Hepatitis A

Last updated: November 20, 2023

Summarytoggle arrow icon

Hepatitis A is a viral disease caused by the hepatotropic hepatitis A virus (HAV) and usually spreads through fecal-oral transmission. About half of all patients with hepatitis A in the US acquire the HAV during visits to countries in which HAV is endemic (tropical or subtropical regions). HAV infection can cause acute viral hepatitis, which initially manifests with prodromal symptoms (fever and malaise), followed by jaundice. The laboratory findings in hepatitis A are similar to those observed in other forms of acute viral hepatitis and include high serum transaminase levels and mixed hyperbilirubinemia. Serological detection of anti-HAV IgM antibodies confirms the diagnosis of hepatitis A. While prodromal symptoms typically resolve within a few weeks, jaundice may persist for 1–3 months. Hepatitis A is typically self-limited with no chronic sequelae, and acute liver failure rarely occurs; therefore, only supportive care is typically required. In the US, routine immunization against HAV is recommended for all children > 12 months of age. Individuals at increased risk of infection, such as travelers to areas in which HAV is endemic, as well as individuals at increased risk of severe disease, such as those with chronic liver disease, should also be immunized against HAV if they have not been previously vaccinated. The hepatitis A immunization series generally provides long-term immunity, without the need for booster doses.

Hepatitis E, caused by the hepatitis E virus (HEV), which is also spread through fecal-oral transmission, is an important differential diagnosis. The clinical features of hepatitis E are almost identical to those of hepatitis A, with the exception that pregnant women are at a higher risk of developing acute liver failure with hepatitis E. Serological tests help to distinguish hepatitis E from hepatitis A.

Epidemiologytoggle arrow icon

  • Incidence (in the US): ∼ 2,000 cases per year (50% acquired during travels abroad) [1]
  • Age: Vaccination programs have made the disease fairly rare in children; infection is now more widespread in adults. [2]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

When it comes to viral hepatitis, vowels (A and E) are bowels (transmitted feco-orally).

Pathophysiologytoggle arrow icon

HAV is not cytopathic in itself; research suggests that liver damage is caused by cellular immunity (especially CD8+ T cells). [2]

Clinical featurestoggle arrow icon

HAV infection in children is typically asymptomatic. The risk of symptomatic disease increases with age and coinfection (e.g., with hepatitis B).

When it comes to viral hepatitis, vowels (A and E) cause only AcutE hepatitis while Consonants (B, C, and D) may have Chronic sequelae as well.

Diagnosticstoggle arrow icon

Laboratory testing [5][6][7]

  • Routine studies
  • Confirmatory testing
    • Anti-HAV IgM antibodies: present in patients with active infection
      • Usually detectable 5–10 days after exposure and 5–10 days before clinical symptoms develop
      • Levels peak commonly ∼ 1 month after infection.
      • May persist for up to 6 months after infection
    • Anti-HAV IgG antibodies
      • Develop during active infection and persist indefinitely after infection or vaccination
      • Production begins within 2–3 weeks of infection.
    • HAV RNA can be detected in stool and serum samples using PCR.

The presence of anti-HAV IgM antibodies or HAV RNA confirms active hepatitis A. Detection of anti-HAV IgG antibodies in the absence of anti-HAV IgM antibodies indicates immunity against HAV due to prior infection or vaccination. [6]

Further testing

Further diagnostic testing is not routinely necessary but may be used to rule out differential diagnoses or in fulminant hepatitis. If performed, additional tests may show the following findings if acute viral hepatitis is present:

Differential diagnosestoggle arrow icon

For an overview comparing the different types of viral hepatitis see “Differential diagnosis of viral hepatitis.”

Hepatitis E [14][15]

Women who are Expecting are FULly aware of the risks: pregnant women with hepatitis E can develop FULminant hepatitis.

A fulminant course is relatively common in pregnant women with HEV infection (occurring in up to 20% of cases) and is life-threatening for both the mother and fetus.

