- Descriptions
- NAFLD: non-alcohol related accumulation of fat in the liver cells
- NASH: NAFLD with chronic inflammation and damage of liver cells
- Epidemiology: very widespread
- Etiology
- Obesity and/or type 2 diabetes (metabolic syndrome)
- Due to excess supply of nutrients in the liver
- Obesity and/or type 2 diabetes (metabolic syndrome)
- Pathophysiology: ↑ Insulin resistance
- ↑ Hepatic uptake of fatty acids
- Essentially, insulin resistance creates a situation where fat storage in the designated areas (fat cells) is impaired, causing the liver to take on an excess burden of processing these fatty acids.
- ↑ Triglyceride synthesis
- ↑ Peripheral lipolysis
- ↑ Hepatic uptake of fatty acids
- Clinical features
- Often asymptomatic
- Hepatomegaly
- May progress to cirrhosis
- Diagnostics
- Initial: RUQ Ultrasound (shows hyperechoic/bright liver, posterior acoustic attenuation). c
- Key Labs:
- Mildly elevated transaminases (ALT > AST; ratio < 1).
- Alk Phos and GGT may be mildly elevated.
- Exclude significant alcohol use (< 20 g/day for women, < 30 g/day for men).
- Non-invasive staging: Transient elastography (FibroScan) or NAFLD Fibrosis Score to assess for advanced fibrosis.
- Confirmatory/Gold Standard: Liver biopsy (shows macrovesicular steatosis; progress to NASH/MASH shows hepatocyte ballooning, lobular inflammation, +/- Mallory-Denk bodies). Note: Rarely performed unless diagnosis is uncertain, or staging is critical.
Mnemonic
There is more ALT than AST (AST/ALT < 1) if the Liver is infiltrated with Lipids.
- Pathology
- Hepatocellular lipid accumulation, mostly macrovesicular