Alcoholic Hepatitis.

Abstract

Alcoholic hepatitis is a common clinical problem confronting gastroenterologists and hepatologists alike. The fundamental issue regarding treatment of this disease is its recognition on the part of the physician. Chronic alcohol abuse, fever, leukocytosis, jaundice, and encephalopathy are key symptoms and signs that should prompt consideration of this diagnosis. Nutrition and abstinence from alcohol are the cornerstones of therapy. In addition, management of seriously ill, hospitalized patients should include prophylaxis for withdrawal and delirium tremens. Alcoholic hepatitis (AH) induces a profound catabolic state, resulting in net negative nitrogen balance. In part, because of malnutrition, AH carries a considerably high mortality rate. Therefore, nutrition remains a key aspect of therapy. In the absence of encephalopathy and in the presence of a functioning gastrointestinal tract, oral intake or nasogastric feedings should be given. If the gastrointestinal tract cannot be used (ie, because of paralytic ileus), then total parenteral nutrition is absolutely essential for recovery. A select subset of patients, based on multiple clinical trials and several meta-analyses, can be treated with corticosteroids provided that the patient does not have active gastrointestinal bleeding and does not have an active infection. The subset of patients with AH who should receive corticosteroids is based on calculation of a modified Maddrey discriminant function, which incorporates the patient's prothrombin time and total serum bilirubin as variables in this equation. Generally, a 4-week course of prednisone or prednisolone is administered. d-penicillamine, colchicine, anabolic steroids, propylthiouracil, and antioxidants have not been shown to be effective in AH and cannot be recommended. After acute illness, patients should be discharged to an inpatient alcohol rehabilitation unit to ensure continued abstinence.