Hepatitis A natural history, complications and prognosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [3]

Overview

Hepatitis A, caused by infection with HAV, has an incubation period of approximately 28 days. HAV infection produces a self-limited disease, rarely leading to acute liver failure. 10-15% of patients experience a relapse of symptoms during the 6 months after acute illness. The risk for symptomatic infection is related to the age of the patient, with >80% of adults showing symptoms compatible with acute viral hepatitis, such as fatigue, malaise, nausea, vomiting and anorexia. Most children have either asymptomatic or unrecognized infection.[1] Possible complications of hepatitis A include: dehydration, electrolyte imbalance, bleeding, and rarely fulminat hepatitis. The prognosis depends on the age of the patient, and underlying liver condition: children are often asymptomatic, while elder patients with chronic liver failure have a higher risk for fulminat hepatitis.

Natural History

Hepatitis A is caused by the hepatitis A virus (HAV). The virus replicates in the liver and is shed in high concentrations in feces from 2 weeks before to 1 week after the onset of clinical illness. It is primarily spread through fecal-oral transmission, commonly after ingesting food or water that is contaminated with the virus. The infected patients have a peak infectivity during the 2 week period before onset of jaundice or elevation of liver enzymes.[2]

The likelihood of having symptoms with HAV infection increases with age. Fewer than 10% of infections among children aged 0-4 years result in jaundice; this percentage increases to 30%-40% among children aged 5-9 years, 60%-80% among youths aged 10-17 years, and 80%-90% among adults aged ≥18 years[3].

Unlike other types of Hepatitis, HAV is always acute.

When signs and symptoms occur, typically they last less 2 months, although 10-15% of symptomatic persons have prolonged or relapsing disease lasting up to 6 months.[4] HAV infection is usually acute and self-limited. The rare cases of fulminant hepatitis are more common among patients with previous liver disease, such as chronic hepatitis C.[5]

The clinical manifestations commonly start after a 30 day incubation period. The disease manifests abruptly, with the following symptoms:[6]

One week after symptom onset, patients experience:

The initial symptoms commonly diminish after the onset of jaundice, which is usually more intense on its second week.

Complications

Possible complications of hepatitis A include:

Prognosis

  • Young children who are infected with hepatitis A typically have a milder form of the disease, usually lasting from 1-3 weeks, whereas adults tend to experience a much more severe form of the disease.
  • Adults are often confined to bed and minimal activity for about 4 weeks and have to stop their work for one to three months or longer.
  • Many adults take up to 36 months and occasionally longer to recover entirely.
  • After the first month of the disease, there may be low immunity, with a consequent increased risk for opportunistic infections
  • It is common for recovering patients to experience occasional "off" days, during which they need to rest more.
  • Approximately 15% of people diagnosed with hepatitis A may experience one or more symptomatic relapse(s) for up to 24 months after contracting this disease.
  • The case-fatality rate for HAV infection increases with age: 1.8% for adults older than 50 years of age, compared with 0.6% for persons below 50 years. The case-fatality rate is also increased among persons with chronic liver disease, who are at increased risk for acute liver failure.[8]

References

  1. Sexually Transmitted Diseases Treatment Guidelines, 2010. Centers for Disease Control and Prevention. Recommendations and Reports December 17, 2010 / 59(RR12);1-110 [1]
  2. Tassopoulos NC, Papaevangelou GJ, Ticehurst JR, Purcell RH (1986). "Fecal excretion of Greek strains of hepatitis A virus in patients with hepatitis A and in experimentally infected chimpanzees". The Journal of Infectious Diseases. 154 (2): 231–7. PMID 3014009. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  3. Armstrong GL, Bell BP (2002). "Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization". Pediatrics. 109 (5): 839–45. PMID 11986444. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  4. Glikson M, Galun E, Oren R, Tur-Kaspa R, Shouval D (1992). "Relapsing hepatitis A. Review of 14 cases and literature survey". Medicine. 71 (1): 14–23. PMID 1312659. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. Vento S, Garofano T, Renzini C, Cainelli F, Casali F, Ghironzi G; et al. (1998). "Fulminant hepatitis associated with hepatitis A virus superinfection in patients with chronic hepatitis C." N Engl J Med. 338 (5): 286–90. doi:10.1056/NEJM199801293380503. PMID 9445408.
  6. Lednar WM, Lemon SM, Kirkpatrick JW, Redfield RR, Fields ML, Kelley PW (1985). "Frequency of illness associated with epidemic hepatitis A virus infections in adults". Am J Epidemiol. 122 (2): 226–33. PMID 3860002.
  7. "Hepatitis A".
  8. Williams I, Bell B, Kaluba J, Shapiro C. Association between chronic liver disease and death from hepatitis A, United States, 1989--92 [abstract no. A39]. IX Triennial International Symposium on Viral Hepatitis and Liver Disease. Rome, Italy, April 21--25, 1996.

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