Alcoholic liver fibrosis: detection and treatment

Alcohol consumption is one of the main risks to public health. Alcohol use disorders (AUDs) cause 80% of hepatotoxic deaths, and approximately 50% of cirrhosis is alcohol-related. The acceptable daily intake (ADI) for ethanol is 2.6 g/day, deduced from morbidity and mortality rates due to liver fibrosis. The relative risk of cirrhosis increases significantly for doses above 60 g/day for men and 20 g/day for women over a period of around 10 years. Twenty to 40% of steatosis cases will evolve into steatohepatitis/steatofibrosis, and 8 to 20% will evolve directly into liver cirrhosis. About 20 to 40% of steatohepatitis cases will evolve into cirrhosis, and 4 to 5% into hepatocellular carcinoma. This cascade of events evolves in 5 to 40 years, with the temporal variability caused by the subjects' genetic patterns and associated risk/comorbidity factors. Steatohepatitis should be considered the rate limiting step: usually, it can be resolved through abstinence, although for some patients, once this situation develops, it is not substantially modified by abstention and there is a risk of fibrotic evolution. Early detection of fibrosis, obtained by hepatic elastography, is a crucial step in patients with AUDs. Such strategy allows patients to be included in a detoxification program in order to achieve abstention. Drugs such as silybin, metadoxine, and adenosylmethionine can be used. Other drugs, with promising antifibrotic effects, are currently under study. In this review, we discuss clinical and pathogenetic aspects of alcohol-related liver fibrosis and present and future strategies to prevent cirrhosis.