Alcoholic hepatitis is hepatitis due to excessive intake of alcohol. It is
usually found in association with fatty liver, an early stage of alcoholic liver
disease, and may contribute to the progression of fibrosis, leading to
cirrhosis. Signs and symptoms of alcoholic hepatitis include jaundice,
ascites, fatigue and hepatic encephalopathy. Mild cases are
self-limiting, but severe cases have a high risk of death. Severe cases may be
treated with glucocorticoids. Signs and symptoms
Alcoholic hepatitis is characterized by a myriad of symptoms, which may include
feeling unwell, enlargement of the liver, development of fluid in the
abdomen, and modest elevation of liver enzyme levels. Alcoholic hepatitis can
vary from mild with only liver enzyme elevation to severe liver inflammation
with development of jaundice, prolonged prothrombin time, and even liver
failure. Severe cases are characterized by either obtundation or the combination
of elevated bilirubin levels and prolonged prothrombin time; the
mortality rate in both severe 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. Some alcoholics develop acute hepatitis as an
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 diagnosis is made in a patient with
history of significant alcohol intake who develops worsening liver function
tests, including elevated bilirubin and aminotransferases. The ratio of
aspartate aminotransferase to alanine aminotransferase is usually 2 or more.
In most cases, the liver enzymes do not exceed 500. The changes on liver biopsy
are important in confirming a clinical diagnosis.
Pathophysiology Some signs and pathological changes in
liver histology include: Mallory's hyaline body - a condition
where pre-keratin filaments accumulate in hepatocytes. This sign is not limited
to alcoholic liver disease, but is often characteristic.
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. 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. If chronic liver disease is also
present: Fibrosis
Cirrhosis - a progressive and permanent type of fibrotic degeneration of liver
tissue. Treatment and management
Clinical practice guidelines by the American College of Gastroenterology
have recommended corticosteroid treatment. Patients should be risk
stratified using a MELD Score or Child-Pugh score.
Corticosteroids: These guidelines suggest that patients with a modified
Maddrey's 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 among patients with a discriminant function score > 32 and at
least one of the following symptoms, 4.6 patients must be treated with
pentoxifylline for 4 weeks to prevent one patient from dying. Subsequent
trials have suggested that pentoxifylline may be superior to
prednisolone in the management of acute alcoholic hepatitis with discriminant
function score >32. Advantage of pentoxifylline over prednisolone was
better tolerability, lesser side effects, with decreased occurrence of
renal dysfunction in patients receiving pentoxifylline.
Potential for combined therapy: A large prospective study of over 1000 patients
investigated whether prednisolone and pentoxifylline produced benefits when
used alone or in combination. Pentoxifylline did not improve survival
alone or in combination. Prednisolone gave a small reduction in mortality at
28 days but this did not reach significance, and there were no
improvements in outcomes at 90 days or 1 year.
See also AST/ALT ratio
Steatohepatitis References