patients due to the bullous disorders, and was permanently discontinued in another four, Dr. Leventhal said.

It’s not clear why patients receiving cancer immunotherapy treatment develop bullous pemphigoid. However, the 180-kd bullous pemphigoid antigen (BP180) is expressed in melanoma and non-small cell lung cancer, which may lead to production of antibodies against tumor cell antigens that also impact the skin, according to Dr. Leventhal.

Further studies are needed to evaluate whether immune-related bullous disorders have any prognostic significance in cancer patients, he added.

Dr. Leventhal reported that he had no relevant disclosures.

MILAN – Among the dermatologic adverse effects of immune checkpoint inhibitor therapy, bullous disorders are relatively infrequent but associated with a high likelihood of treatment interruption, according to results of a single-center study described at the World Congress of Dermatology.

Bullous disorders were seen in about 1% of patients receiving anti-PD-1 or anti-PD-L1 therapy in the single-center retrospective review, and nearly all required systemic steroids and were associated with interruptions and discontinuations of the anti-cancer treatment, reported Jonathan Leventhal, MD, director of the oncodermatology clinic at Yale University, New Haven, Conn.

“This series highlights a very important, clinically relevant, cutaneous immune-related adverse event,” Dr. Leventhal said in an oral presentation at the congress. “These disorders manifested in most patients as bullous pemphigoid, occurred several months after starting therapy, and at a frequency rate of 1%” among all patients treated with these agents, “at least in our institution.”

The retrospective review presented by Dr. Leventhal was based on medical records of patients evaluated at Yale New Haven Hospital between 2016 and 2018. This included a total of 853 patients who received anti-PD-1/PD-L1 therapy, of whom 98 (11.5%) were evaluated at the oncodermatology clinic or inpatient consultative service.

Nine patients – five men, four women – developed bullous disorders, representing about 1% of patients treated with PD-1/PD-L1 blocking therapy, according to Dr. Leventhal. The mean age of the patients was 67.4 years. Seven of the nine patients had received PD-1 inhibitors, while two received PD-L1 inhibitors, for tumors of the lung in four cases, melanoma in two, genitourinary tumors in two, and acute myeloid leukemia in one.

“The time from rash onset to first administration of the drug was over 6 months, which is quite long compared to a lot of the other (checkpoint inhibitor–associated) toxicities that we see more commonly, which often occur in several weeks to just a few months,” Dr. Leventhal said.

Of the 853 patients in this retrospective study, 463 (54.3%) were treated with nivolumab (Opdivo) and 242 (28.4%) were treated with pembrolizumab (Keytruda), both PD-1 blockers. Of the remainder, 112 (13.1%) received the PD-L1 blockers atezolizumab (Tecentriq), 29 (3.4%) received durvalumab (Imfinzi), and 7 (0.8%) received avelumab (Bavencio), Dr. Leventhal reported.

All these patients presented with both pruritus and vesiculobullous eruptions seen mainly on the trunk and extremities, while two patients had oral ulcerations. Other presentations included urticarial-predominant bullous pemphigoid, dyshidrosiform pemphigoid, and lichenoid papules and vesicles. The diagnosis was bullous pemphigoid in seven of nine cases, Dr. Leventhal said.

The best management approach for immune-related bullous disorders would be use of high-potency topical steroids to avoid systemic steroids and avoid interruptions in checkpoint inhibitor therapy, he pointed out. However, eight of the nine patients in this retrospective series required systemic steroids due to progression of the bullae, he added.

Several notable cases were described, including one patient refractory to prednisone and omalizumab who eventually achieved control with methotrexate, a second patient who was well controlled with omalizumab monotherapy and able to resume treatment with an anti PD-1 inhibitor, and another patient who responded to prednisone and dapsone maintenance therapy.

The immunotherapy treatment for cancer was interrupted in four of nine patients due to the bullous disorders, and was permanently discontinued in another four, Dr. Leventhal said.

It’s not clear why patients receiving cancer immunotherapy treatment develop bullous pemphigoid. However, the 180-kd bullous pemphigoid antigen (BP180) is expressed in melanoma and non-small cell lung cancer, which may lead to production of antibodies against tumor cell antigens that also impact the skin, according to Dr. Leventhal.

Further studies are needed to evaluate whether immune-related bullous disorders have any prognostic significance in cancer patients, he added.

Dr. Leventhal reported that he had no relevant disclosures.

MILAN – Hydroxychloroquine sulfate may be an effective and relatively safe treatment option for moderate to severe oral lichen planus, an investigator reported at the World Congress of Dermatology.

Andrew Bowser/MDedge News

In a small retrospective study, 85% of patients treated with the oral antimalarial agent had marked improvement or full remission, according to Ziyad Khamaysi, MD, a dermatologist at Rambam Health Care Campus, Haifa, Israel. Adverse effects leading to discontinuation occurred in a minority of patients and included elevated kidney function tests, hyperpigmentation, and an abnormal eye exam, he said.

“It may be a useful and convenient alternative treatment either as a monotherapy or where a rapid symptomatic relief during periods of exacerbations is needed,” he said in an oral presentation at the meeting.

A variety of medications have been used for palliation of oral lichen planus, including corticosteroids, cyclosporine, calcineurin inhibitors, retinoids, and biologics, but few have been evaluated in larger series of patients, he pointed out.

In the retrospective, nonrandomized study, 15 women and 6 men with erosive, recalcitrant oral lichen planus were treated with hydroxychloroquine (Plaquenil) at a dose of 200 mg/day, which was increased to 400 mg/day at one month. The mean age of the patients was 55 years.

