Alcoholic Liver Disease

Alcoholic liver disease (ALD) encompasses a spectrum of liver injury—hepatic steatosis, alcoholic hepatitis, and cirrhosis—caused by chronic excessive alcohol consumption. It remains a leading cause of cirrhosis and liver-related death worldwide and in Zambia. For Zambian students, ALD is HIGHLY PREVALENT and UNDERDIAGNOSED; ABSTINENCE IS LIFE-SAVING. Pathophysiology: ACETALDEHYDE (ethanol metabolite)—direct hepatotoxin, forms protein/DNA adducts, lipid peroxidation, mitochondrial damage, glutathione depletion. CYP2E1 INDUCTION → oxidative stress, reactive oxygen species. GUT-DERIVED ENDOTOXIN → activation of Kupffer cells (TLR4) → TNF-α, IL-1β, IL-6, profibrotic cytokines. Impaired methionine metabolism (↓SAMe). Spectrum: HEPATIC STEATOSIS (90% heavy drinkers)—reversible with abstinence. ALCOHOLIC HEPATITIS (10-35%)—acute-on-chronic inflammatory injury, variable severity, high short-term mortality. CIRRHOSIS (10-20%)—irreversible, micronodular → macronodular, HCC risk (10-15%). Clinical: STEATOSIS: asymptomatic, hepatomegaly. ALCOHOLIC HEPATITIS: JAUNDICE (90%), FEVER (50%), TENDER HEPATOMEGALY, ANOREXIA, MALAISE, WEIGHT LOSS. SEVERE: ascites, encephalopathy, variceal haemorrhage, coagulopathy, acute kidney injury (hepatorenal syndrome), leukocytosis (20-30,000). CIRRHOSIS: signs of portal hypertension, synthetic dysfunction, HCC. Diagnosis: HISTORY OF SIGNIFICANT ALCOHOL CONSUMPTION (≥40-80 g/day, ≥5 years). ELEVATED AST > ALT (2:1), AST <300 IU/L. ELEVATED GGT (sensitive, not specific). MACROCYTOSIS (MCV). ALCOHOLIC HEPATITIS: Maddrey Discriminant Function (DF) = 4.6 x (PT - control) + total bilirubin (mg/dL). DF ≥32 = SEVERE, 30-50% mortality at 28d. MELD score, Glasgow Alcoholic Hepatitis Score (GAHS). LIVER BIOPSY: not always required; shows macrovesicular steatosis, ballooning, Mallory-Denk hyaline, neutrophil infiltration, 'chicken wire' perisinusoidal fibrosis, cirrhosis. EXCLUDE: NAFLD, viral hepatitis, drug-induced, hemochromatosis, Wilson's. Management: ABSTINENCE—CORNERSTONE, ONLY INTERVENTION THAT IMPROVES SURVIVAL. ALCOHOLIC HEPATITIS: SEVERE (DF≥32, GAHS≥9, MELD≥21): CORTICOSTEROIDS (prednisolone 40 mg/day x 28 days, then taper) OR PENTOXIFYLLINE (400 mg TID)—controversial, corticosteroids superior. Lille score (day 7) identifies non-responders (Lille >0.45) → stop steroids. NUTRITIONAL SUPPORT: enteral nutrition (35-40 kcal/kg, 1.2-1.5 g/kg protein) improves survival. AVOID: acetaminophen, NSAIDs, sedatives. CIRRHOSIS COMPLICATIONS: manage ascites (sodium restriction, diuretics, large-volume paracentesis), varices (beta-blockers, band ligation), encephalopathy (lactulose, rifaximin). HCC SURVEILLANCE: ultrasound q6 months. LIVER TRANSPLANTATION: ALCOHOLIC HEPATITIS—selected patients (severe, non-responders, first presentation, favourable psychosocial profile), 6-month abstinence rule (controversial). CIRRHOSIS—6 months abstinence required. Prognosis: STEATOSIS: reversible 2-4 weeks abstinence. ALCOHOLIC HEPATITIS: 30-50% 28d mortality (severe), 50% 1y mortality. CIRRHOSIS: 60-80% 5y survival if abstinent; <50% if continue drinking. Zambian context: ALCOHOL USE DISORDER IS HIGHLY PREVALENT. Alcohol per capita consumption in Zambia is among highest in Africa. ALD is COMMON, STIGMATIZED, UNDERDIAGNOSED, UNDER-TREATED. SCREEN all patients for alcohol use (AUDIT-C, CAGE). Brief intervention, motivational interviewing, referral to alcohol treatment services (where available) are ESSENTIAL. Corticosteroids (prednisolone) accessible, inexpensive. Nutritional support (RUTF, supplementation). Management of cirrhosis complications (diuretics, lactulose, paracentesis) accessible. Variceal band ligation accessible. HCC surveillance accessible. Liver transplant unavailable. Patient, family, community education: ALCOHOL LIVER DISEASE IS PREVENTABLE AND TREATABLE. ABSTINENCE SAVES LIVES. Do not be nihilistic—INTERVENE.