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Diagnosis of Alcoholic Liver Disease

Last updated on May 27, 2023

Clinical presentation

Alcoholic hepatitis is an acute or chronic illness associated with severe chronic alcoholism, involving extensive hepatocellular necrosis, inflammation, and scarring. It is extremely variable in clinical presentation and may be superimposed on other forms of alcoholic liver disease such as fatty liver and Laennec’s cirrhosis.

Diagnosis of Alcoholic Liver DiseaseAlcoholic liver disease may occur without any symptoms. The most common complaints in symptomatic patients with alcoholic hepatitis are anorexia, nausea, vomiting, and abdominal pain, especially in the right upper quadrant. Most patients lose weight due to anorexia and nausea. One fourth of patients have fever. Fever may be due to severe liver damage in the absence of an infection; however, infections should be excluded in these immunocompromised patients.

Jaundice, when present, is usually mild, but in 20% to 35% of the patients who present with a cholestatic picture, it is severe. Diarrhea and symptoms related to complications of portal hypertension such as ascites, peripheral edema, and esophageal varices are less common. Most patients with acute hepatitis have a tender and somewhat enlarged liver. Jaundice, splenomegaly, ascites, peripheral edema, spider angiomata, palmar erythema, parotid enlargement, gynecomastia, testicular atrophy, finger clubbing, and Dupuytren’s contractures may also be present.

Diagnostic studies

Laboratory studies

The most characteristic laboratory findings in acute alcoholic hepatitis are elevated serum transaminases and bilirubin. Serum glutamic-oxaloacetic transaminase, or aspartate aminotransferase) levels are usually two to ten times normal. Values greater than 500 U/L are rare. Serum glutamic-pyruvic transaminase or alanine aminotransferase) levels are also elevated, but they are increased less than serum glutamic-oxaloacetic transaminase levels. The reduced serum glutamic-pyruvic transaminase levels may be related to mitochondrial injury in alcoholic hepatitis. The serum glutamic-oxaloacetic transaminase/serum glutamic-pyruvic transaminase ratio in alcoholic hepatitis is usually greater than 1.

Serum alkaline phosphatase level is moderately elevated in at least one half of the patients. In patients presenting with a cholestatic picture, the elevation may be marked. Оі-Glutamyltranspeptidase activity is also often elevated in alcoholic hepatitis. This enzyme is quite sensitive for alcoholic injury.

Serum globulins are often increased, and, interestingly, IgA levels are disproportionately elevated compared to the other immunoglobulins.

Serum albumin levels may be normal initially in well-compensated and well-nourished patients but are usually decreased.

Because the liver is the main site of synthesis of the coagulation factors, in severely ill patients the prolongation of prothrombin time by greater than 7 to 10 seconds predicts a poor prognosis.

The hematologic parameters are usually abnormal in alcoholic hepatitis. Leukocytosis with a shift to the left is common. Anemia and thrombocytopenia are usually present. Aside from the fact that alcohol is toxic to the bone marrow, patients may have hypersplenism, disseminated intravascular coagulation, and bone marrow suppression from their acute and chronic disease state.

Other causes of liver injury should be ruled out by appropriate serologic tests and a careful drug history. Acetaminophen even in therapeutic doses may be toxic in alcoholic patients. Aspirin and acetaminophen levels may be helpful in selected patients.


Even though the diagnosis may be easily established in most patients from the history, physical examination, and blood work, it may be helpful in some patients, especially in those presenting with the picture of cholestasis, to obtain an abdominal ultrasound to rule out biliary tract disease, ascites, and the presence of hepatocellular carcinoma. Some patients may require computed tomography scan of the abdomen and endoscopic retrograde cholangiopancreatography.

Liver biopsy should be performed early in the course of the disease in most patients to confirm the diagnosis and to stage the severity of the liver injury. With deterioration of liver function (excessive prolongation of the prothrombin time or the presence of ascites), liver biopsy may not be possible later in the disease process.

Microscopic examination of the liver biopsy is essential for classification of the alcoholic injury with regard to steatosis, early fibrosis, alcoholic hepatitis, or Laennec’s cirrhosis. In patients with alcoholic hepatitis, pathologic features may include the following:

The hepatocellular necrosis is mainly centrilobular but may be panlobular. Hepatocytes in various stages of degeneration are usually present. Many hepatocytes are swollen, balloonlike, or vacuolated and often contain a fibrillar material or alcoholic hyalin called Mallory bodies. This cytoplasmic material, even though commonly seen in patients with alcoholic hepatitis, is not limited to this disease. It has also been reported in diseases such as hepatoma, Indian childhood cirrhosis, liver disease in patients with intestinal bypass surgery, obesity, diabetes, and drug reaction. Occasionally it is seen in primary biliary cirrhosis, primary sclerosing cholangitis, and Wilson’s disease.

The inflammatory exudate consists predominantly of polymorphonuclear leukocytes in addition to some mononuclear cells. Polymorphonuclear leukocytes are seen in portal tracts and sinusoids and are usually concentrated in areas of hepatocellular necrosis with or without alcoholic hyalin. In 50% to 75% of the cases, rosettes of polymorphonuclear leukocytes are seen around degenerating hepatocytes containing Mallory bodies. This finding constitutes the hallmark of the disease.

Fibrosis is usually extensive and seen early in the disease. It frequently surrounds the central veins and extends into the perisinusoidal areas. The stellate fibrosis often remains after inflammation resolves and leads to micronodular cirrhosis.

Fatty infiltration is commonly seen in patients with alcoholic hepatitis. The extent of steatosis depends on recent alcohol intake, dietary fat, and the concomitant presence of obesity or diabetes.

Severe cholestasis may be seen in one third of patients. In these patients, in addition to pericentral injury and scar formation, there is marked periportal necrosis, inflammation, and destruction of small bile ducts.

Hemosiderosis may be seen in some of these patients.

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