Alcohol-associated liver disease

Spectrum of liver injury due to chronic alcohol use, ranging from reversible fatty infiltration to life-threatening hepatitis and irreversible cirrhosis.

• A leading cause of chronic liver disease worldwide (second most common cause of cirrhosis in the US after hepatitis C). Severe alcoholic hepatitis carries a high mortality (~30–50% at 1 month), so recognizing and managing AALD is critical. Frequently tested on exams for its distinct lab findings (AST:ALT ratio, GGT) and treatment decisions (steroids in acute alcoholic hepatitis).

• Often asymptomatic in early stages (simple steatosis); patients may have only mild RUQ discomfort or hepatomegaly. Many cases are first noted incidentally by abnormal labs (AST elevated more than ALT).
• Acute alcoholic hepatitis typically follows a heavy drinking bout and presents with jaundice, fever, anorexia, and a tender enlarged liver. Labs show moderately elevated AST and ALT (AST usually ~2× ALT, rarely >500 U/L), often with high bilirubin and neutrophil-predominant leukocytosis.
• Advanced cirrhosis from alcohol use presents with stigmata of chronic liver disease: ascites, spider angiomata, palmar erythema, gynecomastia, splenomegaly, etc. Decompensation leads to complications of portal hypertension (e.g. variceal hemorrhage causing hematemesis) and liver failure (encephalopathy with confusion/asterixis, coagulopathy).

1. Suspect ALD in patients with long-standing heavy alcohol use and a characteristic AST:ALT ~2:1 pattern (AST often <300 U/L). Supporting labs include elevated GGT and MCV (macrocytosis) from chronic alcohol use.
2. Exclude other causes of liver injury: check viral hepatitis serologies, review medications for drug-induced liver injury, consider autoimmune markers and Wilson disease (in younger patients). Perform imaging (ultrasound) to rule out biliary obstruction or masses; liver biopsy is reserved for uncertain cases (bearing in mind coagulopathy risks).
3. Assess severity in alcoholic hepatitis using prognostic scores. Calculate Maddrey's discriminant function (DF) (uses PT and bilirubin) and MELD score (uses bilirubin, INR, creatinine ± sodium). A DF ≥32 or MELD ≥20 correlates with ~50% 1-month mortality and indicates severe disease (consider steroids). Also evaluate for hepatic encephalopathy or rapidly rising INR, which signal acute liver failure risk.
4. Address management priorities: foremost stop alcohol (enforce abstinence, involve addiction support) and provide nutritional rehabilitation (high-protein diet if possible, replete thiamine, folate, etc.). In severe alcoholic hepatitis (DF ≥32 or high MELD), begin corticosteroids (e.g. prednisolone 40 mg/day for 4 weeks) after ruling out infection or GI bleeding. If steroids are contraindicated, start pentoxifylline as an alternative.
5. Monitor response to therapy: if on steroids, check a 7-day Lille score (assesses bilirubin change). A Lille >0.45 (poor response) → stop steroids; a Lille ≤0.45 → continue the 4-week course. Concurrently treat any cirrhosis complications (e.g. diuretics & paracentesis for ascites, beta-blockers and endoscopy for varices, lactulose for encephalopathy). For end-stage ALD, arrange evaluation for liver transplant once sobriety is established (typically ≥6 months).

1. Complete abstinence from alcohol – the single most important intervention (can stabilize or improve early disease). Provide nutritional support (high-protein diet if no encephalopathy) and replace vitamins (thiamine, folate, etc.).
2. Corticosteroids for severe alcoholic hepatitis (if DF ≥32 or MELD ≥20): e.g. prednisolone 40 mg daily for 4 weeks. Must first rule out active infection or GI bleeding (contraindications). If steroids contraindicated or not effective, use pentoxifylline (400 mg TID × 4 weeks) as an alternative (modest benefit).
3. Manage cirrhosis complications: Nonselective β-blockers (e.g. nadolol) and periodic endoscopic banding to prevent variceal hemorrhage; diuretics (spironolactone ± furosemide) and paracentesis for ascites; lactulose (plus rifaximin) for encephalopathy, etc. Screen for HCC every 6 months. Consider liver transplant for end-stage alcoholic cirrhosis, typically after ≥6 months of documented sobriety.

• AST > ALT (~2:1) in Alcoholic liver damage (think "A Scotch and Tonic" for AST) – contrast with viral hepatitis (ALT tends to be higher). Alcohol causes vitamin B6 depletion, limiting ALT elevation.
• Mallory bodies (eosinophilic Mallory–Denk hyaline inclusions) are classically associated with alcoholic hepatitis. They represent tangled intermediate filaments in hepatocytes and also appear in other diseases (e.g. NASH, Wilson's).
• Chronic alcohol use often raises GGT (gamma-glutamyl transferase) and causes macrocytosis (↑MCV) on CBC – useful lab clues pointing to alcohol as the etiology.

• Any signs of decompensation in ALD: new-onset tense ascites (risk of SBP), variceal GI bleeding (hematemesis), or encephalopathy (confusion, asterixis) indicate severe disease and warrant urgent evaluation.
• Severe alcoholic hepatitis with jaundice and coagulopathy (e.g. INR >1.5) plus hepatic encephalopathy signifies a high risk of liver failure and death (high short-term mortality) – ICU care and specialist intervention needed.

1. Chronic heavy alcohol use + abnormal LFTs (AST > ALT) → suspect ALD. Take a thorough alcohol history and obtain labs (AST, ALT, bilirubin, INR, CBC, metabolic panel).
2. Exclude other etiologies: test viral hepatitis panel; perform abdominal ultrasound to rule out biliary obstruction or masses. If diagnosis remains uncertain, consider liver biopsy (careful if coagulopathic).
3. If alcoholic hepatitis is present (e.g. patient with jaundice): calculate severity scores (Maddrey DF, MELD). Severe cases (DF ≥32 or MELD ~≥20) → begin steroid therapy, provided no infection or bleeding is ongoing.
4. Provide aggressive supportive care throughout: IV fluids, correct electrolytes, nutritional support (enteral feeding if needed), and prevent alcohol withdrawal (use benzodiazepines like lorazepam if high risk). Treat intercurrent infections promptly (frequent in severe ALD).
5. Reassess in 1 week if on steroids (compute Lille score). If Lille >0.45 (poor response) → stop steroids. If improving, continue full 4-week course. Ensure plans for long-term abstinence (rehab, support groups) and follow closely. Refer for transplant evaluation in patients with end-stage disease once a period of sobriety is achieved.

• Middle-aged patient with long-term heavy drinking found to have mildly elevated LFTs (AST 150, ALT 70; AST:ALT ~2:1) and an elevated GGT → suggests alcoholic fatty liver disease.
• Patient after a binge presents with painful hepatomegaly, fever, and new jaundice → acute alcoholic hepatitis (look for AST ~2× ALT and neutrophils on biopsy with Mallory bodies).
• Known alcoholic with cirrhosis develops hematemesis and melena → likely variceal bleed from portal hypertension (common in alcoholic cirrhosis). Another scenario: chronic drinker with confusion and asterixis → think hepatic encephalopathy due to decompensated ALD.