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  • Chronic alcohol intake usually exceeds 80 g/day in men and 30–40 g/day in women with alcohol-associated hepatitis or cirrhosis.

  • Fatty liver is often asymptomatic.

  • Fever, right upper quadrant pain, tender hepatomegaly, and jaundice characterize alcohol-associated hepatitis, but the patient may be asymptomatic.

  • AST is usually elevated but infrequently > 300 U/L (6 mckat/L); AST is > ALT, often by a factor of two or more.

  • Alcohol-associated hepatitis is often reversible, but it is the most common precursor of cirrhosis in the United States.


Excessive alcohol intake can lead to fatty liver, hepatitis, and cirrhosis. Validated tools, such as the Alcohol Use Disorders Inventory Test (AUDIT), can be used to identify persons with alcohol abuse and dependence (see Table 1–7). Alcohol-associated hepatitis is characterized by acute or chronic inflammation and parenchymal necrosis of the liver induced by alcohol and is often a reversible disease, but it is the most common precursor of cirrhosis in the United States. It is associated with four to five times the number of hospitalizations and deaths as hepatitis C. Mortality from alcohol-associated liver disease has been increasing since 1999. The incidence of alcohol-associated liver disease in the United States is rising fastest among those aged 20–29, and the increase accelerated during the COVID-19 pandemic.

The frequency of alcohol-associated cirrhosis is estimated to be 10–15% among persons who consume over 50 g of alcohol (4 oz of 100-proof whiskey, 15 oz of wine, or four 12-oz cans of beer) daily for over 10 years (although the risk of cirrhosis may be lower for wine than for a comparable intake of beer or spirits). The risk of cirrhosis is lower (5%) in the absence of other cofactors such as chronic viral hepatitis and obesity. Genetic factors, including polymorphisms of the genes encoding 555(PNPLA3), membrane bound O-acyltransferase (MBOAT1), transmembrane 6 superfamily member 2 (TM6SF2), tumor necrosis factor, cytochrome P450 2E1, glutathione S-transferase, galectin-9, mitochondrial amidoxime reducing component 1, heterogeneous nuclear ribonucleoprotein U like 1, and heterozygosity of the Z allele of the gene for alpha-1-antitrypsin deficiency, may also account for differences in susceptibility to and severity of liver disease. Women appear to be more susceptible than men, in part because of lower gastric mucosal alcohol dehydrogenase levels, but young men who drink excessively are at increased risk for liver disease later in life when they are no longer drinking as much. Over 80% of patients with alcohol-associated hepatitis have been drinking 5 years or more before symptoms that can be attributed to liver disease develop; the longer the duration of drinking (10–15 or more years) and the larger the alcohol consumption, the greater the probability of developing alcohol-associated hepatitis and cirrhosis. In individuals who drink alcohol excessively, the rate of ethanol metabolism can be sufficiently high to permit the consumption of large quantities without raising ...

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