| pubmed-article:11944632 | pubmed:abstractText | Hepatic steatosis and steatohepatitis are encountered with great frequency in people who consume large amounts of ethanol (more than 6 drinks per day). Ethanol causes steatosis by altering several steps in the hepatic processing of fatty acids, including their uptake from plasma, their use as fuel substrates, and their export as triglyceride. When clinically mild, alcoholic steatosis and steatohepatitis can be difficult to distinguish from nonalcoholic fatty liver disease. This is particularly true among individuals at high risk of accelerated alcoholic liver injury, such as women, the obese, and those with hepatitis C. In the outpatient setting, history and aspartate aminotransferase:alanine aminotransferase ratio offer the best clues to diagnosis. Liver biopsy cannot determine the cause of steatohepatitis, but can show the extent of disease. The etiology of disease is important to prognosis, as alcoholic fatty liver carries a much higher risk of progression and mortality than nonalcoholic fatty liver disease. Patients with moderate to severe alcoholic steatohepatitis are typically hospitalized. Derangements in white blood cell count, prothrombin time, and bilirubin identify those with the highest early mortality. Survival in this severely ill subgroup is improved with the short-term use of corticosteroids; patients who have contraindications to steroids may benefit from other forms of therapy, either pharmacologic, nutritional, or both. | lld:pubmed |
