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Hepatic steatosis, commonly known as fatty liver, is the accumulation of triglycerides within hepatocytes exceeding 5% of liver weight or >5% of hepatocytes on histology.

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It represents a spectrum ranging from simple steatosis to steatohepatitis (NASH) and can progress to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC).

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Etiopathogenesis

1. Major Causes

• Alcoholic liver disease (ALD) – chronic excessive ethanol intake.
• Non-alcoholic fatty liver disease (NAFLD) – associated with:
  • Obesity, diabetes mellitus, metabolic syndrome, dyslipidemia, insulin resistance.
  • Drugs: corticosteroids, methotrexate, tamoxifen, amiodarone.
  • Rapid weight loss, parenteral nutrition.
• Other causes: Viral hepatitis (esp. HCV genotype 3), Wilson’s disease, pregnancy (AFLP).

2. Pathogenesis

• Imbalance between lipid acquisition (increased uptake and de novo synthesis) and lipid disposal (oxidation and export as VLDL).
• Insulin resistance plays a central role in NAFLD.
• Two-hit hypothesis:
  1. First hit – steatosis due to fat accumulation.
  2. Second hit – oxidative stress, cytokine release → inflammation → fibrosis (NASH).

Clinical Features

• Often asymptomatic, detected incidentally on imaging.
• Non-specific symptoms: fatigue, vague right upper quadrant discomfort.
• Physical findings: hepatomegaly, signs of metabolic syndrome.