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Alcohol Induced Liver Disease

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Clinical Cases in Hepatology
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Abstract

Genetic predisposition, including the presence of PNPLA3 and the single nucleotide polymorphism in the Solute Carrier Family 38, Member A4 (SLC38A), seems to play a role in developing alcoholic liver disease (ALD), considering that only 15% of the subjects who drink alcohol excessively develop cirrhosis.

The prevention of ALD starts with the identification of patients with alcohol use disorder (AUD). The question “How many times in the past year have you had X or more drinks in a day?” X being five for men and four for women, and the response of at least one being considered positive can be used in all clinical settings.

Patients with AUD with or without ALD may experience an alcohol withdrawal syndrome, which can progress to delirium tremens; thus, patients at risk should be identified with the Prediction of Alcohol Withdrawal Severity Scale and treated prophylactically.

Patients with ALD may be asymptomatic. The typical liver profile of ALD is increased serum activity of aspartate and alanine aminotransferases at a 2:1 ratio. Patients with alcoholic hepatitis (AH), a severe form of liver injury, also present with hyperbilirubinemia, and hepatic synthetic dysfunction, and may have encephalopathy.

Alcohol abstinence is the treatment foundation of all forms of alcohol-related disease. Pharmacotherapy includes baclofen and opiate antagonists.

The treatment of AH is steroids, based on severity scores. Nutrition is fundamental in patients with all degrees of liver disease, with the provision of a protein night snack.

Liver transplantation for patients with liver failure from alcoholic hepatitis is an option.

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Acknowledgments

The author acknowledges Dr. Cesar del Rosario for having contributed Figures 8.1, 8.2, 8.3 and 8.5.

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Bergasa, N.V. (2022). Alcohol Induced Liver Disease. In: Bergasa, N.V. (eds) Clinical Cases in Hepatology. Springer, London. https://doi.org/10.1007/978-1-4471-4715-2_8

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