To the Editor.—
Porphyria cutanea tarda results from deficient activity of uroporphyrinogen decarboxylase in liver. Cutaneous manifestations of porphyria cutanea tarda are variable and include skin fragility, vesicles, bullae, hypertrichosis, hyperpigmentation, and sclerodermoid changes found frequently on sun-exposed areas. Alcohol, estrogens, and increased hepatic iron stores are major contributing factors. Various hepatic abnormalities, commonly siderosis, accompany porphyria cutanea tarda. A characteristic profile of excessive urinary porphyrin metabolites is seen.Porphyria cutanea tarda has been reported to presage development of acquired immunodeficiency syndrome in five previous case reports.1-3 Two additional cases are presented here, and the literature is reviewed.
Report of Cases.—Case 1.—
A 42-year-old homosexual businessman presented with Pneumocystis carinii pneumonia. Five months earlier he had tested positive for antibody to human immunodeficiency virus and had developed skin hyperpigmentation and a vesicular rash on the dorsa of his hands. His history was devoid of alcoholism, familial