Table 4.

A Summary of Studies Evaluating Bile Acids in Alcoholic Liver Disease and Hepatocellular Carcinoma.

Author	Study population	Parameter studied	Type of study	Duration of study	Outcome
Brandl et al. Journal of hepatology 2018136	Alcoholic hepatitis (n = 132), alcohol use disorder (n = 9), and controls (n = 9)	Serum BAs	Multicenter prospective cohort study	–	Alcoholic hepatitis vs controls: Significant ↑ total and conjugated BAs, serum FGF19 ↓ De novo bile acid synthesis
Kakiyama et al Am J Physiol Gastrointest Liver Physiol. 201425	N = 103; HC (n = 19), alcohol intake w/o liver disease (n = 6), cirrhotic patients (n = 78): currently drinking (n = 10), no history of alcohol consumption (n = 30), and alcoholic cirrhosis and abstinent for >6 m (n = 38)	Fecal BAs	Prospective cohort study	–	MELD score significantly negatively correlated with total fecal BAs, total secondary BAs, and the secondary-to-primary BA ratio. Active alcohol intake influences BA composition independent of cirrhosis
Thomas et al. Cancers 2021137	N = 32,535; incident HCC N = 216 among participants who provided a prediagnostic serum sample	Serum BAs	Prospective population-based cohort study Nested case–control study	10 years	↑ serum primary BAs and T:G ratio were strongly associated with HCC risk of ↑ 2°:1° primary BAs inversely associated with HCC risk
Petrick et al. International journal of cancer 2020138	HBV N = 185; matched controls N = 61 from REVEAL-HBV cohort; HCV cases N = 96; matched controls N = 96 from REVEAL-HCV cohort	15 serum BAs measured using LC-MS	Case–control study	Mean duration of follow-up HBV: 13 years HCV: 15 years	↑ glycine- and taurine-conjugated primary BAs a/w 2–8 fold ↑ risk of HBV- and HCV-related HCC. ↑ DCA inversely a/w HBV-related HCC risk No ↑ risk of liver cancer with ↑ secondary BAs observed

MELD, model for end-stage liver disease; BA, bile acid; FGF19, fibroblast growth factor 19; HCC, hepatocellular carcinoma; HBV, hepatitis B virus; HCV, Hepatitis C virus; T:G, taurine:glycine.