Fatty liver disease

Fatty liver (steatosis) is the initial and most common consequence of excessive alcohol ingestion. It is potentially reversible. Fatty liver is the accumulation of macrovesicular fat as large droplets of triglyceride that displaces the hepatocyte nucleus. Less often, fat appears in a microvesicular form as small droplets that do not displace the nucleus. Microvesicular fat represents mitochondrial damage. The liver enlarges, and the cut surface is yellow.

Symptoms and Signs

Symptoms match the stage and severity of disease. Symptoms generally become apparent in patients during their mid 30s; severe problems appear about a decade later. Fatty liver usually causes no symptoms. In 1⁄3 of patients, the liver is enlarged, smooth, and occasionally tender.

In any chronic alcoholic liver disease, Dupuytren's contracture of the palmar fascia, vascular spiders, peripheral neuropathy, Wernicke's encephalopathy, Korsakoff's psychosis, and, in men, signs of hypogonadism and feminization (eg, smooth skin, gynecomastia, testicular atrophy) may be present. These manifestations more likely reflect the effect of alcoholism than that of liver disease. Malnutrition may also lead to enlarged parotid glands. Hepatitis C virus infection occurs in about 25% of alcoholics, a combination that markedly worsens the progression of liver disease.

Diagnosis

Alcohol is usually suspected as the cause of liver disease in any patient whose consumption exceeds 80 g/day. If the diagnosis is suspected, liver function tests, CBC, and hepatitis serology are performed. No specific test exists just for alcoholic liver disease.

Patients with abnormalities suggesting alcoholic liver disease must undergo screening tests for other treatable forms of liver disease, especially viral hepatitis. Describing the precise findings is more useful than assigning the patient to this diseace, which can only be determined by liver biopsy. Liver biopsy is performed to stage the severity of liver disease. In addition to confirming liver disease, biopsy also helps identify excessive alcohol use as the most likely cause and establishes the stage of liver injury. If iron accumulation is observed, quantitation of iron content and genetic testing can eliminate hereditary hemochromatosis as the cause.

Prognosis and Treatment

The prognosis for alcoholic liver disease is determined by the degree/ amount of hepatic fibrosis and inflammation. Fatty liver and alcoholic hepatitis without fibrosis are reversible but only if alcohol is avoided; with abstinence, complete resolution of fatty liver occurs within 6 wk.

Abstinence is generally the mainstay of treatment; it can prevent further damage from alcoholic liver disease and thus prolong life. Because compliance is problematic, a compassionate team approach is essential. Excellent results can come from support groups such as Alcoholics Anonymous as long as the patient is motivated (see Drug Use and Dependence: Maintenance).

General management usually emphasizes supportive care. A nutritious diet and vitamin supplements (especially B vitamins) are provided, especially during the first few days of abstinence. However, supplements have not proved to affect outcomes, even in hospitalized patients with alcoholic hepatitis. Alcohol withdrawal sometimes requires benzodiazepines (eg, diazepam)