Alcohol-associated hepatitis is an acute clinical syndrome, identified from the history and laboratory findings rather than from a single test, that heavy drinking can precipitate. It usually arises on a background of established alcohol-associated liver disease, and it carries the highest short-term mortality of any ALD presentation.
Definition and presentation
The diagnosis rests on a consensus definition:
- onset of jaundice within 60 days after heavy drinking, defined as more than 50 g/day for more than 6 months
- increased serum bilirubin above 3 mg/dL
- increased AST of 50–400 U/L
- AST:ALT ratio of 1.5 or more
- no other obvious cause of hepatitis
Jaundice is the only clinical sign required, but patients often also report fever, right upper quadrant pain, anorexia and weakness. Most have an established or newly discovered cirrhosis underneath, and the syndrome is frequently complicated by infection, acute kidney injury and a systemic inflammatory response, which are the main drivers of death.
Assessing severity
Severity is measured with laboratory-based scores, and it decides treatment:
- the Maddrey discriminant function (MDF), calculated from prothrombin time and total bilirubin, defines severe disease at a score of 32 or more and is the score used to decide on corticosteroids
- the Model for End-Stage Liver Disease (MELD), which adds creatinine and INR, gives a more graded prognosis, and a score above 20 also prompts consideration of steroids
- the Lille score is not used at presentation but after treatment begins, to judge response
Severe alcohol-associated hepatitis has a 28-day mortality of roughly 16–30%, and mortality continues to rise over the following year in those who do not recover.
Treatment
Abstinence from alcohol is the mainstay of treatment and the strongest influence on long-term survival. Nutritional support is given at a daily energy intake of 35–40 kcal/kg and a daily protein intake of 1.2–1.5 g/kg, preferably enterally, and thiamine and other micronutrients are replaced. Because infection is common and can be occult, patients are screened with cultures and a chest radiograph, and any infection is treated before or alongside specific therapy.
In severe disease (MDF of 32 or more, or MELD above 20) without contraindications such as uncontrolled infection, upper gastrointestinal bleeding, or severe kidney injury, prednisolone 40 mg/day is given orally. Response is judged with the Lille score on day 7: a score below 0.45 means the patient is responding, and steroids are continued to a total of 28 days; a score of 0.45 or more means non-response, and steroids are stopped. Pentoxifylline is no longer recommended. Adding intravenous N-acetylcysteine to prednisolone may improve short-term survival but needs further confirmation. Patients with moderate disease (MDF below 32) are managed with abstinence and supportive care rather than steroids.
For patients with severe disease who do not respond to medical treatment, or who are ineligible for it and presenting with their first episode of liver decompensation, early liver transplantation — before the traditional six months of abstinence — can be life-saving in carefully selected patients with a favourable psychosocial profile.