Steatosis (NAFLD / NASH)
Formal Definition
Hepatic steatosis — the accumulation of fat (triglycerides) in hepatocytes exceeding 5% of liver weight, broadly categorized as non-alcoholic fatty liver disease (NAFLD, now reclassified as metabolic dysfunction-associated steatotic liver disease / MASLD) when not due to alcohol or other causes; non-alcoholic steatohepatitis (NASH / MASH) is the inflammatory subtype with hepatocyte ballooning and fibrosis that can progress to cirrhosis, hepatocellular carcinoma, and liver-related death.
How It's Used on the Ward
"Fatty liver" — the patient's liver imaging or biopsy shows fat accumulation; the spectrum ranges from benign steatosis (reversible with weight loss) to NASH with active inflammation and fibrosis (progresses to cirrhosis); commonly diagnosed incidentally on imaging or elevated LFTs.
Example
""52-year-old man with obesity (BMI 34), type 2 diabetes, hypertriglyceridemia, found to have ALT 78 / AST 62 on routine labs. Abdominal ultrasound: increased hepatic echogenicity consistent with hepatic steatosis. FIB-4 score 1.8. Diagnosis: presumed NAFLD/MASLD with intermediate fibrosis risk. Recommended: weight loss 7-10%, GLP-1 agonist for diabetes and steatosis, repeat FIB-4 in 1 year, consider transient elastography if not improving.""
Clinical Context
Spectrum: simple steatosis → NASH/MASH (inflammation + injury) → fibrosis (stages F0-F4) → cirrhosis → hepatocellular carcinoma. Diagnosis: usually clinical + imaging (US, CT, MRI-PDFF for quantification). Biopsy remains gold standard for NASH diagnosis but rarely done due to invasiveness. Non-invasive fibrosis assessment: FIB-4 score (age, AST, ALT, platelets), NAFLD fibrosis score, transient elastography (FibroScan), MR elastography. Causes of secondary hepatic steatosis: alcohol (>20g/day women, >30g/day men), hepatitis C (genotype 3), medications (methotrexate, amiodarone, tamoxifen, valproate), Wilson disease, rapid weight loss, total parenteral nutrition. Treatment: weight loss (7-10% improves steatosis and inflammation), GLP-1 agonists (semaglutide, tirzepatide — strong evidence for MASH resolution), pioglitazone, vitamin E (caution: increased hemorrhagic stroke risk at high dose), resmetirom (newly approved THR-β agonist for MASH). Avoid: alcohol, hepatotoxic drugs. HCC surveillance: once cirrhosis develops (US + AFP q6 months).