Porphyria cutanea tarda appears in its familial form with an autosomal dominant transmission of the defect of uroporphyrinogen decarboxylase in all tissues of the body, or in its sporadic form with the defect in the liver only, in our population with a prevalence of 1:15.000. Etiologically there participate in its appearance the iron overload (often caused by a mutation of the HFE gene of hereditary hemochromatosis), chronic alcohol intoxication, long-term estrogen therapy, and hepatitis C infection. Reliable treatments are serial phlebotomies and oral therapy with low doses of quinoline antimalarial drugs, or the combination of both. The report speaks of factors and conditions for the appearance of the disorder and of the mechanisms of the therapeutic action of both the treatments. It also presents a draft of a rational scheme for the optimal therapy of PCT.

        Key words: porphyria cutanea tarda – iron overload – uroporphyrinogen decarboxylase – HFE gene mutation – hepatitis C – alcohol – estrogens – venepuncture – antimalarial drugs