• Clinical science

Hepatitis A

Summary

Hepatitis A infection is caused by the hepatotropic hepatitis A virus (HAV) and is usually transmitted via the fecal-oral route. About half of all cases of HAV infection that occur in the US are acquired during visits to countries that are endemic for HAV (e.g., tropical or subtropical regions). HAV infection results in acute hepatitis with a clinical course characterized by prodromal symptoms of fever and malaise, followed by jaundice. As in any other case of acute viral hepatitis, high levels of serum transaminase, and mixed hyperbilirubinemia are observed. Serological detection of anti-HAV IgM, which is elevated during acute infection, confirms the diagnosis. While prodromal symptoms resolve within a few weeks, jaundice usually resolves within 1–3 months. No chronic sequelae occur and acute hepatic failure occurs only in very rare cases. Therefore, supportive care is usually the only treatment required. As of 2006, routine immunization against hepatitis A is recommended for all children older than 12 months. Certain high-risk groups, such as tourists to areas where HAV is endemic, should also be immunized against HAV if they have not been vaccinated in the past.

An important differential diagnosis is another feco-orally transmitted viral infection caused by the hepatitis E virus (HEV). The clinical presentation of hepatitis E is almost identical to that of hepatitis A, with the exception that pregnant women are at a high risk of developing acute liver failure. Serological tests help to distinguish HEV from HAV.

Epidemiology

  • Incidence (in the US): ∼ 2,000 cases per year (50% acquired during travels abroad) [1]
    • Hepatitis A infection is the second most common cause of acute hepatitis in the US.
    • Hepatitis A is very common in tropical and subtropical regions.
  • 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.

Etiology

  • Pathogen: hepatitis A virus [2]
    • Belongs to the family of Picornaviridae and the genus Hepatoviridae
    • Small (27 nm in diameter), non-enveloped virus with single-stranded, positive-sense RNA
    • Resistant to denaturation by gastric acid, heat, and chemicals, and can remain viable for months in fresh and saltwater
    • Humans are the only reservoir for the hepatitis A virus. [3]
  • Route of transmission: fecal-oral [4]
    • Contaminated water and food (e.g., raw shellfish)
    • Risk groups: nursing home residents, international travelers, prison inmates, men who have sex with men, IV drug users.
  • Infectious period: 2 weeks before to 1 week after the onset of the illness [3]

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

Pathophysiology

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

Clinical features

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.

Diagnostics

Positive IgG values indicate immunity against HAV due to prior infection or vaccination.

Differential diagnoses

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

Hepatitis E [9][10]

  • Pathogen: hepatitis E virus (HEV)
  • Epidemiology
    • Uncommon in the US
    • An important cause of endemic viral hepatitis in developing countries and equatorial regions (e.g., India, western and northern Africa, Middle East, and Mexico)
  • Route of transmission: fecal-oral (especially via contaminated water, food, or sources)
  • Pathophysiology: The degree of hepatic injury is usually mild and the patient may present with clinical features of acute hepatitis.
  • Clinical features: similar to those of hepatitis A (see “Clinical features” above). [2]
    • Incubation period: 2–8 weeks
    • In the majority of cases, the disease is self-limiting with complete recovery.
    • Fulminant hepatitis in pregnant women (high risk of mortality for both mother and fetus)
    • Affected individuals do not become carriers nor do they develop chronic hepatitis (unlike in hepatitis B and hepatitis C). [12]
  • Diagnostics [2]
    • Laboratory findings are the same as in hepatitis A.
    • Confirmatory test
      • Anti-HEV IgM: active infection
      • Anti-HEV IgG: past infection
      • HEV RNA can be detected by PCR in stool and serum samples during the prodromal phase and up to 3 months after the onset of symptoms.
    • Liver biopsy (not normally necessary): patchy necrosis
  • Treatment: supportive care
  • Prevention: no vaccine available

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.

Treatment

Disease is self-limiting; only supportive care is required.

Prevention

Hepatitis A pre-exposure prophylaxis [3][13]

  • Travelers should be advised to follow primary preventive measures such as hand-washing and following proper food and water safety.
  • Routine active immunization is now recommended for all children over 12 months consisting of a first IM dose of hepatitis A vaccine followed by a booster dose after 6 months (see also “Immunization schedule”).
  • Active immunization is also recommended for certain high-risk groups who have not been immunized in the past:
    • Travelers to foreign countries where HAV is endemic.
    • Men who have sex with men
    • Patients with chronic liver disease

Hepatitis A post-exposure prophylaxis [3][4]

Post-exposure prophylaxis is indicated for all previously unvaccinated individuals who have been exposed to a serologically confirmed case of HAV infection. In order to be effective, post-exposure prophylaxis should be administered within two weeks of exposure.

  • 1. Lai M, Chopra S. Hepatitis A Virus Infection in Adults: An Overview. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-a-virus-infection-in-adults-an-overview. Last updated October 17, 2016. Accessed March 24, 2017.
  • 2. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Philadelphia, PA: Elsevier Saunders; 2014.
  • 3. Centers for Disease Control and Prevention. Hepatitis A Questions and Answers for Health Professionals. https://www.cdc.gov/hepatitis/hav/havfaq.htm#B1. 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. New York, NY: McGraw-Hill Education; 2015.
  • 5. Kim J-Y, Joung J-Y, Kang J-Y, Son C-G, Cho J-H. Acute Viral Hepatitis A with Cholestatic Hepatitis Treated with Traditional Korean Medicine: A Case Report. Journal of Korean Medicine. 2015; 36(4): pp. 114–121. doi: 10.13048/jkm.15038.
  • 6. Watanabe H, Sekine H, Uruma T, et al. Increase of atypical lymphocytes expressing CD4+/CD45RO+ in an infectious mononucleosis-like syndrome associated with hepatitis A virus infection. Journal of Infection and Chemotherapy. 2009; 15(3): pp. 187–190. doi: 10.1007/s10156-009-0677-9.
  • 7. De los Angeles Rodríguez Lay L, Larralde Díaz O, Martínez Casanueva R, Gutiérrez Moreno A. Anti-Hepatitis A Virus Immunoglobulin M Antibodies in Urine Samples for Rapid Diagnosis of Outbreaks. Clinical Diagnostic Laboratory Immunology. 2003; 10(3): pp. 492–494. doi: 10.1128/cdli.10.3.492-494.2003.
  • 8. Matheny SC, Kingery JE. Hepatitis A. Am Fam Physician. 2012; 86(11): pp. 1027–34; quiz 1010–2. pmid: 23198670.
  • 9. World Health Organization. Hepatitis E. http://www.who.int/mediacentre/factsheets/fs280/en/. Updated July 1, 2016. Accessed March 24, 2017.
  • 10. Centers for Disease Control and Prevention. Hepatitis E FAQs for Health Professionals. https://www.cdc.gov/hepatitis/hev/hevfaq.htm. Updated May 31, 2015. Accessed March 24, 2017.
  • 11. 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.
  • 12. Kamar N, Izopet J, Dalton HR. Chronic Hepatitis E Virus Infection and Treatment. Journal of Clinical and Experimental Hepatology. 2014; 3(2): pp. 134–140. doi: 10.1016/j.jceh.2013.05.003.
  • 13. Chopra S, Lai M. Hepatitis A Virus Infection: Prevention. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-a-virus-infection-prevention. Last updated November 2, 2016. Accessed March 24, 2017.
  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
  • Umashanker R, Chopra S. Hepatitis E Virus Infection. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-e-virus-infection. Last updated December 14, 2016. Accessed March 24, 2017.
last updated 10/22/2020
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