Pathology · Year 2 · from Pathology
Case 2: Alcoholic Fatty Liver Disease (Steatosis)
Patient Demographics
- Age: 48 years old
- Sex: Male
- Occupation: Restaurant owner
Chief Complaint
"My doctor said my liver tests are abnormal"
History of Present Illness
A 48-year-old male is referred to hepatology after routine blood work revealed elevated liver enzymes. He reports drinking 4-6 beers daily for the past 20 years, with occasional binge drinking on weekends. He denies jaundice, abdominal pain, or abdominal distension. He has noticed some fatigue and mild right upper quadrant discomfort after eating fatty foods.
Physical Examination
- Vital Signs: BP 138/88 mmHg, HR 78 bpm, BMI 31 kg/m²
- General: Overweight male, no acute distress
- Abdomen: Soft, mild hepatomegaly (liver edge 3 cm below costal margin), non-tender, no splenomegaly, no ascites
- Skin: No spider angiomata, no palmar erythema
- Extremities: No edema
Diagnostic Workup
Laboratory Studies:
| Test | Result | Reference Range |
|---|---|---|
| AST | 85 U/L | 10-40 U/L |
| ALT | 52 U/L | 7-56 U/L |
| AST:ALT ratio | 1.6:1 | - |
| GGT | 180 U/L | 8-61 U/L |
| Alkaline phosphatase | 95 U/L | 44-147 U/L |
| Total bilirubin | 1.1 mg/dL | 0.1-1.2 mg/dL |
| Albumin | 3.9 g/dL | 3.5-5.5 g/dL |
| Platelets | 195,000/µL | 150,000-400,000/µL |
Imaging:
- Ultrasound: Hepatomegaly with increased echogenicity ("bright liver"), consistent with hepatic steatosis
- FibroScan: Liver stiffness 7.2 kPa (mild fibrosis, F1)
Liver Biopsy:
- Macrovesicular steatosis affecting >60% of hepatocytes
- Large fat droplets displacing nuclei peripherally
- Minimal inflammation, no Mallory-Denk bodies
- Mild perisinusoidal fibrosis
Pathology Correlation
This case demonstrates reversible cell injury manifesting as fatty change (steatosis):
- Mechanism: Alcohol metabolism produces excess NADH, shifting metabolism toward lipid synthesis and inhibiting fatty acid oxidation
- Morphology: Macrovesicular steatosis with large, clear vacuoles pushing the nucleus to the cell periphery
- Reversibility: Steatosis is completely reversible with alcohol cessation
- Progression risk: Without abstinence, may progress to alcoholic hepatitis and cirrhosis
Clinical Image
Liver biopsy showing macrovesicular steatosis. Hepatocytes contain large clear vacuoles (lipid droplets) that displace the nucleus to the cell periphery. This represents reversible cell injury.
Image Source: Wikimedia Commons - "Fatty liver" License: CC BY-SA 3.0 URL: https://commons.wikimedia.org/wiki/File:Non-alcoholic_fatty_liver_disease1.jpg
Diagnosis
Alcoholic Fatty Liver Disease (Steatosis) with mild fibrosis
Treatment
- Alcohol cessation (primary intervention)
- Nutritional counseling and weight management
- Thiamine supplementation
- Referral to addiction medicine/counseling
- Follow-up liver function tests in 3 months
- Hepatitis A and B vaccination
Teaching Points
- Fatty change is a manifestation of reversible cell injury
- The AST:ALT ratio >2:1 is characteristic of alcoholic liver disease
- Steatosis results from imbalance between lipid uptake/synthesis and export
- Intracellular accumulations represent a form of sublethal cell injury
- Early intervention with abstinence can prevent progression to irreversible injury