Severe alcoholic hepatitis is associated with a high mortality and the presence of liver failure, manifested by jaundice, coagulopathy, and often encephalopathy. Whereas insights into the pathophysiology of this devastating disease have improved over the past years, clinical progress in the last two decades has been minor. For more than two decades, steroids have remained the only moderately effective treatment option. One key confounder to most therapy studies has been the use of the discriminant function to identify patients at highest risk of mortality in the absence of better scoring systems more accurately predicting the outcome of severe alcoholic steatohepatitis. The now reported Glasgow alcoholic hepatitis score might represent a substantial improvement in clinical phenotyping and could catalyse the development of new treatments in this disease.

The appearance of steatohepatitis is an important rate limiting step in the development of progressive alcoholic liver disease. One month mortality rates of 40–50% have been reported in patients hospitalised with acutely decompensated liver disease due to alcohol induced steatohepatitis.¹ Patients with severe alcoholic steatohepatitis typically present with fever, hepatomegaly, jaundice, and anorexia. The presence of liver failure manifested by coagulopathy, jaundice, and/or encephalopathy is an indicator of poor outcome, usually highlighting the presence of limited hepatic functional reserve. Approximately 40–50% of patients have ascites and tender hepatomegaly is common. Leucocytosis is frequent and correlates with the severity of hepatic injury.² Neutrophilic infiltration is commonly seen on liver biopsy and these cells may play an important role in the hepatic injury. Although the diagnosis can be confirmed by liver biopsy, clinical and laboratory features are often adequate for establishing the diagnosis. Absolute values for serum aspartate …