Alcoholic hepatitis

Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake of alcohol. While distinct from cirrhosis, it is regarded as the earliest stage of alcoholic liver disease. Symptoms are jaundice, ascites (fluid accumulation in the abdominal cavity), fatigue and hepatic encephalopathy (brain dysfunction due to liver failure). Mild cases are self-limiting, but severe cases have a high risk of death. Severe cases may be treated with corticosteroids.

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Symptoms and signs

Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.

Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C. The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis in Western countries.

Some alcoholics get an acute hepatitis or inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.

Diagnosis

The ratio of aspartate aminotransferase to alanine aminotransferase is usually > 2.^[1]

Pathophysiology

Some signs and pathological changes in liver histology include:

• Mallory's Hyaline - a condition where pre-keratin filaments accumulate in hepatocytes. This sign is not limited to alcoholic liver disease, but is often characteristic.^[2]
• Ballooning degeneration - hepatocytes in the setting of alcoholic change often swell up with excess fat, water and protein; normally these proteins are exported into the bloodstream. Accompanied with ballooning, there is necrotic damage. The swelling is capable of blocking nearby biliary ducts, leading to diffuse cholestasis.^[2]
• Inflammation - Neutrophilic invasion is triggered by the necrotic changes and presence of cellular debris within the lobules. Ordinarily the amount of debris is removed by Kupffer cells, although in the setting of inflammation they become overloaded, allowing other white cells to spill into the parenchyma. These cells to hepatocytes with Mallory bodies.^[2]

If chronic liver disease is also present:

• fibrosis
• Cirrhosis - a progressive and permanent type of fibrotic degeneration of liver tissue.

Treatment/Management

Clinical practice guidelines by the American College of Gastroenterology recommend corticosteroids.^[3]

Corticosteroids

Patients with a discriminant function score > 32 or hepatic encephalopathy should be considered for treatment with prednisolone 40 mg daily for four weeks followed by a taper.^[3]

Pentoxifylline

A randomized controlled trial found that among patients with a discriminant function score > 32 and at least one of the following symptoms (palpable tender hepatomegaly, fever, leukocytosis, hepatic encephalopathy, or hepatic systolic bruit), 4.6 patients must be treated with pentoxifylline 400 mg orally 3 times daily for 4 weeks to prevent one patient from dying. ^[4]

References

1. ^ Sorbi D, Boynton J, Lindor KD (1999). "The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease". Am. J. Gastroenterol. 94 (4): 1018-22. PMID 10201476.
2. ^ ^{a b c} Cotran; Kumar, Collins. Robbins Pathologic Basis of Disease. Philadelphia: W.B Saunders Company. 0-7216-7335-X. 
3. ^ ^{a b} McCullough AJ, O'Connor JF (1998). "Alcoholic liver disease: proposed recommendations for the American College of Gastroenterology". Am. J. Gastroenterol. 93 (11): 2022-36. PMID 9820369.
4. ^ Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O (2000). "Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial". Gastroenterology 119 (6): 1637-48. doi:10.1053/gast.2000.20189. PMID 11113085. (ACP Journal Club synopsis)

See also

Biliary tree (Cholangitis, Cholestasis/Mirizzi's syndrome, PSC, Biliary fistula, Ascending cholangitis)

Malabsorption (celiac, Tropical sprue, Blind loop syndrome, Whipple's)

postprocedural: Gastric dumping syndrome - Postcholecystectomy syndrome