From the Guidelines

Alcoholic Hepatitis (AH) is a severe and potentially life-threatening liver disease caused by excessive alcohol consumption.

AH is characterized by the onset of jaundice within 8 weeks of last period of drinking, heavy drinking (> 40 g/day) for more than 6 months, serum bilirubin > 3.0 mg/dL, serum AST > 50 IU/L but < 400 IU/L, and serum AST/ALT ratio > 1.5 1.
A liver biopsy specimen showing macrovesicular steatosis, neutrophil infiltration, ballooning degeneration of hepatocytes, megamitochondria, and Mallory-Denk bodies is helpful but not required for the clinical diagnosis 1.

The Maddrey Discriminant Function (MDF) and the MELD score are recommended scores for identifying severe forms of AH, with an MDF score ≥ 32 or a MELD score > 20 indicating severe disease 1.
The Lille score, calculated on the seventh day of treatment, is used to assess therapeutic response to corticosteroid therapy, with a score ≥ 0.45 indicating poor response 1.

Abstinence from alcohol is the cornerstone of treatment for AH 1.
Corticosteroids, such as methylprednisolone 32 mg daily, may be considered in patients with severe AH to reduce short-term mortality, but do not influence medium to long-term survival 1.
Nutritional support, with a daily energy intake ≥ 35-40 kcal/kg BW and 1.2-1.5 g/kg protein, is essential for recovery 1.
Systematic screening for infection should be performed before initiating therapy, during corticosteroid treatment, and during the follow-up period 1.

The mortality rate within 90 days is 40-50% without treatment and abstinence from drinking alcohol 1.
Early non-response to corticosteroids is associated with poor prognosis, and highly selected patients may be considered for early liver transplantation 1.
Long-term outcomes depend mainly on achieving abstinence, with addiction treatment strongly recommended after an episode of AH 1.

From the Research

Alcoholic hepatitis (AH) is an acute and often devastating form of alcohol-associated liver disease 2
AH is characterized by elevated bilirubin, model for end stage liver disease scores >20, and nonspecific symptoms caused by underlying inflammation, hepatocyte injury, and impaired intestinal barrier function 2
Clinically, AH is characterized by jaundice, hepatomegaly, and abdominal pain, and histologically by macrovesicular steatosis and necroinflammation 3
AH is an inflammatory disorder of the liver that can occur in patients with steatosis or underlying cirrhosis 4

The pathogenesis of AH is multifactorial, involving genetic factors, alcohol-induced hepatocyte damage, reactive oxygen species, and gut-derived microbial components 4
Continued alcohol use and pro-inflammatory cytokines induce stellate cell activation and result in progressive fibrosis 4
Compromised immune defense in AH contributes to infections, sepsis, and organ failure 2

AH is characterized by the rapid onset of jaundice and the development of myriad complications 5
The diagnosis of AH has been controversial for many years, but it is now accepted that there are clear clinical criteria that can be used to diagnose AH without the need for a liver biopsy 6
Clinical criteria such as the Glasgow Alcoholic Hepatitis score and model for end-stage liver disease can be used to diagnose AH 6

Corticosteroids are the only recommended treatment for severe AH, but they do not provide survival benefits beyond 1 month 2
Abstinence from alcohol is critically important in patients with AH, but recidivism is high 5
Other treatments such as N-acetylcysteine, granulocyte colony stimulating factor, faecal microbiota transplantation, and routine antibiotics show promise, but adequate controlled trials are needed to confirm efficacy 6
Liver transplant has an emerging role for some patients with severe AH not responding to corticosteroids 6