Alcohol: A Fibrogenic Cocktail in Genetic Haemochromatosis?

Background: The interpretation of moderate alcohol consumption varies worldwide. In Ireland, recommended sensible limits for men and women are no more than 21 IU and 14 IU of alcohol per week respectively. Excess alcohol consumption is thought to act as a fibrogenic cofactor in the progression of haemochromatosis.

Aim: The aim of this study was to evaluate the influence of alcohol consumption on disease expression in Irish haemochromatosis subjects.

Method: One hundred and seventy one C282Y homozygous patients (133 men, 38 women) were evaluated. The data were analysed with respect to age, sex, declared alcohol consumption, serum ferritin (SF), transferrin saturation (TS%), liver enzymes, liver histopathology and iron deposition.

Results: Within this cohort, 14.2% of men and 5.3% of women consumed excess alcohol at presentation. The mean SF and >2+ hepatocyte iron staining prevelance increased with alcohol consumption. Hepatic iron concentrations (HIC) and hepatic iron indicies (HII) did not significantly differ between individuals consuming less than or greater than 14 IU of alcohol/ week. There was no statistically significant difference in either sex between age, SF, TS%, liver fibrosis/ cirrhosis and >2+ hepatocyte iron staining between non-drinkers and those exceeding the recommended sensible limits of alcohol consumption.

Conclusion: Increasing alcohol consumption was not associated with progressive fibrotic change in either sex. Therefore, it appears that haemochromatosis patients may consume alcohol within recommended sensible limits and not experience further hepatocellular deleterious effects.