tic and Statistical Manual of Mental Disorders. 3rd ed revised. Washington, DC: American Psychiatric Association; 1987:346-347. 3. Koblenzer CS. Psychocutaneous Disease. Orlando, Fla: Grune & Stratton Inc; 1987:103-104. 4. Hartman EL. Sleep. In: Kaplan HL, Sadock BJ, eds. Comprehensive Textbook of Psychiatry. 4th ed. Baltimore, Md: Williams & Wilkins; 1985:56\x=req-\ 57.
Psoriatic Alopecia To the Editor.\p=m-\Since my article on psoriatic alopecia1 could be ambiguous unless read with care, I write to correct its misquotation by Headington et al.2 First, I found hair loss in patches of psoriasis on the trunk and limbs. Second, I observed three types of psoriatic alopecia on the scalp: (1) The most common was hair loss confined to the lesions, which was due to dystrophic anagen follicles that produced fine hair. I published the evidence for this, with photographs of dystrophic follicles and the frequency distribution of hair thickness in scalp lesions. (2) I found an acute hair fall that was not confined to the lesions and that was a telogen effluvium occurring mostly with severe psoriasis. (3) Finally, and surprisingly, I also found a destructive alopecia, although this was the least common. Biopsy showed paucity of follicles and perifollicular inflammation. I therefore wrote that "the hair loss shows every appearance of permanency although neither the patients nor I are likely to live long enough to prove this." Although the first part of that sentence remains correct, one of the patients has lived long enough to disprove the second part, because, despite the appearance of destructive alopecia, regrowth of hair was reported 10 years later (rather like the regrowth sometimes seen in children with an apparently destructive alopecia following a kerion). Headington et al say "no attempt was made to clinically identify or grade alopecia" in their patients. This is unfor¬ tunate because, although their limited studies do confirm those I made earlier, their failure to touch clinical base precludes any advance in the problem. A fuller study of the various types of psoriatic alopecia remains as desirable now as it did when I defined them. Sam Shuster, FRCP University Department of Dermatology The Royal Victoria Infirmary Newcastle Upon Tyne NE14LP, England 1. Shuster S. Psoriatic alopecia. Br J Dermatol. 1972;87:73-77. 2. Headington JT, Gupta AK, Goldfarb MT, et al. A morphometric and histological study of the scalp in psoriasis. Arch Dermatol. 1989;125:639-642.
ported use of cyclosporine for treatment of dermatological disease is increasing in frequency, and favorable responses have been observed in the treatment of psoriasis, Beh\l=c;\et's disease, bullous pemphigoid, pemphigus vulgaris, dermatomyositis, polymyositis, ichthyosis, and several other cutaneous disorders.1 We
report on the successful treatment of a patient with severe bullous erythema multiforme that had previously responded only partially to high dosages of systemic corticosteroids. Report of a Case.\p=m-\A23-year-old white woman was referred to dermatology service in August 1987 for evaluation of a bullous eruption of 3 years' duration. The patient was in good health until 1984 when, approximately 1 week after a dental procedure, she developed a generalized eruption and oral ulcerations. The initial eruption cleared after an intramuscular dose of penicillin. Four months later the patient developed continuing crops of lesions primarily on her arms, legs, and flanks consisting of small papules that would evolve into plaques with central bullae. These lesions would then crust over and heal in 1 to 2 weeks' time. The patient also noted oral mucosal ulcérations during the cutaneous outbreaks. Her dis¬ ease-free intervals shortened, and, over the last 2 years, she was rarely without cutaneous lesions. The patient denied prior herpes or other virus infection, chronic bacterial infections, medication use, symptoms, or allergies. Her initial skin biopsy specimen was interpreted as erythema multiforme, and she was treated with a tapered dosage of prednisone (60 mg/d to 10 mg/d). This partially cleared her lesions. The lesions recurred again in 2 to 3 weeks' time. She developed a severe flare of her disease requiring hospitalization, and was then referred to our dermatology service after a regimen of 80 mg/d of prednisone our
failed to clear her skin. On our initial examination her skin had le¬ sions in various stages of development. The smallest primary lesion was a 4-mm pink papule that matured into a plaque by enlarging centrifugally while developing a central bulla (Figure). Multiple annular plaques ranging in size from 2 to 20 cm in diameter were distributed on her lower arms, legs, flanks, and lumbosacral region. Dusky pink-to-gray flaccid bullae were present in the center of al¬ most all lesions. The outer border of these plaques showed the brightest pink-to-red coloration. No atrophy or scarring was present; however, milia and postinflammatory pigmentation were evident in areas of previous lesions. Examination of her oral cav¬ ity revealed small erosions on the buccal mucosa. Conjunctival and
genital mucosa were spared. Extensive laboratory analysis was within normal limits. Chest and sinus roentgenograms were normal. Skin biopsy specimens were obtained for routine, immunofluorescent, and electron micro¬ scopic processing and evaluation. All findings were consistent with the diagnosis of erythema multiforme.
Cyclosporine Therapy for Bullous Erythema Multiforme To the
Editor.\p=m-\Immunosuppressivetherapy with cyclosporine introduced in the 1970s dramatically improved the survival of kidney, liver, and heart transplants. The re-
Annular plaque with central bullae and erosions tient with cyclosporine.
