Colchicine decreases
liver fibrosis in experimental and human disease, but a meta-analysis recently concluded that
colchicine should not be used for
liver fibrosis or
cirrhosis irrespective of the aetiology. In this issue, Cortez-Pinto et al. confirm such negative conclusions in their series of 55 outpatients with biopsy-proven
alcoholic cirrhosis followed for a median of 3.5 years. Although well tolerated,
colchicine did not affect either the annual incidence rate of complications or liver function tests. Current treatment of
alcoholic cirrhosis includes correction of
nutritional deficiencies, exogenous administration of
antioxidants (notably
S-adenosylmethionine and
polyenylphosphatidylcholine), and
liver transplantation. In the future, preventive/therapeutic strategies will include campaigns to decrease
alcohol abuse aimed at subjects genetically prone to develop alcoholic liver injury, prevention of
liver fibrosis via inhibition of the Na+/H+ exchange, stimulation of apoptosis of stellate cells, antagonism of
cytokines involved in liver injury, degradation of extracellular matrix, and reversal of
ethanol-induced inflammatory and fibrotic changes via increased
nitric oxide levels. On the grounds that it renders the hepatocyte more vulnerable to
necrosis, steatosis has a key role in the pathogenesis of alcoholic and non-
alcoholic liver disease. Conditions associated with
insulin resistance have been recognized as risk factors for chronic
liver disease and
hepatocellular carcinoma in the alcoholic. This suggests that, through steatosis,
insulin resistance could be a co-factor of
alcoholic liver disease. Were such a hypothesis confirmed, it would unify our view of the pathogenesis of alcoholic and non-
alcoholic liver disease, with all its inherent therapeutic implications.