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Prevalence of Cholelithiasis According to Alcoholic Liver Disease: A Possible Role of Apolipoproteins AI and AII
Author(s) -
Poynard Thierry,
Lonjon Isabelle,
Mathurin Philippe,
Abella Annie,
Musset Dominique,
Bedossa Pierre,
Aubert Alain,
Naveau Sylvie,
Chaput JeanClaude
Publication year - 1995
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1995.tb01473.x
Subject(s) - gallstones , medicine , gastroenterology , cirrhosis , steatosis , fatty liver , alcoholic liver disease , liver disease , prospective cohort study , apolipoprotein b , logistic regression , alcohol consumption , disease , cholesterol , alcohol , biochemistry , chemistry
Moderate alcohol intakes decreases the risk of gallstones; in contrast, the prevalence of gallstones is increased in patients with alcoholic cirrhosis. The aims of this prospective study were to assess the prevalence of cholethiasis among drinkers according to the histological severity of liver disease, and to estimate the importance of serum apolipoproteins AI and apolipoprotein All as risk factors for gallstones. Among the 320 drinkers included, 53 patients had cholelithiasis. The prevalence increased ( p < 0,0001) from 5% in patients with normal liver (1 of 22) and 6% in patients with steatosis only (3 of 47) to 13% in patients with fibrosis (7 of 54), reaching 27% among patients with biopsy‐proven cirrhosis (28 of 103). Among patients with clinically obvious cirrhosis on whom biopsy was not performed mainly because of the severity of liver disease, the prevalence of cholelithiasis reached a maximum of 46% (6 of 13). Among drinkers with nonsevere liver disease, patients with cholelithiasis were older (59 ± 9 years, mean ± SD vs. 45 ± 11, p = 0.003) with lower apolipoprotein AI (118 ± 37 vs. 163 ± 45mg/dl; p = 0.002) and apolipoprotein All (30 ± 12 vs. 53 ± 20 mg/dl; p = 0.0002) in comparison with patients without cholelithiasis. These differences persisted after considering by multiple logistic regression analysis, sex, and ideal body weight. Alcohol consumption during the last 5 years was lower in patients with cholelithiasis (83 g/day) in comparison with patients without cholelithiasis (142 g/day; p = 0.04). Among drinkers with severe liver disease, patients with cholelithiasis were slightly older (56 ± 13 vs. 52 ± 12 years; p = 0.07) and were more often female (46% vs. 29%; p = 0.06). Unconjugated serum bilirubin was also slightly higher (30 ± 43 vs. 19 ± 40 μmol/liter; p = 0.08). In conclusion, alcohol intake could protect drinkers against cholesterol gallstones as long as apolipoprotein Al and apolipoprotein All secretions are increased. In contrast, heavy ethanol‐induced fibrosis in the liver results in decreased apolipoprotein Al and apolipoprotein All secretions and thus, may promote the occurrence of cholesterol gallstones. These relationships could explain the paradox of decrease gallstones prevalence among moderate drinkers and the high prevalence among alcoholic cirrhotics.