Ethanol, mostly in
alcoholic beverages, is a significant cause of
hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption.
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.
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.
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.
[3]
★
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 are particularly attracted to hepatocytes with Mallory bodies.
[3]
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.
[5]
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.
Pentoxifylline
A randomized controlled trial found that 5 patients with a
discriminant function score > 32 and at least one of palpable tender hepatomegaly, fever, leukocytosis, hepatic encephalopathy, or hepatic systolic bruit
must be treated with
pentoxifylline 400 mg orally 3 times daily for 4 weeks for one to prevent one patient from dying.
[6]
References
1. The ratio of aspartate aminotransferase to alanine aminotransferase: potential value in differentiating nonalcoholic steatohepatitis from alcoholic liver disease, Sorbi D, Boynton J, Lindor KD, , , Am. J. Gastroenterol., 1999
2. Robbins Pathologic Basis of Disease, , , Cotran, W.B Saunders Company, , 0-7216-7335-X
3.
4.
5. Alcoholic liver disease: proposed recommendations for the American College of Gastroenterology, McCullough AJ, O'Connor JF, , , Am. J. Gastroenterol., 1998
6. Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial, Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O, , , Gastroenterology, 2000 (ACP Journal Club synopsis)
See also
External links