An acquired (“symptomatic”) chronic hepatic porphyria (CHP) is described, which develops secondarily following damage to the liver tissue and is characterized by the absence of clinical symptoms. It can be differentiated biochemically from latent porphyria cutanea tarda (PCT) by a lower total porphyrin excretion (0.18–0.64 mg/l) and a relatively increased excretion of corproporphyrin (C) (18–55 %) in urine. In liver biopsies from 4 patients with chronic aggressive hepatitis (CAH) and 2 patients with fibrosis of the liver, uro-(U) and heptacarboxylic porphyrin (VII) were found to have accumulated in the liver, just as in PCT. The elevated excretion of porphyrins with the urine involved all components, especially U, VII, and C. Independently of an inversion of the C/U ratio, VII increases in accordance with the rule of the biochemical PCT index: VII/C increases (U+VII)/C by 18–37 %. U was found to predominate in 3 patients with CAH; in fibrosis, however, larger amounts of C were present in the urine, although the liver stored U and VII. On the basis of the relative distributions of the individual urinary porphyrins, two types of CHP are distinguished: Type A with C/U>1 (in fibrosis), and type B, in which C/U<1 (in CAH). Apparently, enhanced renal excretion of U in type B of CHP is indicative of an active hepatic process. The concentrations of U and VII in the liver are greater in type B than in type A. CHP can remain stable, or undergo remission: type A can develop into type B; PCT can arise from type B with an increase of U plus VII. The key to the biochemical pathogenesis is probably to be found in the induction ofδ-aminolevulinic acid synthetase and, in addition, a reduced decarboxylation of heptacarboxylic porphyrinogen.