eMedicine Specialties > Gastroenterology > Liver

Hepatitis A: Differential Diagnoses & Workup

Author: Richard K Gilroy, MBBS, FRACP, Associate Professor, Medical Director of Liver Transplantation and Hepatology, Department of Internal Medicine, Kansas University Medical Center
Coauthor(s): Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Contributor Information and Disclosures

Updated: Aug 26, 2008

Differential Diagnoses

Budd-Chiari Syndrome
Cytomegalovirus
Hepatitis, Viral

Other Problems to Be Considered

Acute drug-induced liver injury (eg, Tylenol, ecstasy)
Acute HIV infection
Drug-induced hypersensitivity reactions (eg, sulfasalazine hypersensitivity)

Workup

Laboratory Studies

  • Anti–hepatitis A virus immunoglobulin M
    • The diagnosis of acute hepatitis A virus infection is based on serologic testing for IgM antibody to the hepatitis A virus. Test results for anti-hepatitis A virus IgM are positive at the time of onset of symptoms and usually accompany the first rise in alanine aminotransferase (ALT) level. This test is sensitive and specific, and the results remain positive for 3-6 months after the primary infection and for as long as 12 months in 25% of patients.
    • False-positive results are uncommon and should be considered in the event that anti-hepatitis A virus IgM persists.
    • IgM persists in patients with relapsing hepatitis for the duration of this pattern of disease.
  • Anti–hepatitis A virus immunoglobulin G
    • Anti-hepatitis A virus IgG appears soon after IgM and generally persists for many years.
    • The presence of anti-hepatitis A virus IgG in the absence of IgM indicates past infection or vaccination rather than acute infection.
    • IgG provides protective immunity.
  • Liver enzymes
    • Rises of levels in ALT and aspartate aminotransferase (AST) assays are sensitive for this disease. Levels may exceed values of 10,000 mIU/mL, with ALT levels generally greater than AST levels. Levels usually return to reference ranges over 5-20 weeks.
    • Rises in alkaline phosphatase accompany the acute disease and may progress during the cholestatic phase of the illness following the rises in transaminase levels.
  • Hepatic synthetic function
    • Bilirubin level rises soon after the onset of bilirubinuria and follows rises in ALT and AST levels. Levels may be impressively high and can remain elevated for several months; persistence beyond 3 months indicates cholestatic hepatitis A virus infection.
    • Older individuals have higher bilirubin levels.
    • Both direct and indirect fractions increase because of hemolysis, which often occurs in acute hepatitis A virus infection.
  • Modest falls in serum albumin level may accompany the illness.
  • Prothrombin time
    • Prothrombin time usually remains within or near the reference range. Significant rises should raise concern and support closer monitoring.
    • In the presence of encephalopathy, an elevated prothrombin time has ominous implications (eg, fulminant hepatic failure).
  • CBC count
    • Mild lymphocytosis is not uncommon. Pure red cell aplasia and pancytopenia may rarely accompany infection.
    • Indices of low-grade hemolysis are not uncommon.

Imaging Studies

  • Imaging studies are usually not indicated in hepatitis A virus infection.
  • An ultrasound scan may be required when alternative diagnoses warrant exclusion and should assess vessel patency and evaluate any evidence supporting unsuspected underlying chronic liver disease. Ultrasound scanning is essential in patients with fulminant hepatic failure.

Other Tests

  • Molecular diagnostic techniques performed on blood and feces for hepatitis A virus RNA are purely research tools.
  • Other investigations (eg, serum acetaminophen) may be necessary as suggested by history and clinical examination findings.

Procedures

  • Liver biopsy has a minimal role in acute hepatitis A virus infection. This procedure may play a part in chronic relapsing hepatitis A virus infection or when the diagnosis is uncertain.

Histologic Findings

Histopathology reveals pronounced portal inflammation early in the illness, which is consistent with viral hepatitis. Focal necrosis and acidophilic bodies are less pronounced than with infections of hepatitis B virus (HBV) and hepatitis C virus (HCV). In fulminant hepatic failure, biopsy findings may show extensive cell loss with ballooning in many of the remaining hepatocytes. Immunofluorescent stains for hepatitis A virus antigen provide positive results.

More on Hepatitis A

Overview: Hepatitis A
Differential Diagnoses & Workup: Hepatitis A
Treatment & Medication: Hepatitis A
Follow-up: Hepatitis A
Multimedia: Hepatitis A
References

References

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Further Reading

Keywords

hepatitis A, infectious hepatitis, hepatitis A virus, acute hepatitis, hepatitis A vaccine, hepatitis A vaccination, hep A, HAV, HAV infection, fulminant hepatic failure, liver transplant, liver transplantation, hepatomegaly, jaundice, hepatitis B virus, HBV, hepatitis C virus, HCV, hepatitis D virus, HDV, hepatitis E virus, HEV, Picornaviridae

Contributor Information and Disclosures

Author

Richard K Gilroy, MBBS, FRACP, Associate Professor, Medical Director of Liver Transplantation and Hepatology, Department of Internal Medicine, Kansas University Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center
Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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