Editor,—We read with interest the recent paper by Grove et al (Gut1998;43:262–6) which concludes that the two haemochromatosis mutations (C282Y and H63D) influence neither the liver iron content nor risk of fibrosis in alcoholic liver disease. Two factors in this study may have led to an underestimation of the contribution of the haemochromatosis gene (HFE) to hepatic iron loading.

Most of the patients in the study had established cirrhosis. Cirrhosis, particularly alcoholic cirrhosis, may itself be a potent cause of hepatic iron loading once it has developed.1 This rapid iron loading may result in hepatic iron concentrations usually associated with the homozygous haemochromatosis state and might obscure the effect of any iron loading that might occur due to the heterozygous genotype. Also, in haemochromatosis, excess alcohol consumption, although not affecting the hepatic iron concentration, seems to cause iron to redistribute from hepatocytes to reticuloendothelial cells.2 The same may be true of hepatic iron stores in heterozygous haemochromatosis when excess alcohol is consumed, thus causing an underestimation of the hepatic iron stores if only hepatocellular …