Abstract
Human porphyrias are rare inborn disorders of porphyrin metabolism. Porphyria cutanea tarda is one such disorder, which may occur spontaneously after the ingestion of drugs and alcohol. This is the "constitutional" type and is associated with a deficiency of uroporphyrinogen decarboxylase in the liver. This constitutional type must be differentiated from the "acquired" type, which occurred in hundreds of people poisoned by hexachlorobenzene in Turkey. Morphological changes observed in the livers of animals and humans vary greatly. Porphyria cutanea tarda may be associated with very little liver pathology or with very pronounced changes, depending on the agent causing the porphyria. Usually, the liver has an increased iron load, and mitochondria contain a crystalline material.
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