Alcoholic hepatitis is a multi-system disease seen in patients who have abused large quantities of alcohol over an extended period of time, often years. The development of alcoholic hepatitis is complex and dependent on a variety of genetic and environmental factors. In general, men who ingest more than 100 g of ethanol daily for more than 5 years are at highest risk of developing alcoholic hepatitis; however, women may develop alcoholic hepatitis after ingesting smaller amounts of ethanol for shorter periods of time. Alcoholic hepatitis can adversely affect multiple organ systems: the gastrointestinal system, central nervous system, hematologic system, cardiovascular system, and renal system. Symptoms are non-specific and may include fatigue, right upper quadrant abdominal pain, anorexia, weight loss, jaundice, and fever. There is usually a history of recent binge drinking. Clinical signs may include tender hepatomegaly often with a systolic hepatic bruit, jaundice, fever, ascites, and encephalopathy in more severe cases. Physical stigmata of underlying chronic liver disease may be present including spider angiomata, splenomegaly, palmar erythema, gynecomastia, parotid gland enlargement, testicular atrophy, and Dupuytren’s contractures. Laboratory tests classically show modest elevations in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) (typically not greater than 300 mg/dL), with AST greater than ALT, bilirubin levels as high as 30 mg/dL, marked coagulopathy, leukocytosis, anemia, and renal failure in the most severe cases. Diagnosis can be made on clinical and biochemical grounds and liver biopsy is not routinely needed to confirm the diagnosis. Based on the American Association for the Study of Liver Disease (AASLD) guidelines set forth in 2010 for alcoholic liver disease, it is recommended that for patients with a clinical diagnosis of severe alcoholic hepatitis for whom medical treatment is contemplated, or for those in whom reasonable uncertainty exists regarding the underlying diagnosis, a liver biopsy should be considered[1
Patients with severe alcoholic hepatitis frequently deteriorate within a few days to weeks in the hospital with progressive hepatic and renal failure despite supportive measures. Severe alcoholic hepatitis is associated with a high short-term mortality rate, approaching that of fulminant hepatic failure without orthotopic liver transplantation. Indeed, nearly one-half of patients with severe alcoholic hepatitis die within one month of hospitalization. In an effort to determine prognostic criteria for these gravely ill patients with acute alcoholic hepatitis, Maddrey et al[2
] found significant independent associations with prothrombin time prolongation, peak serum bilirubin and mortality. Using these parameters, the discriminant function (DF) was devised as a disease specific prognostic scoring system [DF = 4.6 × prothrombin time (seconds prolonged more than control) + serum total bilirubin (mg/dL)]. Patients with the most severe disease, as defined by a DF greater than 32 have the highest risk of dying, with a one month mortality of 30%-50%[3
]. Furthermore, spontaneous hepatic encephalopathy or the model for end-stage liver disease score greater than 18 in patients with acute alcoholic hepatitis carries a similar poor prognosis and has been used along with the DF to predict disease severity. Moreover, in patients who survive the initial hospitalization, alcoholic hepatitis is a well-known precursor of alcoholic cirrhosis, especially in patients who continue to drink.