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Hepatol Commun. 2017 Nov 11;2(1):29-34. doi: 10.1002/hep4.1123. eCollection 2018 Jan.

Interaction between the patatin-like phospholipase domain-containing protein 3 genotype and coffee drinking and the risk for acute alcoholic hepatitis.

Author information

1
Division of Gastroenterology and Hepatology, Department of Medicine Indiana University School of Medicine Indianapolis IN.
2
Roudebush Veterans Administration Medical Center Indianapolis IN.
3
Department of Biochemistry and Molecular Biology Indiana University School of Medicine Indianapolis IN.
4
Division of Pharmacotherapy and Experimental Therapeutics, Center for Pharmacogenomics and Individualized Therapy, Eshelman School of Pharmacy University of North Carolina Chapel Hill NC.
5
Division of Gastroenterology and Hepatology Mayo Clinic Rochester MN.
6
Division of Gastroenterology and Hepatology, Department of Medicine Virginia Commonwealth University Richmond VA.
7
Department of Biostatistics Indiana University School of Medicine and Richard M. Fairbanks School of Public Health Indianapolis IN.
8
Eskenazi Health Indianapolis IN.

Abstract

Only a subset of subjects with excessive alcohol consumption develops alcoholic liver disease (ALD). One of the major risk factors for ALD is the genetic variant of the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene. Coffee is one of the most commonly consumed beverages, and coffee consumption has been associated with lower levels of serum alanine aminotransferase. The aim of this study was to investigate the role of coffee drinking and PNPLA3 rs738409 and their association with alcoholic hepatitis (AH) in a well-characterized cohort of subjects from the Translational Research and Evolving Alcoholic Hepatitis Treatment consortium. AH subjects and heavy drinking controls without a history of liver disease who were enrolled between May 2013 and May 2016 were included (n = 339), and the details of alcohol and coffee consumption were assessed. The PNPLA3 variant was determined among participants of European ancestry (n = 183). Relationships between baseline data and AH status were determined, and multivariable logistic regression modeling was performed. During the study period, 189 cases with AH and 150 heavy drinking controls were prospectively enrolled. The prevalence of regular coffee consumption was significantly lower in patients with AH compared to controls (20% versus 43%; P < 0.0001). The overall minor allele frequency of the PNPLA3 variant was higher in AH cases. Multivariable logistic regression revealed that coffee consumption and PNPLA3 were significantly associated with AH status at baseline after adjusting for relevant patient characteristics. Conclusion: We found a higher prevalence of AH among heavy drinkers with PNPLA3 G/G and G/C genotypes regardless of coffee consumption status and a higher prevalence of AH among heavy drinkers who were not regular coffee drinkers. These findings remained after considering relevant baseline patient characteristics. Further studies are needed to confirm our observation. (Hepatology Communications 2018;2:29-34).

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