Alcohol-associated liver disease
- Lesion
Heavy drinking first fills liver cells with fat, can then inflame and kill them, and over years leaves the liver scarred.
What it is
Alcohol-associated liver disease has three overlapping lesions: hepatocellular steatosis, alcoholic steatohepatitis (alcoholic hepatitis) and cirrhosis. Steatosis appears in most heavy drinkers and reverses with abstinence; steatohepatitis and cirrhosis develop in a minority, depending on amount and pattern of drinking, sex, genetics and coexisting obesity or viral hepatitis. Ethanol metabolism produces acetaldehyde, oxidative stress and an excess of NADH that shifts the liver toward fat synthesis.
Structure
- Steatosis: enlarged, soft, yellow, greasy liver; macrovesicular fat beginning around central veins.
- Steatohepatitis: ballooned hepatocytes with Mallory-Denk bodies, neutrophils (satellitosis), megamitochondria, cholestasis.
- Fibrosis: perivenular and pericellular collagen around single hepatocytes (chicken-wire), central vein sclerosis.
- Cirrhosis: shrunken brown liver with fine nodules (Laennec cirrhosis) that grow coarser over time.
Step by step
- Ethanol is oxidized by alcohol dehydrogenase, CYP2E1 and catalase to acetaldehyde, then to acetate.
- The excess NADH favours fatty acid synthesis and blocks their oxidation: fat accumulates.
- Acetaldehyde forms protein adducts and damages microtubules and mitochondria.
- CYP2E1 induction generates reactive oxygen species and lipid peroxidation.
- Gut-derived endotoxin activates Kupffer cells, which release TNF and IL-8: neutrophils attack hepatocytes.
- Stellate cells are activated, first around central veins and sinusoids, leading to cirrhosis.
The three lesions of alcohol-associated liver disease
| Lesion | Main features | Reversible? |
|---|---|---|
| Steatosis | Macrovesicular fat in zone 3, big yellow liver | Yes, with abstinence |
| Steatohepatitis | Ballooning, Mallory-Denk bodies, neutrophils, chicken-wire fibrosis | Partly; repeated episodes lead to scar |
| Cirrhosis | Micronodular, later mixed nodules; small brown liver | Largely no, though fibrosis may regress somewhat |
Clinical notes
- Death in advanced disease comes from liver failure, variceal bleeding, infection, hepatorenal syndrome and hepatocellular carcinoma.
- Alcohol use is a major cause of liver disease in Latin America; abstinence is the key to recovery.
Test yourself
Think of the answer, then tap the question to see it.
Why does alcohol cause fat to accumulate in hepatocytes?
Ethanol oxidation generates excess NADH, which favours fatty acid synthesis and inhibits their beta-oxidation; lipid export also falls.
What is chicken-wire fibrosis?
Pericellular and perisinusoidal collagen surrounding single hepatocytes or small groups, typical of steatohepatitis.
Which lesion of alcohol-associated liver disease is fully reversible?
Steatosis, which resolves with abstinence.
Which cell recruited by IL-8 is typical of alcoholic steatohepatitis?
The neutrophil, which surrounds damaged ballooned hepatocytes.
Elsewhere in DurgiPedia
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Alcoholic liver disease: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Alcohol (World Health Organization, 2026).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.