Alcohol-associated hepatitis presents as a clinical syndrome of jaundice and elevated liver enzymes, typically with an AST-to-ALT ratio greater than two, following significant alcohol exposure. Pathophysiologically, it functions as an immune-mediated response triggered by gut barrier disruption, necessitating rigorous infection surveillance and aggressive nutritional support as first-line therapies. Patients require 30 kilocalories per kilogram daily to combat catabolic states. While corticosteroids may improve 28-day survival in select cases, they are not a substitute for infection control and should be guided by the Lille score, which uses bilirubin trends to assess treatment response by day four. Long-term management centers on alcohol use disorder pharmacotherapy, such as naltrexone and acamprosate, which remain underutilized despite their efficacy in preventing relapse even in patients with stable cirrhosis.
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