The porphyrias are a heterogeneous group of inherited or acquired disorders. Each of the individual porphyrias is a distinct clinical condition resulting from an abnormality of a specific heme synthesis enzyme. Porphyria cutanea tarda (PCT) is biochemically characterized by the reduced activity of uroporphyrinogen decarboxylase. In the familial form of PCT, both erythrocyte and hepatocyte enzyme activity is deficient, whereas in its acquired form, usually only the liver cells have diminished enzyme activity. Patients with PCT typically develop cutaneous lesions secondary to chronic or delayed photosensitivity. Increased skin fragility, bruising, vesicles, bullae, hyperpigmentation, and hypertrichosis are early features, whereas mild to mutilating scarring, milia, and sclerodermoid changes are late manifestations of PCT-associated sensitivity.1
A 48-year-old, homosexual, human immunodeficiency virus (HIV)—seropositive man was evaluated for blisters on his hands and forehead. Prior acquired immunodeficiency syndrome (AIDS)—related infection included oral candidiasis; he was currently receiving zidovudine, trimethoprim and sulfamethoxazole, and nystatin.