alcoholic fatty liver

Alcoholic fatty liver results from chronic ethanol metabolism disrupting normal hepatic lipid handling. Ethanol is metabolized by alcohol dehydrogenase (and CYP2E1 with chronic use) to acetaldehyde, generating excess NADH. This altered NADH/NAD+ ratio inhibits fatty acid oxidation and the TCA cycle, promoting fatty acid synthesis and triglyceride accumulation within hepatocytes (macrovesicular steatosis). Additionally, acetaldehyde impairs lipoprotein assembly/secretion and damages mitochondria, further worsening lipid accumulation. Histologically, hepatocytes show large lipid vacuoles displacing the nucleus (macrovesicular steatosis), typically most pronounced in the centrilobular (zone 3) region. Clinically, patients are often asymptomatic, though some may have mild right upper quadrant discomfort, hepatomegaly, and mildly elevated liver enzymes (AST > ALT, typically both <500 IU/L, with AST:ALT ratio >2:1 suggestive of alcoholic etiology). This is the first stage in the spectrum of alcoholic liver disease, which can progress to alcoholic hepatitis (with inflammation, hepatocyte ballooning, Mallory-Denk bodies, neutrophilic infiltrate) and ultimately cirrhosis with continued alcohol use. Importantly, hepatic steatosis is fully reversible within weeks with alcohol cessation, distinguishing it from the more severe, potentially irreversible later stages. Diagnosis is primarily clinical/biochemical with supportive imaging (ultrasound showing hyperechoic liver) or biopsy when needed. Management centers on complete alcohol abstinence, nutritional support, and treatment of any concurrent alcohol use disorder.