Hepatitis

Hepatitis: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter

Susan C. Cullom

Viral hepatitis is the most common cause of liver disease in the world. In the United States, more than 300,000 cases of acute viral hepatitis occur annually. Hepatitis B and C give rise to chronic hepatitis, with 5 million cases worldwide (1). In addition to the six hepatitis viruses (A,B,C,D,E,G) identified to date (2), multiple other causes of hepatitis exist: viruses (e.g., cytomegalovirus, Epstein-Barr, coxsackie virus), alcohol, drugs, and biliary tract disease. Drug-induced disease accounts for approximately 10% of hepatitis cases among all adult patients and for more than 40% of cases among patients aged more than 50 years (3).

Approach

 The important tasks in the diagnosis are to identify infectious causes, so as to limit infectivity through appropriate precautions, and to identify those patients with fulminant hepatitis from noninfectious causes in an attempt to limit their morbidity (4). Hepatitis can be classified into five broad categories:

 A. Viral

B. Drug-induced

C. Alcoholic

D. Chronic

E. Autoimmune

History

Patients may complain of anorexia, fever, arthralgia, malaise, vomiting, diarrhea, or chills. Complaints of dark urine or jaundice are highly suggestive of hepatitis. As these symptoms are seen in many types of hepatitis, specific questions help categorize the cause.

 A. Viral hepatitis. Does the patient have exposure to blood (transfusions before 1990, tattoos, body piercing, shared razor, needlestick, sharing needles, intranasal cocaine use)? Hepatitis B is most commonly transmitted via contaminated blood or sexually via risky sexual behaviors (anal intercourse, prostitution, multiple sexual partners). Hepatitis A and E are transmitted via the fecal-oral route. Does the patient have a history of travel to developing countries, raw shellfish ingestion, or work in an institution or daycare?

 B. Drug-induced hepatitis. Does the patient use prescription or over-the-counter medication? The drugs most often associated with hepatitis are anesthetics (halothane), neuropsychotropics (chlorpromazine, haloperidol, tricyclics), anticonvulsants (phenytoin), analgesics (acetaminophen, ibuprofen), antigout (allopurinol), hormonal derivatives and drugs used in endocrine disease (glipizide, tamoxifen, anabolic steroids, oral contraceptives), antimicrobials (tetracyclines), cardiovascular drugs (amiodarone, procainamide), antineoplastic (cisplatin), vitamin A, propoxyphene, cimetidine, and ferrous sulfate.

 C. Alcoholic hepatitis. Could the patient be an alcoholic? Inquire about quantitative alcohol intake and obtain a history from both patient and family members. Use the CAGE questionnaire to help identify individuals at high risk. Inquire about alcohol-associated illnesses (pancreatitis) and motor vehicle citations.

 D. Chronic hepatitis. Has the patient ever been jaundiced or diagnosed with hepatitis before (Chapter 9.10)? Has the patient had elevated liver enzymes for at least 6 months? The most common cause of chronic hepatitis and cirrhosis is alcohol. Viral hepatitis B and C often cause chronic hepatitis, cirrhosis, or hepatocellular carcinoma. Other causes of chronic hepatitis are drug-induced, Wilson’s disease, and α₁-antitrypsin deficiency.

E. Autoimmune hepatitis. Is there a history of arthritis, amenorrhea, or rash? Mediated by the deposition of circulating immune complexes, this disease is also referred to as “chronic active hepatitis.” It is more common in female patients and adolescents; prior hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is a triggering factor.

Physical examination

 A. General examination. Common findings in viral, alcoholic, or drug-induced hepatitis include fever, jaundice, scleral icterus, weight loss, muscle tenderness or weakness, and a palpable tender liver. Ecchymosis or petechiae indicates significant clotting factor abnormalities and, coupled with a small liver which diminishes in size, is suggestive of severe hepatitis or impending hepatic failure.

 B. Chronic liver disease results in progressive liver dysfunction, fluid retention, and portal hypertension. The liver plays a key role in the detoxification of endogenous hormones, drugs, and ingested substances. Abnormalities in estrogen metabolism have often been considered the cause of peripheral stigmata such as spider angiomata, palmar erythema, gynecomastia, parotid enlargement, and testicular atrophy.

