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Liver and intrahepatic bile ducts-nontumor

Hepatitis - noninfectious

Alcoholic hepatitis and alcoholic liver disease

Reviewers: Komal Arora, M.D. (see Reviewers page)
Revised: 28 April 2012, last major update April 2012
Copyright: (c) 2004-2012, PathologyOutlines.com, Inc.


● U.S. has 10 million alcoholics, 200,000 alcohol related deaths/year, 25% of hospitalized patients have problems related to alcohol abuse
● Alcohol is largest single cause of liver failure in US; damage affected by duration and quantity of consumption and patient’s genetic makeup
● 8 beers/day causes reversible fatty liver; 16 beers/day for 10 years is associated with severe injury
● Alcohol related liver disease consists of hepatic steatosis (50%), alcoholic hepatitis (20%) and cirrhosis (10%); 20% have other liver pathology, including Hepatitis C infection
Alcoholic cirrhosis: only 10% of alcoholics develop cirrhosis
● May develop without steatosis or alcoholic hepatitis
● Resembles cirrhosis from other causes
● Women are more susceptible to hepatic injury than men
Symptoms of alcoholic hepatitis: acute onset, usually after heavy drinking
● Variable symptoms ranging from none to acute hepatic failure; may have acute cholestatic syndrome
● 10% risk of death with each bout of hepatitis, cirrhosis in 1/3 within a few years with repeated bouts
● Hepatitis may persist and progress even with abstinence
5 year survival: 90% in abstainers without jaundice, ascites or hematemesis vs. 50% if continue to drink
● Death due to hepatic coma, GI bleed, infection, hepatorenal syndrome after bout of alcoholic hepatitis, hepatocellular carcinoma (3%)
● Sudden death may be due to abnormality in heart conduction system (Arch Pathol Lab Med 2001;125:21)
Fibrosis: initially sinusoidal and perivenular; periportal fibrosis may predominate with repeated bouts of heavy alcohol intake
Alcoholic cirrhosis: final and irreversible form of alcoholic liver disease
● Initially cirrhotic liver is yellow, fatty, enlarged (> 2 kg); eventually becomes brown, shrunken, nonfatty, < 1 kg
● Initial fibrous septa are delicate, regenerative micronodules; nodules then become larger and have hobnail appearance on hepatic surface, and bands of fibrous tissue become wider
Laennec cirrhosis: broad expanses of tough, pale scar tissue due to ischemic necrosis and fibrous obliteration of nodules
● Also bile stasis; Mallory’s hyaline rare


● Alcohol consumption results in translocation of gut bacteria into the portal system along with lipopolysaccharides that interact with toll-like receptors, and results in production of inflammatory and immunogenic mediators such as tumor necrosis factor-α and interferons (World J Hepatol 2011;3:114)
● Alcohol consumption causes shunting of normal substrates away from catabolism and toward lipid biosynthesis due to (a) excess NADH generation from alcohol dehydrogenase and acetaldehyde dehydrogenase, (b) impaired assembly/secretion of lipoproteins and (c) increased peripheral fat catabolism
● P450 induction causes other drugs to be transformed to toxic metabolites; free radicals, from microsomal oxidation of alcohol, damage proteins and membranes
● Alcohol directly affects microtubular and mitochondrial function, also induces immunologic attack on hepatic neoantigens
● Acetaldehyde (alcohol metabolite) causes lipid peroxidation and acetaldehyde-protein adduct formation
● Collagen deposition by perisinusoidal hepatic stellate (Ito) cells is due to Kupffer cell activation (release of TNF-alpha, IL1/6, TGF-beta), platelet-activating factor, influx of neutrophils into parenchyma
● Alcohol also causes derangements of vascular perfusion


● Corticosteroids and pentoxifylline (World J Hepatol 2011;3:205); alcohol abstinence

Gross description

● Initially liver is 4-6 kg, yellow, greasy, easily fractured
● Later liver becomes red with bile-stained areas
● May contain visible nodules and fibrosis

Micro description

Early - hepatocyte swelling and necrosis, macrovesicular fatty change due to triglyceride in centrilobular area, Mallory’s hyaline with surrounding neutrophils
● Also portal lymphocytes (40%, even without hepatitis B/C, Hum Pathol 2002;33:1170) and macrophages
● Reversible macrovesicular steatosis occurs after moderate alcohol intake, fibrosis may develop late around central veins and extend into parenchyma (sclerosing hyaline necrosis, highlighted with trichrome stain)
● May have marked cholestatic features or giant mitochondria that appear as globular eosinophilic hyaline inclusions larger than hepatocyte nuclei

Micro images

Macro and microsteatosis, Mallory bodies

Mallory bodies

Fat stain (osmium tetraoxide)

Electron microscopy description

● Giant mitochondria

Differential diagnosis

● Jejunoileal bypass, drug reactions, nonalcoholic steatohepatitis, megamitochondria (resemble Mallory’s hyaline but coarsely granular and more regular in contour, and trichrome stains them red)

Additional references

Clin Liver Dis 2005;9:37, N Engl J Med 2009;360:2758

End of Liver and intrahepatic bile ducts-nontumor > Hepatitis - noninfectious > Alcoholic hepatitis and alcoholic liver disease

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