The overall mortality rate for alcohol-associated hepatitis is 34% (20% within 1 month) without corticosteroid therapy. Individuals in whom the prothrombin time prohibits liver biopsy have a 42% mortality rate at 1 year. Other unfavorable prognostic factors are older age, a serum bilirubin greater than 10 mg/dL (171 mcmol/L), hepatic encephalopathy, coagulopathy, azotemia, leukocytosis, sepsis and other infections, systematic inflammatory response syndrome (which is associated with multiorgan failure), lack of response to corticosteroid therapy, and possibly a paucity of steatosis on a liver biopsy specimen and reversal of portal blood flow by Doppler ultrasonography. Concomitant gastrointestinal bleeding does not appear to worsen survival. Failure of the serum bilirubin level to decline after 7 days of treatment with corticosteroids predicts nonresponse and poor long-term survival, as does the Lille model (which includes age, serum creatinine, serum albumin, prothrombin time [or INR], serum bilirubin on admission, and serum bilirubin on day 7). The MELD score used for cirrhosis and the Glasgow alcohol-associated hepatitis score (based on age, white blood cell count, blood urea nitrogen, prothrombin time ratio, and bilirubin level) also correlate with mortality from alcohol-associated hepatitis and have higher specificities than the discriminant function and Lille score. A scoring system based on age, serum bilirubin, INR, and serum creatinine (ABIC) has been proposed, and at least one study has shown that the development of acute kidney injury is the most accurate predictor of 90-day mortality. Another scoring system based on hepatic encephalopathy, systemic inflammatory response syndrome, and MELD score has also been reported to predict acute kidney injury and mortality. The combination of the MELD score and Lille model has been reported to be the best predictor of short-term mortality among the scoring systems. Histologic features associated with 90-day mortality include the degree of fibrosis and neutrophil infiltration, presence of megamitochondria, and bilirubinostasis.
Overall mortality from alcohol-associated liver disease has declined slightly in the United States since 1980. Nevertheless, the 3-year mortality rate of persons who recover from acute alcohol-associated hepatitis is 10 times greater than that of control individuals of comparable age; the 5-year mortality rate is as high as 85%. Histologically severe disease is associated with continued excessive mortality rates after 3 years, whereas the death rate is not increased after the same period in those whose liver biopsy specimens show only mild alcohol-associated hepatitis. Complications of portal hypertension (ascites, variceal bleeding, hepatorenal syndrome), coagulopathy, and severe jaundice following recovery from acute alcohol-associated hepatitis also suggest a poor long-term prognosis.
The most important long-term prognostic factor is continued excessive drinking. In many European countries, ethanol conjugated ethyl glucuronide in urine is used as a direct marker of alcohol consumption. The risk of alcohol-associated cirrhosis is greater in women than in men, associated with obesity, cigarette smoking, chronic hepatitis C, and low vitamin D levels; the risk is inversely associated with coffee drinking. Alcohol-associated cirrhosis is a risk factor for hepatocellular carcinoma, and the risk is highest in carriers of the C282Y mutation for hemochromatosis or those with increased hepatic iron. A 6-month period of abstinence is generally required before liver transplantation is considered, although this requirement has been questioned and early liver transplantation has been performed in selected patients with alcohol-associated hepatitis, with good outcomes. Optimal candidates have adequate social support, do not smoke, have no psychosis or personality disorder, are adherent to therapy, and have regular appointments with a psychiatrist or psychologist who specializes in addiction treatment. Patients with alcohol-associated liver disease are at higher risk for posttransplant malignancy than those with other types of liver disease because of alcohol and tobacco use.