Abstract
Three patients with porphyria cutanea tarda and evidence of liver disease on biopsy were treated with chloroquine in doses of 0.5 gm daily for eight days. In each instance an initial febrile episode was followed by evidences of hepatocellular injury, which soon reverted to pretreatment status. Associated with this was an increased excretion of delta-aminolevulinic acid, uroporphyrin, coproporphyrin and protoporphyrin in the urine and feces. In two of three patients the proportion of type I porphyrin isomers was not influenced by therapy. Porphyrin excretion became normal following therapy, and the patients experienced prolonged remissions, free of skin manifestations. These findings for the most part support the thesis that the responses are secondary to a reduction in hepatic porphyrins rather than interference of chloroquine in the porphyrin biosynthetic pathway. In one patient transient ascites and a hemolytic episode developed following administration of chloroquine.
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