 C. Does the abdominal examination reveal hepatosplenomegaly? Modest enlargement of the liver occurs in acute viral and chronic hepatitis, whereas marked enlargement (>10 cm below the costal margin) is seen in alcoholic hepatitis. Ascites, prominent abdominal collateral veins, bruits, rubs, abdominal masses, or a palpable gallbladder can also indicate hepatitis, whereas a small liver can indicate cirrhosis.

Testing

Laboratory tests differentiate between hepatocellular disorders (e.g., viral hepatitis) and cholestatic syndromes (e.g., primary biliary cirrhosis and bile duct obstruction).

 A. Liver function tests (LFTs)

1. Elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are nonspecific indicators of hepatocellular damage and do not distinguish viral from drug-induced hepatitis. Alcoholic liver disease is suggested when the AST:ALT ratio is greater than 2:1.

2. Total serum bilirubin is not a sensitive indicator of hepatic dysfunction. Hepatitis impairs the excretion phase of bilirubin metabolism, resulting in an elevated direct (conjugated) bilirubin greater than 0.1 mg/dl.

 3. γ-Glutamyl transpeptidase (GGT) is a very sensitive indicator for minimal hepatocellular damage. Elevations are seen in alcoholic liver disease before other LFTs are abnormal.

 4. Alkaline phosphatase indicates cholestasis or obstruction. Approximately 75% of patients with prolonged cholestasis have alkaline phosphatase values increased fourfold or greater.

 5. Immunoglobulins (IgA, IgG, IgM) in acute hepatitis are normal or minimally increased. A moderate increase is seen in chronic active or autoimmune hepatitis. Indices are useful in monitoring response to immunotherapy.

 6. Circulating autoantibodies (e.g., antinuclear, smooth muscle, liver-kidney microsomal) may be seen in autoimmune hepatitis.

 B. Hepatitis serology. Serologic testing (anti-HDV, anti-HCV) is now available for each type, except hepatitis E virus (HEV) (5) (Fig. 9.1). Hepatitis G virus (HGV) and GB virus C (GBV-C) are the most recently discovered hepatitis viruses (2). HGV is present in asymptomatic blood donors and, although it is thought to cause chronic hepatitis, no causal relationship between HGV and hepatitis has been convincingly established (3).

C. Radiologic and diagnostic procedures

1. Abdominal films are useful in detecting splenomegaly.

2. Ultrasound is helpful in detecting gallstones in patients with jaundice and in detecting mass lesions (tumors or liver abscesses).

3. Abdominal computerized tomography aids in the diagnosis of mass lesions of the liver and abnormalities of the gallbladder.

4. Percutaneous needle biopsy of the liver permits an accurate diagnosis of diffuse parenchymal disorders such as hepatitis, drug reaction, cirrhosis, and liver tumors.

Diagnostic assessment

 Viral hepatitis can be diagnosed by a thorough history and serology used in tandem. Individual susceptibility to hepatic injury in drug-induced hepatitis can be affected by genetic factors, age, gender, nutritional status, exposure to other drugs and chemicals, systemic disease, and other factors (4). Liver injury produced by drugs is either cytotoxic (hepatocellular), cholestatic, or a combination of the two. Knowledge of these mechanisms is extremely important in diagnosing the inciting agent. Alcoholic hepatitis is identified by the history coupled with the typical laboratory abnormalities. Chronic hepatitis requires elevated LFTs for at least 6 months and can result from infection with HBV or HCV, alcoholic liver disease, drug toxicity, or autoimmune causes. Liver biopsy is required for accurate assessment and classification of chronic hepatitis. Although effective vaccines are available for HAV and HBV and have yielded protection for decades, vaccines for HCV and HEV are only in early development and no vaccine exists for HDV.

References

1. Schiff ER, Sorrell MF, Maddrey WC. Diseases of the liver, 8th ed. Philadelphia:
Lippincott Williams & Wilkins, 1999:234–235, 919–921.

2. Blum HE. Update hepatitis A-G. Digestion 1997;58(Suppl 1):33–36.

3. Zimmerman HJ. General aspects of drug-induced liver disease. Gastroenterol Clin North Am 1995;24:739–757.

4. Kools AM. Hepatitis A,B,C,D, and E. Update on testing and treatment. Postgrad Med 1992;91:109–114.

5. Schiff ER. Update in hepatology. Ann Intern Med 1999;130:52–59.

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Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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