Downloaded From: http://archderm.jamanetwork.com/ by a Western University User on 06/10/2015
prior to treatment of pa¬
Psoriatic Alopecia To the Editor.\p=m-\Since my article on psoriatic alopecia1 could be ambiguous unless read with care, I write to correct its misquotation by Headington et al.2 First, I found hair loss in patches of psoriasis on the trunk and limbs. Second, I observed three types of psoriatic alopecia on the scalp: (1) The most common was hair loss confined to the lesions, which was due to dystrophic anagen follicles that produced fine hair. I published the evidence for this, with photographs of dystrophic follicles and the frequency distribution of hair thickness in scalp lesions. (2) I found an acute hair fall that was not confined to the lesions and that was a telogen effluvium occurring mostly with severe psoriasis. (3) Finally, and surprisingly, I also found a destructive alopecia, although this was the least common. Biopsy showed paucity of follicles and perifollicular inflammation. I therefore wrote that "the hair loss shows every appearance of permanency although neither the patients nor I are likely to live long enough to prove this." Although the first part of that sentence remains correct, one of the patients has lived long enough to disprove the second part, because, despite the appearance of destructive alopecia, regrowth of hair was reported 10 years later (rather like the regrowth sometimes seen in children with an apparently destructive alopecia following a kerion). Headington et al say "no attempt was made to clinically identify or grade alopecia" in their patients. This is unfor¬ tunate because, although their limited studies do confirm those I made earlier, their failure to touch clinical base precludes any advance in the problem. A fuller study of the various types of psoriatic alopecia remains as desirable now as it did when I defined them. Sam Shuster, FRCP University Department of Dermatology The Royal Victoria Infirmary Newcastle Upon Tyne NE14LP, England 1. Shuster S. Psoriatic alopecia. Br J Dermatol. 1972;87:73-77. 2. Headington JT, Gupta AK, Goldfarb MT, et al. A morphometric and histological study of the scalp in psoriasis. Arch Dermatol. 1989;125:639-642.
ported use of cyclosporine for treatment of dermatological disease is increasing in frequency, and favorable responses have been observed in the treatment of psoriasis, Beh\l=c;\et's disease, bullous pemphigoid, pemphigus vulgaris, dermatomyositis, polymyositis, ichthyosis, and several other cutaneous disorders.1 We
report on the successful treatment of a patient with severe bullous erythema multiforme that had previously responded only partially to high dosages of systemic corticosteroids. Report of a Case.\p=m-\A23-year-old white woman was referred to dermatology service in August 1987 for evaluation of a bullous eruption of 3 years' duration. The patient was in good health until 1984 when, approximately 1 week after a dental procedure, she developed a generalized eruption and oral ulcerations. The initial eruption cleared after an intramuscular dose of penicillin. Four months later the patient developed continuing crops of lesions primarily on her arms, legs, and flanks consisting of small papules that would evolve into plaques with central bullae. These lesions would then crust over and heal in 1 to 2 weeks' time. The patient also noted oral mucosal ulcérations during the cutaneous outbreaks. Her dis¬ ease-free intervals shortened, and, over the last 2 years, she was rarely without cutaneous lesions. The patient denied prior herpes or other virus infection, chronic bacterial infections, medication use, symptoms, or allergies. Her initial skin biopsy specimen was interpreted as erythema multiforme, and she was treated with a tapered dosage of prednisone (60 mg/d to 10 mg/d). This partially cleared her lesions. The lesions recurred again in 2 to 3 weeks' time. She developed a severe flare of her disease requiring hospitalization, and was then referred to our dermatology service after a regimen of 80 mg/d of prednisone our
failed to clear her skin. On our initial examination her skin had le¬ sions in various stages of development. The smallest primary lesion was a 4-mm pink papule that matured into a plaque by enlarging centrifugally while developing a central bulla (Figure). Multiple annular plaques ranging in size from 2 to 20 cm in diameter were distributed on her lower arms, legs, flanks, and lumbosacral region. Dusky pink-to-gray flaccid bullae were present in the center of al¬ most all lesions. The outer border of these plaques showed the brightest pink-to-red coloration. No atrophy or scarring was present; however, milia and postinflammatory pigmentation were evident in areas of previous lesions. Examination of her oral cav¬ ity revealed small erosions on the buccal mucosa. Conjunctival and
genital mucosa were spared. Extensive laboratory analysis was within normal limits. Chest and sinus roentgenograms were normal. Skin biopsy specimens were obtained for routine, immunofluorescent, and electron micro¬ scopic processing and evaluation. All findings were consistent with the diagnosis of erythema multiforme.
Cyclosporine Therapy for Bullous Erythema Multiforme To the
Editor.\p=m-\Immunosuppressivetherapy with cyclosporine introduced in the 1970s dramatically improved the survival of kidney, liver, and heart transplants. The re-
Annular plaque with central bullae and erosions tient with cyclosporine.
Downloaded From: http://archderm.jamanetwork.com/ by a Western University User on 06/10/2015
prior to treatment of pa¬
