Alcohol-Associated Liver Disease (ALD) 1. Background Defin…
Alcohol-Associated Liver Disease (ALD) 1. Background Definition: Spectrum of liver injury due to chronic alcohol use — fatty liver → alcoholic hepatitis → cirrhosis. Pathophysiology: Alcohol → ↑NADH/NAD⁺ ratio → impaired fatty acid oxidation → steatosis. Acetaldehyde causes oxidative stress, mitochondrial injury, and inflammation. Chronic exposure leads to fibrosis and portal hypertension. Epidemiology: Second most common cause of cirrhosis in the U.S. Risk rises with intake >40–60 g/day in men, >20–40 g/day in women. Synergistic injury with obesity or viral hepatitis. 2. History Symptoms: Early: fatigue, anorexia, nausea, or vague RUQ pain. Advanced: jaundice, pruritus, edema, abdominal distension, confusion (encephalopathy). Risk factors: Long-term heavy alcohol use, poor nutrition (especially folate, thiamine). Coexistent hepatitis C or metabolic syndrome accelerates damage. Alcohol timeline: Steatosis can appear after weeks of heavy intake; hepatitis requires sustained use; cirrhosis follows years of abuse. 3. Exam Findings General: Fever (alcoholic hepatitis), cachexia, jaundice. Skin: Spider angiomas, palmar erythema, ecchymoses. Abdomen: Hepatomegaly (early), splenomegaly, ascites, caput medusae. Neurologic: Asterixis, confusion, tremor (encephalopathy). Endocrine: Gynecomastia, testicular atrophy, menstrual irregularities. 4. Diagnosis A. Laboratory Findings Stage Typical Findings Steatosis Mild ↑AST/ALT (2 : 1 (values 100 fL) common due to folate deficiency. AST > ALT hallmark due to mitochondrial damage. B. Imaging Ultrasound: Fatty infiltration, nodular liver, splenomegaly, ascites. Elastography: Estimates fibrosis. CT/MRI: Excludes alternate causes or HCC. C. Severity Scoring (Alcoholic Hepatitis) Maddrey Discriminant Function (MDF): ≥32 → severe disease. MELD or Lille score guide prognosis and treatment response. D. Differential Diagnosis Viral hepatitis, drug-induced injury, hemochromatosis, MAFLD, autoimmune hepatitis. 5. Management A. Alcohol Cessation (Essential) Abstinence halts progression and can reverse steatosis. Refer to counseling, behavioral therapy, and pharmacologic support (acamprosate, naltrexone, disulfiram). B. Nutritional Support High-protein, high-calorie diet; supplement thiamine, folate, and zinc. Correct electrolyte abnormalities. C. Specific Therapy (Alcoholic Hepatitis) Corticosteroids (prednisolone 40 mg/day × 28 days) if MDF ≥ 32 or MELD ≥ 20 and no infection. Pentoxifylline if steroids contraindicated. Treat concurrent infections before starting steroids. D. Cirrhosis Management Complication Key Treatment Ascites Sodium restriction, spironolactone ± furosemide, paracentesis Varices Nonselective β-blockers, endoscopic band ligation Encephalopathy Lactulose ± rifaximin HCC screening Ultrasound ± AFP every 6 months E. Advanced Disease Liver transplant for end-stage cirrhosis; many centers require ≥6 months sobriety. F. Prevention Routine screening for alcohol misuse. Vaccinate against HAV and HBV. Address comorbid obesity, diabetes, and viral hepatitis. A 54-year-old man presents with two weeks of fatigue, jaundice, and right upper quadrant discomfort. He drinks approximately six beers daily and has done so for 20 years. Laboratory results: Test Result Reference Range AST 180 U/L (10–40 U/L) ALT 75 U/L (7–56 U/L) Alkaline phosphatase 130 U/L (44–147 U/L) Total bilirubin 4.2 mg/dL (0.2–1.2 mg/dL) INR 1.8 (0.8–1.2) MCV 104 fL (80–96 fL) Which of the following findings is most characteristic of this patient’s condition?