Alcohol abuse with/without cirrhosis is associated with an impaired gut barrier and inflammation. Gut microbiota can transform primary bile acids(BA) to secondary BAs which can adversely impact the gut barrier. Aim: Define the effect of active alcohol intake on fecal BA levels, ileal & colonic inflammation in cirrhosis. Methods: Five age-matched groups; two non-cirrhotic (control and drinkers) & three cirrhotic [(NAlc:non-alcoholic (non-drinkers),AbsAlc: abstinent alcoholic for >3mths & CurrAlc:(currently drinking)] were included. Fecal and serum BA analysis, serum endotoxin and stool microbiota using pyro-sequencing were performed. A subgroup of controls, NAlc and CurrAlc underwent ileal and sigmoid colonic biopsies on which mRNA expression of TNF-α, IL1β,IL6 and Cox-2 were performed. Results: 103 patients (19 healthy, 6 non-cirrhotic drinkers, 10 CurrAlc, 38 AbsAlc and 30 NAlc, age 56 yrs, median MELD:10.5) were included. Five each of healthy, CurrrAlc and NAlc underwent ileal/colonic biopsies. Endotoxin, serum conjugated DCA and stool total BAs and secondary/primary BA ratios were highest in current drinkers. On biopsies, a significantly higher mRNA expression of TNF-α, IL1β,IL6 and Cox-2 in colon but not ileum was seen in CurrAlc compared to NAlc & controls. Conclusion: Active alcohol use in cirrhosis is associated with a significant increase in the secondary BA formation compared to abstinent alcoholic cirrhotics and non-alcoholic cirrhotics. This increase in secondary BAs is associated with a significant increase in expression of inflammatory cytokines in colonic mucosa but not ileal mucosa, which may contribute to alcohol-induced gut barrier injury.