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 is caused by infection with hepatitis A virus (HAV) which has an incubation period of approximately 28 days. HAV infection produces a self-limited disease, rarely leading to acute liver failure. The risk for symptomatic infection is related to the age of the patient. While children most commonly have either asymptomatic or unrecognized infection, more than 80% of adults exhibit symptoms of acute viral hepatitis, such as fatigue, malaise, nausea, vomiting, and anorexia.[1] Possible complications of hepatitis A include dehydration, electrolyte imbalance, bleeding, and rarely fulminant hepatitis. The prognosis depends on the age of the patient and the underlying liver condition. Approximately 10 to 15% of patients experience a relapse of symptoms during the 6 months following acute illness.
Natural History
Hepatitis A is caused by the hepatitis A virus (HAV) infection. Unlike other types of hepatitis, HAV infection is always acute. 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 developing 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]
When signs and symptoms occur, they typically last less than 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:
- Jaundice
- Pruritus
- Dark urine
- Acholic stool
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:
- Severe dehydration
- Electrolyte imbalance
- Bleeding
- After the first month of the disease, there may be low immunity, with a consequent increased risk for opportunistic infections.
- Fulminant hepatitis
- Death (particularly in elderly and adults with chronic liver disease, such as hepatitis C)
Prognosis
- 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.
- 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 United States Centers for Disease Control and Prevention (CDC) reported that the mortality rate of hepatitis A in 2010 was 0.03 deaths per 100,000 population.[7]
- 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
- ↑ Sexually Transmitted Diseases Treatment Guidelines, 2010. Centers for Disease Control and Prevention. Recommendations and Reports December 17, 2010 / 59(RR12);1-110 [1]
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.
- ↑ 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.
- ↑ "Hepatitis A".
- ↑ 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.