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A. Bourlond, Ch. Pirard, Department of Dermatology, Faculty of Medicine, Catholic University of Louvain, 52, avenue E. Mounier (Tour Vésale), B–1200 Brussels (Belgium) We were interested to read the paper of Tegelberg-Stassen et al. [1], and we adhere without restriction to their conclusions. As a matter of fact, at the Department of Dermatology, we have treated all our cases of toxic epidermal necrolysis (excluded of course the cases of staphylococcal scalded skin syndrome) in the same way, i.e. reserved barrier nursing, control of fluid balance, timely antibiotics and overall high doses of corticosteroids. From our experience, we would like to add some comments: High doses of corticosteroid must be resorted to as soon as possible in order to control the intensity of the eruption. The treatment does not prevent the shedding of the epidermis already severely aggressed, but it minimizes the oozing. Improvement must be achieved in a few days only; if delayed for more than 7 days, prognosis gets much worse, and infections multiply unavoidably. The comfort of patients and the rapidity of recovery are definitively enhanced. 238 Letters to the Editor Reference In Reply 1 Tegelberg-Stassen MJAM, Vloten WA van, Baart de la Faille H Management of nonstaphylococcal toxic epidermal necrolysis Follow-up study of 16 case histories. Dermatologica 1990; 180 124-129. Chronic Vulvar Purpura Sir, In a recent issue of Dermatologica, Kato et al. [1] described a chronic vulvar purpura in a 56year-old Japanese woman. The purpuric lesion was persistent during a follow-up time of 8 years and has been related by the authors to an abdominal ptosis. A cause of persistent purpuric lesions with hemosiderin deposits in the vestibulum vaginae is the plasma cell vulvitis of Zoon (vulvitis cir-cumscripta plasmacellularis). This circumscribed chronic vulvitis is usually located around the posterior circumference of the introitus vaginae or on the inner side of the labia minora; most often it presents as a dark red colored smooth lesion or a slightly erosive inflammatory erythroplasia [2]. The main histologic hallmarks are: atrophy of the epithelium, dense lymphoplasmocytic infiltration of the upper corium with invasion of the lower epithelial layers and extravasation of erythrocytes leading to a less or more dense deposition of hemosiderin [3]. Persistent lesions heavily laden with hemosiderin look clinically dark pigmented. In histologic specimens of older