The classic histologic features of alcoholic hepatitis include inflammation and necrosis, which are most prominent in the centrilobular region of the hepatic acinus ( Figure 2 ). Hepatocytes are classically ballooned, which causes compression of the sinusoid and reversible portal hypertension. The inflammatory cell infiltrate, located primarily in the sinusoids and close to necrotic hepatocytes, consists of polymorphonuclear cells and mononuclear cells. In addition to inflammation and necrosis, many patients with alcoholic hepatitis have fatty infiltration and Mallory bodies, which are intracellular perinuclear aggregations of intermediate filaments that are eosinophilic on hematoxylin-eosin staining. Neither fatty infiltration nor Mallory bodies are specific for alcoholic hepatitis or necessary for the diagnosis. 16
Side effects are minimized by taking the lowest doses possible (that still yields positive results) and following doctor's orders. It is important to avoid self-regulation of the dosage, either by adding more or stopping the drug without a schedule. After prolonged use, steroids must be gradually reduced to permit the adrenal glands to resume natural cortisol production. Eliminating doses too quickly can result in glucocorticoid withdrawal symptoms, worsening of underlying inflammatory disease (rebound effect), or rarely, adrenal crisis (a life-threatening state caused by insufficient levels of adrenal steroids).