Hepatitis B natural history
Hepatitis B |
Diagnosis |
Treatment |
Case Studies |
Hepatitis B natural history On the Web |
American Roentgen Ray Society Images of Hepatitis B natural history |
Risk calculators and risk factors for Hepatitis B natural history |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor In Chief: Cafer Zorkun, M.D., Ph.D. [2]
Prognosis
Hepatitis B virus infection may be either acute (self-limiting) or chronic (long-standing). Persons with self-limiting infection clear the infection spontaneously within weeks to months.
Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus. However, this drops to 30% for younger children, and only 5% of newborns that acquire the infection from their mother at birth will clear the infection.[1] This population has a 40% lifetime risk of death from cirrhosis or hepatocellular carcinoma.[2] Of those infected between the age of one to six, 70% will clear the infection.[3]
Hepatitis D (HDV) can occur only with a concomitant hepatitis B infection, because HDV uses the HBV surface antigen to form a capsid.[4] Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer.[5] Polyarteritis nodosa is more common in people with hepatitis B infection.
Reactivation
Hepatitis B virus DNA persists in the body after infection, and in some people the disease recurs.[6] Although rare, reactivation is seen most often in people with impaired immunity.[7] HBV goes through cycles of replication and non-replication. Approximately 50% of people experience acute reactivation. Males with baseline ALT of 200 UL/L are three times more likely to develop a reactivation than people with lower levels. People who undergo chemotherapy are at risk for HBV reactivation. The current view is that immunosuppressive drugs favor increased HBV replication while inhibiting cytotoxic T cell function in the liver.[8]
References
- ↑ Bell, S J; Nguyen, T (2009). "The management of hepatitis B" (Free full text). Aust Prescr. 23 (4): 99–104.
- ↑ Dienstag JL (2008). "Hepatitis B virus infection". The New England Journal of Medicine. 359 (14): 1486–500. doi:10.1056/NEJMra0801644. PMID 18832247. Retrieved 2012-02-08. Unknown parameter
|month=
ignored (help) - ↑ Kerkar N (2005). "Hepatitis B in children: complexities in management". Pediatric Transplantation. 9 (5): 685–91. doi:10.1111/j.1399-3046.2005.00393.x. PMID 16176431. Retrieved 2012-02-08. Unknown parameter
|month=
ignored (help) - ↑ Taylor JM (2006). "Hepatitis delta virus". Virology. 344 (1): 71–6. doi:10.1016/j.virol.2005.09.033. PMID 16364738. Retrieved 2012-02-08. Unknown parameter
|month=
ignored (help) - ↑ Oliveri F, Brunetto MR, Actis GC, Bonino F (1991). "Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC)". The Italian Journal of Gastroenterology. 23 (8): 498–502. PMID 1661197. Unknown parameter
|month=
ignored (help);|access-date=
requires|url=
(help) - ↑ Vierling JM (2007). "The immunology of hepatitis B". Clinics in Liver Disease. 11 (4): 727–59, vii–viii. doi:10.1016/j.cld.2007.08.001. PMID 17981227. Retrieved 2012-02-08. Unknown parameter
|month=
ignored (help) - ↑ Katz LH, Fraser A, Gafter-Gvili A, Leibovici L, Tur-Kaspa R (2008). "Lamivudine prevents reactivation of hepatitis B and reduces mortality in immunosuppressed patients: systematic review and meta-analysis". Journal of Viral Hepatitis. 15 (2): 89–102. doi:10.1111/j.1365-2893.2007.00902.x. PMID 18184191. Retrieved 2012-02-08. Unknown parameter
|month=
ignored (help) - ↑ Bonacini, Maurizio, MD. "Hepatitis B Reactivation". University of Southern California Department of Surgery. Retrieved 2009-01-24.