Quantitative liver function was assessed before and after therapy in 4 patients with porphyria cutanea tarda. Three patients underwent phlebotomy, which produced clinical and biochemical remission. Concomitantly, functional liver cell mass, as measured by galactose elimination capacity, normalized. In the last patient, treated with chloroquine, liver function did not improve during therapy. The aminopyrine breath test, a measure of microsomal function, was inconclusive. These results show that decreased hepatic function in porphyria cutanea tarda is reversible and emphasize the potential role of iron accumulation in the pathogenesis of hepatic dysfunction in porphyria cutanea tarda.