Impaired iron metabolism in patients with porphyria cutanea tarda (PCT) participates in the development of its sporadic form and manifestation of its familial form via partial inhibition of liver uroporphyrinogen decarboxylase. The cause of iron accumulation is sometimes infection with the HCV virus, in other instances chronic alcoholism, frequently mutation of the C282Y gene of hereditary haemochromatosis (HFE). To elucidate conditions of iron metabolism the authors made an investigation in three groups of PCT patient: the first one with a HFE mutation, the second one without it but with the presence of anti-HCV antibodies and the third one without mutation of the gene and without antibodies against HCV. In porphyric patients on average normal sideraemia was recorded which however was significantly higher in subjects with a heterozygous gene mutation (p=0.05). The serum ferritin values were markedly higher than normal in all PCT groups but the results did not differ significantly when mutually compared. The same applied also to transferrin saturation.The values of serum concentration of transferrin receptors examined in the first group of patients was within a normal range. A suitable marker for non-invasive evaluation of an iron overload in PCT patients is the serum ferritin concentration. Serum iron is not necessarily significantly elevated in these patients and the same applies to transferrin saturation.

        Key words: porphyria cutanea tarda, iron, hepatitis C, C282HFE mutation