The alcoholic fatty liver may develop in some people with modest alcohol consumption or after acute episodes of alcohol consumption. It is always found in heavy drinkers in whom the disease may progress to alcoholic hepatitis and cirrhosis. Distinguishing alcoholic fatty liver from the non-alcoholic fatty liver is not without problems; however, certain combinations of symptoms have been found helpful in differentiating the two conditions. Alcoholic fatty liver is reversible if abstinence is practiced.
Alcoholic fatty liver, which may occur after even moderate (about 10g per day) consumption of alcohol , is invariably found in people who drink heavily . It is the initial stage in alcoholic liver disease when pathologic changes are reversible. Consumption of excessive amounts of alcohol over extended periods will lead to the appearance of more severe manifestations, such as alcoholic hepatitis and cirrhosis.
The buildup of fats (triglycerides) in the liver is the consequence of the metabolism of alcohol by the liver. The enzymes that oxidize alcohol to the toxic acetaldehyde and then to acetic acid also produce reduced nicotinamide adenine dinucleotide (NADH). Excess NADH inhibits the oxidation of fatty acids and promotes their synthesis, which favors their accumulation in the form of triglycerides . A multitude of other molecular and cellular effects of alcohol metabolism, such as oxidative stress, and the activation of hepatic macrophages, leads to further damage, inflammation, and fibrosis.
Alcoholic fatty liver does not usually cause symptoms. Hepatomegaly may be observed and supports the diagnosis. Rare symptoms are portal hypertension and extrahepatic problems such as muscle wasting, cardiomyopathy, and pancreatitis. Cholestasis is another rare occurrence in people with fatty liver. The American Association for the Study of Liver Diseases recommends using an organized questionnaire if excessive alcohol consumption is suspected .
Patient history is extremely important because fatty liver can occur in obese patients and in conditions of hyperlipidemia, insulin resistance, and malnutrition, and can be caused by various drugs. However, patient history may not be accurate, and single biomarkers (for example, amino acid transferase or gamma-glutamyl transpeptidase levels) do not distinguish efficiently between alcoholic and non-alcoholic hepatic steatosis. However, a combination of results of diagnostic markers can differentiate between the two types of conditions reliably  .
In alcoholic liver disease, laboratory studies show elevated aminotransferases (aspartate aminotransferase and alanine aminotransferase) in about 30% of the patients, with aspartate aminotransferase being higher than alanine aminotransferase. Bilirubin concentrations may also be elevated because of hemolysis.
Liver biopsy is not usually performed for fatty liver but may be useful to exclude more advanced disease (steatohepatitis or fibrosis), or other unrelated conditions that cause liver damage. The biopsy of fatty liver will show fat accumulation in the hepatocytes, which tends to be macrovesicular, consisting of a single or very few large lipid droplets resulting in the displacement of the nucleus to a peripheral position. Microvesicular lipid accumulation is sometimes observed, which leads to foamy degeneration of hepatocytes . Fatty deposition most often affects the centrilobular part of the acinus, but in advanced cases of fatty liver, the whole acinus is affected .
Ultrasonography, computed tomography, and magnetic resonance imaging can demonstrate the condition of steatosis in a patient. Ultrasonography shows a diffusely echogenic liver in alcoholic steatosis.