Hepatitis B natural history: Difference between revisions

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===Acute Hepatitis B===
===Acute Hepatitis B===
* The acute form of the disease often resolves spontaneously after a 4-8 week illness. Most patients recover without significant consequences and without recurrence. However, a favourable [[prognosis]] is not certain, especially in the elderly who can develop fulminating, fatal cases of acute hepatic [[necrosis]]. Young children rarely develop acute clinical disease, but many of those [[infected]] before the age of seven will become chronic carriers.
* The acute form of the disease often resolves spontaneously after a 4-8 week illness. Most patients recover without significant consequences and without recurrence. However, a favourable [[prognosis]] is not certain, especially in the elderly who can develop fulminating, fatal cases of acute hepatic [[necrosis]]. Young children rarely develop acute clinical disease, but many of those [[infected]] before the age of seven will become chronic carriers.
* [[Incubation period]] - usually varies between 45 and 120 days, with an average of 60 to 90 days. The variation is related to:
:* Amount of virus in the inoculum (larger initial dose of virus is associated with shorter incubation period)
:* Mode of transmission
:* Host factors


===Chronic Hepatitis B===
===Chronic Hepatitis B===

Revision as of 22:41, 29 July 2014

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Natural History

The course of hepatitis B may be extremely variable. Hepatitis B virus infection has different clinical manifestations, depending on the patient’s age at infection and immune status, and the stage at which the disease is recognized.[1]

During the incubation phase of the disease (6 to 24 weeks), patients may feel unwell with possible nausea, vomiting, diarrhea, anorexia and headaches. Patients may then become jaundiced although low grade fever and loss of appetite may improve. Sometimes HBV infection produces neither jaundice nor obvious symptoms.[1]

The asymptomatic cases may become silent carriers of the virus and constitute a reservoir for further transmission to others.

The persons infected with hepatitis B may:[1]

In general, the frequency of clinical disease increases with age, whereas the percentage of carriers decreases.[1]

Acute Hepatitis B

  • The acute form of the disease often resolves spontaneously after a 4-8 week illness. Most patients recover without significant consequences and without recurrence. However, a favourable prognosis is not certain, especially in the elderly who can develop fulminating, fatal cases of acute hepatic necrosis. Young children rarely develop acute clinical disease, but many of those infected before the age of seven will become chronic carriers.
  • Incubation period - usually varies between 45 and 120 days, with an average of 60 to 90 days. The variation is related to:
  • Amount of virus in the inoculum (larger initial dose of virus is associated with shorter incubation period)
  • Mode of transmission
  • Host factors

Chronic Hepatitis B

Complications

While most acute HBV infections in adults result in complete recovery, fulminant hepatitis occurs in about 1% to 2% of acutely infected persons. About 200 to 300 Americans die of fulminant disease each year (case-fatality rate 63% to 93%). Although the consequences of acute HBV infection can be severe, most of the serious complications associated with HBV infection are due to chronic infection. Common complications of Hepatitis are:

Chronic Infection

Approximately 5% of all acute HBV infections progress to chronic infection, with the risk of chronic HBV infection decreasing with age. As many as 90% of infants who acquire HBV infection from their mothers at birth become chronically infected. Of children who become infected with HBV between 1 year and 5 years of age, 30% to 50% become chronically infected. By adulthood, the risk of acquiring chronic HBV infection is approximately 5%.

Persons with chronic infection are often asymptomatic and may not be aware that they are infected; however, they are capable of infecting others and have been referred to as carriers. Chronic infection is responsible for most HBV-related morbidity and mortality, including chronic hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma. Approximately 25% of persons with chronic HBV infection die prematurely from cirrhosis or liver cancer. Chronic active hepatitis develops in more than 25% of carriers and often results in cirrhosis. An estimated 3,000 to 4,000 persons die of hepatitis B-related cirrhosis each year in the United States. Persons with chronic HBV infection are at 12 to 300 times higher risk of hepatocellular carcinoma than noncarriers. An estimated 1,000 to 1,500 persons die each year in the United States of hepatitis B-related liver cancer.

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.[2] This population has a 40% lifetime risk of death from cirrhosis or hepatocellular carcinoma.[3] Of those infected between the age of one to six, 70% will clear the infection.[4]

Hepatitis D (HDV) can occur only with a concomitant hepatitis B infection, because HDV uses the HBV surface antigen to form a capsid.[5] Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer.[6] Polyarteritis nodosa is more common in people with hepatitis B infection.

References

  1. 1.0 1.1 1.2 1.3 "Hepatitis B" (PDF).
  2. Bell, S J; Nguyen, T (2009). "The management of hepatitis B" (Free full text). Aust Prescr. 23 (4): 99–104.
  3. 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)
  4. 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)
  5. 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)
  6. 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)

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