Liver iron distribution, histological activity and mutations in the hemochromatosis gene (HFE) in chronic hepatitis C

Sampietro, Maurizio; Boldorini, Renzo; Corbetta, Noemi; Amato, Massimo; Casatta, A.; Lupica, L.; Nunziata, Raffaele; Mattioli, Massimo; Vitto, M. Del; Molteni, V.; Fracanzani, A.L.; Fiorelli, G.

doi:10.1016/s0168-8278(98)80589-8

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“…In this review, we summarize current knowledge of these associations and emphasize important unresolved questions that require further study hepatic iron, inflammation, fibrosis or cirrhosis, or abnormal serum iron parameters [15,16,17]. Other studies have suggested an association between the presence of the mutations and elevated laboratory variables (transferrin saturation, ALT, and serum iron) [18,19] or histologic variables (liver iron content and fibrosis but, interestingly, not inflammation) [20,21]. A recent study [22] in 137 patients supported the existence of an association and showed that the amount of serum ferritin, level of transferrin saturation, presence of stainable iron, and existence of liver fibrosis and cirrhosis were significantly higher in patients who were heterozygous for the C282Y mutation when compared with normal homozygous patients.…”

Section: Iron Hfe Gene Testing and Chronic Viral Hepatitismentioning

confidence: 97%

Role of HFE gene mutations in liver diseases other than hereditary hemochromatosis

Bonkovsky

Obando

1999

Curr Gastroenterol Rep

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Heavy iron overload, as occurs in primary and secondary hemochromatosis, may cause fibrosis of parenchymal organs, including the heart, liver, and pancreas, and it is a risk factor for the development of hepatocellular carcinoma. Recent evidence indicates that lesser degrees of hepatic iron deposition are also risk factors for nonhemochromatotic liver disease. For example, several recent studies showed extraordinarily high prevalences (about 60% to 75%) of HFE mutations in patients with porphyria cutanea tarda and significantly increased prevalences of these mutations in patients with nonalcoholic steatohepatitis from Australia and the United States. It is less well established that the prevalence of the HFE mutations is increased in alcoholic liver disease and in chronic viral hepatitis, but in both conditions, patients harboring one of these mutations, especially C282Y, are more likely to have advanced hepatic fibrosis or cirrhosis. Thus, these mutations both incite and exacerbate nonhemochromatotic liver disease. In this review, we summarize current knowledge of these associations and emphasize important unresolved questions that require further study.

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