AIM

The impact of mild drinking habit (less than 20 g/d of ethanol) on the clinical course of non-alcoholic fatty liver disease (NAFLD) has not been determined. We examined the influence of a mild drinking habit on liver carcinogenesis from NAFLD.

METHODS

A total of 301 patients who had been diagnosed as having NAFLD by liver biopsy between 2003 and 2016 [median age: 56 years, 45% male, 56% with non-alcoholic steatohepatitis, 26% with advanced fibrosis (F3-4)] were divided into the mild drinking group with ethanol consumption of less than 20 g/d (mild drinking group, = 93) and the non-drinking group ( = 208). Clinicopathological features at the time of liver biopsy and factors related to hepatocellular carcinoma (HCC) occurrence were compared between the groups.

RESULTS

We observed significant differences in male prevalence ( = 0.01), platelet count ( = 0.04), and gamma-glutamyl transpeptidase ( = 0.02) between the test groups. Over 6 years of observation, the HCC appearance rate was significantly higher in the mild drinking group (6.5% 1.4%, = 0.02). Multivariate survival analysis using Cox's regression model revealed that hepatic advanced fibrosis (F3-4) ( < 0.01, risk ratio: 11.60), diabetes mellitus ( < 0.01, risk ratio: 89.50), and serum triglyceride ( = 0.04, risk ratio: 0.98) were factors significantly related to HCC in all NAFLD patients, while the effect of a drinking habit was marginal ( = 0.07, risk ratio: 4.43). In patients with advanced fibrosis (F3-4), however, a drinking habit ( = 0.04, risk ratio: 4.83), alpha-fetoprotein ( = 0.01, risk ratio: 1.23), and diabetes mellitus ( = 0.03, risk ratio: 12.00) were identified as significant contributors to HCC occurrence.

CONCLUSION

A mild drinking habit appears to be a risk factor for hepatocarcinogenesis in NAFLD patients, especially those with advanced fibrosis.