In one patient, treatment was stopped after a month because of side effects, Dr. Khamaysi said. Among the remaining patients, 5 (25%) had a complete remission, while 12 (60%) had moderate to marked improvement, and 3 (15%) had no improvement, he said. In the patients who did respond, improvement was noted within 2-4 months of treatment initiation, he added. “Hydroxychloroquine kept the disease under control, with either full remission or marked improvement as long as the patients took it.”

Treatment appeared to be more effective in male patients and those under age 65 years, the investigator commented.

These data corroborate the findings of a smaller study evaluating hydroxychloroquine for oral lichen planus, published in 1993, according to Dr. Khamaysi. In that report, 9 of 10 patients had an “excellent” response to treatment, according to the investigator (J Am Acad Dermatol. 1993 Apr;28[4]:609-12).

Of the 10 patients in that study, 6 had erosions at the start of treatment, and 3 of these patients had complete healing with 3-6 months of therapy, and the other 3 had reepithelialization and at least a 50% reduction in lesion size, according to the report.

Dr. Khamaysi had no disclosures relevant to his presentation.

MILAN – Hydroxychloroquine sulfate may be an effective and relatively safe treatment option for moderate to severe oral lichen planus, an investigator reported at the World Congress of Dermatology.

Andrew Bowser/MDedge News

In a small retrospective study, 85% of patients treated with the oral antimalarial agent had marked improvement or full remission, according to Ziyad Khamaysi, MD, a dermatologist at Rambam Health Care Campus, Haifa, Israel. Adverse effects leading to discontinuation occurred in a minority of patients and included elevated kidney function tests, hyperpigmentation, and an abnormal eye exam, he said.

“It may be a useful and convenient alternative treatment either as a monotherapy or where a rapid symptomatic relief during periods of exacerbations is needed,” he said in an oral presentation at the meeting.

A variety of medications have been used for palliation of oral lichen planus, including corticosteroids, cyclosporine, calcineurin inhibitors, retinoids, and biologics, but few have been evaluated in larger series of patients, he pointed out.

In the retrospective, nonrandomized study, 15 women and 6 men with erosive, recalcitrant oral lichen planus were treated with hydroxychloroquine (Plaquenil) at a dose of 200 mg/day, which was increased to 400 mg/day at one month. The mean age of the patients was 55 years.

In one patient, treatment was stopped after a month because of side effects, Dr. Khamaysi said. Among the remaining patients, 5 (25%) had a complete remission, while 12 (60%) had moderate to marked improvement, and 3 (15%) had no improvement, he said. In the patients who did respond, improvement was noted within 2-4 months of treatment initiation, he added. “Hydroxychloroquine kept the disease under control, with either full remission or marked improvement as long as the patients took it.”

Treatment appeared to be more effective in male patients and those under age 65 years, the investigator commented.

These data corroborate the findings of a smaller study evaluating hydroxychloroquine for oral lichen planus, published in 1993, according to Dr. Khamaysi. In that report, 9 of 10 patients had an “excellent” response to treatment, according to the investigator (J Am Acad Dermatol. 1993 Apr;28[4]:609-12).

Of the 10 patients in that study, 6 had erosions at the start of treatment, and 3 of these patients had complete healing with 3-6 months of therapy, and the other 3 had reepithelialization and at least a 50% reduction in lesion size, according to the report.

Dr. Khamaysi had no disclosures relevant to his presentation.

MILAN – Hydroxychloroquine sulfate may be an effective and relatively safe treatment option for moderate to severe oral lichen planus, an investigator reported at the World Congress of Dermatology.

Andrew Bowser/MDedge News

In a small retrospective study, 85% of patients treated with the oral antimalarial agent had marked improvement or full remission, according to Ziyad Khamaysi, MD, a dermatologist at Rambam Health Care Campus, Haifa, Israel. Adverse effects leading to discontinuation occurred in a minority of patients and included elevated kidney function tests, hyperpigmentation, and an abnormal eye exam, he said.

“It may be a useful and convenient alternative treatment either as a monotherapy or where a rapid symptomatic relief during periods of exacerbations is needed,” he said in an oral presentation at the meeting.

A variety of medications have been used for palliation of oral lichen planus, including corticosteroids, cyclosporine, calcineurin inhibitors, retinoids, and biologics, but few have been evaluated in larger series of patients, he pointed out.

In the retrospective, nonrandomized study, 15 women and 6 men with erosive, recalcitrant oral lichen planus were treated with hydroxychloroquine (Plaquenil) at a dose of 200 mg/day, which was increased to 400 mg/day at one month. The mean age of the patients was 55 years.

In one patient, treatment was stopped after a month because of side effects, Dr. Khamaysi said. Among the remaining patients, 5 (25%) had a complete remission, while 12 (60%) had moderate to marked improvement, and 3 (15%) had no improvement, he said. In the patients who did respond, improvement was noted within 2-4 months of treatment initiation, he added. “Hydroxychloroquine kept the disease under control, with either full remission or marked improvement as long as the patients took it.”

Treatment appeared to be more effective in male patients and those under age 65 years, the investigator commented.

These data corroborate the findings of a smaller study evaluating hydroxychloroquine for oral lichen planus, published in 1993, according to Dr. Khamaysi. In that report, 9 of 10 patients had an “excellent” response to treatment, according to the investigator (J Am Acad Dermatol. 1993 Apr;28[4]:609-12).

Of the 10 patients in that study, 6 had erosions at the start of treatment, and 3 of these patients had complete healing with 3-6 months of therapy, and the other 3 had reepithelialization and at least a 50% reduction in lesion size, according to the report.

Dr. Khamaysi had no disclosures relevant to his presentation.