Gastrointestinal · Year 2 · from Gastrointestinal
Case 2: Non-Alcoholic Steatohepatitis (NASH) with Cirrhosis
Patient Presentation
Demographics: 58-year-old female
Chief Complaint: Fatigue, abdominal distension, and leg swelling for 3 months
History of Present Illness: The patient has experienced progressive fatigue, abdominal bloating, and bilateral leg swelling over the past 3 months. She has gained 15 pounds, mostly in her abdomen. She has noticed easy bruising. She has no history of alcohol abuse and denies IV drug use.
Past Medical History: Type 2 diabetes (12 years), hypertension, hyperlipidemia, obesity (BMI 38), obstructive sleep apnea
Medications: Metformin, lisinopril, atorvastatin
Social History: Never drinks alcohol, non-smoker
Physical Examination
- Vital Signs: BP 138/82 mmHg, HR 84 bpm
- General: Obese female with central adiposity
- HEENT: Mild scleral icterus
- Abdomen: Distended with shifting dullness (ascites), hepatomegaly, no splenomegaly initially detected due to body habitus
- Extremities: 2+ pitting edema bilaterally
- Skin: Multiple spider angiomata on chest, palmar erythema
Workup and Results
- Liver Function Tests: AST 68 U/L, ALT 52 U/L (AST:ALT ratio <1), ALP 145 U/L, Total bilirubin 2.8 mg/dL
- Albumin: 2.6 g/dL
- INR: 1.4
- Platelet Count: 98,000 (low, suggesting portal hypertension)
- HbA1c: 8.2%
- Hepatitis B and C Serologies: Negative
- Autoimmune Markers: ANA, ASMA negative; normal ceruloplasmin, ferritin/transferrin saturation
- FIB-4 Score: 4.8 (high, suggesting advanced fibrosis)
- Transient Elastography (FibroScan): 28 kPa (cirrhosis range)
- Abdominal Ultrasound: Nodular liver contour, splenomegaly, moderate ascites
Liver biopsy in NASH showing macrovesicular steatosis (large fat droplets displacing nuclei), ballooning hepatocyte degeneration, and early bridging fibrosis. These findings distinguish NASH from simple steatosis.
Image Source: Wikimedia Commons, CC BY-SA 3.0
Diagnosis
NASH-related Cirrhosis (Decompensated - Ascites)
Clinical Correlation
Non-alcoholic fatty liver disease (NAFLD/MASLD) exists on a spectrum from simple steatosis to steatohepatitis (NASH/MASH) to cirrhosis. NASH is distinguished by hepatocyte injury (ballooning degeneration) and inflammation in addition to steatosis. Risk factors align with metabolic syndrome: obesity, type 2 diabetes, dyslipidemia, and hypertension. NAFLD has become the most common liver disease worldwide and a leading indication for liver transplantation. The transition to decompensated cirrhosis (ascites, variceal bleeding, encephalopathy, jaundice) marks a significant prognostic threshold. Insulin resistance drives the pathophysiology through increased hepatic lipogenesis and oxidative stress.
Treatment
- Ascites management: Sodium restriction (<2g/day) + spironolactone (with furosemide if needed)
- Weight loss target 7-10% (improves histology even in cirrhosis)
- Optimize diabetes control (consider pioglitazone for NASH without decompensation)
- Statin continuation is safe and may be beneficial
- Consider GLP-1 receptor agonists (weight loss + potential hepatic benefit)
- Screen for esophageal varices (upper endoscopy)
- HCC surveillance: Ultrasound every 6 months
- Liver transplant evaluation given decompensation
- Vaccinations: Hepatitis A, Hepatitis B, pneumococcal, influenza