How Do I Treat
نویسنده
چکیده
It is well known that hepatic siderosis and high serum iron levels occur in most PCT patients. The role of genetic hemochromatosis in the pathogenesis of iron overload in PCT has been hypothesized for many years but it is only recently that the genetic defect causing hemochromatosis has been identified. There are two known mutations in the hemochromatosis gene (HFE): cystein 282 tyrosine (Cys282Tyr) and histidine 63 asparagine (His63Asp) (7, 8, 9). A recent Swedish study including both familial and sporadic PCT patients showed that 60% of the patients were carriers of one or two mutations in the gene for hemochromatosis (P.␣ Harper, personal communication). Iron overload is one of the factors that trigger off the clinical manifestations of PCT, and iron depletion remains an important factor in the therapy (10, 11). Iron inhibits catalytic activity of URO-D without decreasing the concentration of enzyme protein, and this inhibition is reversible (12, 13).
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