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Iron, haemochromatosis and thalassaemia as risk factors for fibrosis in hepatitis C virus infection
  1. Mark Thursz
  1. Correspondence to:
    Professor M Thursz
    Gastroenterology and Hepatology Research, Imperial College St Mary’s Hospital Campus, Norfolk Place, London W2 1NY, UK; m.thursz{at}imperial.ac.uk

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Iron depletion is required in patients with HCV and iron overload to retard liver fibrosis

Excess iron is an important cause of liver damage. Aerobic metabolism generates oxygen species as a by-product of the reduction of O2 but these are generally of low reactivity. The presence of transition metal ions such as iron (Fe2+) catalyses the generation of highly reactive oxygen species, the most important of which is the hydroxyl radical (•OH).

Fe2++H2O2→Fe3++OH+OH

H2O2+O2-(Fe)OH+OH+O2

The hydroxyl radical causes oxidation of lipids, lipoproteins, proteins, DNA and carbohydrates leading to injury to the cell membranes and genomic damage. Mitochondrial cell membranes are particularly susceptible to iron-catalysed, hydroxyl-mediated damage.1 Reactive oxygen species may also activate hepatic stellate cells and stimulate transformation into the collagen-producing myofibroblast phenotype associated with hepatic fibrosis2

The presence of excess iron in the liver in the absence of other aetiologies of liver damage may not be sufficient to cause liver disease. However, excess liver iron is now clearly recognised as a cofactor for the development of advanced fibrosis and cirrhosis in patients with hepatitis C virus (HCV) infection and alcohol-related liver disease.3–8

There is enormous variation in the rate at which fibrosis develops and the time taken for cirrhosis or decompensated liver disease to occur among patients with chronic HCV infection.9,10 Certain factors influencing the progression of disease have been identified through cross-sectional and cohort studies so that some of this variation in …

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