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

Preventiontoggle arrow icon

Hepatitis A preexposure prophylaxis [6][7]

Hepatitis A vaccine

See “ACIP immunization schedule” for scheduling details.

Hepatitis A vaccination is considered suitable for use during pregnancy in previously unvaccinated individuals with an increased risk of infection or severe disease. [6]

Hepatitis A postexposure prophylaxis [6]

Postexposure prophylaxis is indicated for all previously unvaccinated individuals who have been in contact with an individual with serologically confirmed hepatitis A within the past two weeks. Hepatitis A is a notifiable disease.

Recommended regimens for hepatitis A postexposure prophylaxis
Type of postexposure prophylaxis Indications
Active immunization
  • Healthy individuals who are 1–40 years of age
Passive immunization with immune globulin
Both active and passive immunization

Referencestoggle arrow icon

  1. Lai M, Chopra S. Hepatitis A Virus Infection in Adults: An Overview. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: October 17, 2016. Accessed: March 24, 2017.
  2. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014
  3. Hepatitis A Questions and Answers for Health Professionals. Updated: July 13, 2016. Accessed: March 24, 2017.
  4. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  5. Matheny SC, Kingery JE. Hepatitis A.. Am Fam Physician. 2012; 86 (11): p.1027-34; quiz 1010-2.
  6. Nelson NP, Weng MK, Hofmeister MG, et al. Prevention of Hepatitis A Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices, 2020. MMWR Recomm Rep. 2020; 69 (5): p.1-38.doi: 10.15585/mmwr.rr6905a1 . | Open in Read by QxMD
  7. Desai AN, Kim AY. Management of Hepatitis A in 2020-2021. JAMA. 2020; 324 (4): p.383-384.doi: 10.1001/jama.2020.4017 . | Open in Read by QxMD
  8. Botros M, Sikaris KA. The De Ritis Ratio: The Test of Time. Clin Biochem Rev. 2013; 34 (3): p.117-30.
  9. Cuthbert JA. Hepatitis A: Old and New. Clin Microbiol Rev. 2001; 14 (1): p.38-58.doi: 10.1128/cmr.14.1.38-58.2001 . | Open in Read by QxMD
  10. Okuno T, Sano A, Deguchi T, et al. Pathology of Acute Hepatitis A in Human: Comparison with Acute Hepatitis B. Am J Clin Pathol. 1984; 81 (2): p.162-169.doi: 10.1093/ajcp/81.2.162 . | Open in Read by QxMD
  11. Sciot R, Oord JJ, Wolf-Peeters C, Desmet VJ. In situ characterisation of the (peri)portal inflammatory infiltrate in acute hepatitis A. Liver. 1986; 6 (6): p.331-336.doi: 10.1111/j.1600-0676.1986.tb00300.x . | Open in Read by QxMD
  12. Rubin R, Strayer DS, Rubin E. Rubin's Pathology: Clinicopathologic Foundations of Medicine. Lippincott Williams & Wilkins ; 2012
  13. Kurtz AB, Rubin CS, Cooper HS, et al. Ultrasound findings in hepatitis. Radiology. 1980; 136 (3): p.717-723.doi: 10.1148/radiology.136.3.7403553 . | Open in Read by QxMD
  14. Hepatitis E. Updated: July 1, 2016. Accessed: March 24, 2017.
  15. Hepatitis E FAQs for Health Professionals. Updated: May 31, 2015. Accessed: March 24, 2017.
  16. Park W-J, Park B-J, Ahn H-S, et al. Hepatitis E virus as an emerging zoonotic pathogen. Journal of Veterinary Science. 2016; 17 (1): p.1.doi: 10.4142/jvs.2016.17.1.1 . | Open in Read by QxMD
  17. Kamar N, Izopet J, Dalton HR. Chronic Hepatitis E Virus Infection and Treatment. Journal of Clinical and Experimental Hepatology. 2014; 3 (2): p.134-140.doi: 10.1016/j.jceh.2013.05.003 . | Open in Read by QxMD

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