Griseofulvin ineffective in balanitis circumscripta plasmacellularis

Griseofulvin ineffective in balanitis circumscripta plasmacellularis

CORRESPONDENCE Griseofulvin circumscripta REFERENCE ineffective in balanitis plasmacellularis To the Editor: We read with great interest the brief ...

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CORRESPONDENCE Griseofulvin circumscripta

REFERENCE

ineffective in balanitis plasmacellularis

To the Editor: We read with great interest the brief communication by Tamaki et al. entitled “Treatment of Plasma Cell Cheilitis with Griseofulvin” (J AM ACAD DERMATOL 1994;30:789-90). Because balanitis circumscripta plasmacellularis (Zoon’s erythroplasia) shares at least some histologic features with plasma cell cheilitis and its treatment often is similarly disappointing, we tried griseofulvin in our next two patients with histologically confiied plasma cell balanitis. Although 500 mg of griseofulvin was administered during a 6-week period, improvement was not seen in any of our patients. Thus in contrast to plasma cell cheilitis, in our experience griseofulvin did not help in balanitis circumscripta plasmacellularis. Andreas W. Gerbig, MD Thomas Hunziker, MD Department of Dermatology University of Beme CH-3010 Beme, Switzerland

1. Humphreys F, Cox NH. Thiabendazole-induced erythema multiforme with lesions around melanocytic nevi. Br J Dermatol 1988;118:855-6.

Reply To the Editor: I thank Dr. Cox for bringing to my attention his previously reported case of erythema multiforme in which some lesions encircled melanocytic nevi.l I only wish that reports such as these were as easy to retrieve from the electronic memory of medical literature databases as they are from the biologic memory of published authors. Robert J. Pariser, MD Division of Dermatology Eastern Virginia Medical School Nor@4 Virginia REFERENCE 1. Humphreys F, Cox NH. Thiabendazole-induced erythema mukiforme with lesions around melanocytic nevi. Br J Dermatol 1988;118:855-6.

“Nevocentric” unique

erythema

multiforme:

Not

To the Editor: Pariser reports an interesting case of erythema multiforme and concludes that this appears to be unique (J AM ACAD DERMATOL 1994;3 1:49 l-2). Few things in medicine are. We described this phenomenon in 1988’ and one of us (N. H. C.) has subsequently seen a patient with a similar condition. As in Pariser’s report, the erythema multiforme does not affect all nevi and is not confined to clinically apparent nevi. Presumably this pattern is not restricted to any specific cause of erythema multiforme, as Pariser’s case was caused by herpes simplex, but ours was drug induced (our unreported case occurred in a patient with preceding pharyngitis and malaise). We hypothesize that it may occur because of abnormal vasculature in nevi, which exaggerates deposition of immune complexes. Neil H. Cox Department of Dermatology Cumberland Injirmary Carlisle, CA2 7HY, UK Frances Humphreys Department of Dermatology Royal Injirmary Edinburgh, UK

Prevalence of autoimmune diseases in the family members of patients with pemphigus vulgaris To the Editor: This paper (Firooz et al. J AM ACAD DERMATOL 1994;3 1:434-7) as published neglects to provide cmcial information for its readers. The “Patients and Methods” section does not provide sufficient information to document and understand the methodology of this large study. It is not specified how patients with pemphigus were selected (Were these outpatients selected from one center? Were they randomly selected from a universal regional regisb-y?). The methodology of the way in which control subjects were selected was not specified (Were they selected from the New England population as a whole? Were they patients with other dermatologic diseasesattending the same clinic?). The number of relatives of the patients who were not studied and the response rate for the control subject were not specified. The number of relatives with diseasesnot confirmed by the treating physician was not specified. It would be highly fortuitous for

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