Dramatic resolution of skin lesions associated with porphyria cutanea tarda after interferon-α therapy in a case of chronic hepatitis C

Porphyria cutanea tarda (PCT) has an estimated prevalence of 1 per 25,000 in North America (1). This disease results from a deficiency of hepatic uroporphyrinogen decarboxylase, either acquired or inherited as an autosomal dominant trait. A strong association between PCT and hepatitis C virus has been recently reported (2-6). Hepatitis C virus (HCV) is thought to be responsible for all hepatic complications in these patients, including cirrhosis and hepatocellular carcinoma (2, 5). HCV infection usually occurs before cutaneous manifestation of porphyria (5). The mechanism by which HCV triggers the development of PCT is still unknown. Interferon-α can improve biochemical, virological, and histological parameters in some patients with chronic hepatitis C (7-9). Recently interferon-α therapy has been shown to induce remission in three patients with porphyria cutanea tarda who simultaneously had chronic hepatitis C (10-12). We describe a patient in whom such a syndrome remitted after six months of therapy with interferon-α without any significant decrease in HCV RNA level.