Hepatitis A overview: Difference between revisions
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HAV infection produces a self-limited disease that does not result in chronic infection or chronic liver disease. However, 10–15% of patients might experience a relapse of symptoms during the 6 months after acute illness. Acute liver failure from Hepatitis A is rare (overall case-fatality rate: 0.5%). The risk for symptomatic infection is directly related to age, with >80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infection.<ref name="pmid10683554">{{cite journal |doi=10.1016/S0264-410X(99)00470-3 |author=Ciocca M. |title=Clinical course and consequences of hepatitis A infection |journal=Vaccine |volume=18 |pages=71–4 |year=2000 |pmid=10683554}}</ref> Antibody produced in response to HAV infection persists for life and confers protection against reinfection. The disease can be prevented by [[vaccination]], and [[hepatitis A vaccine]] has been proven effective in controlling outbreaks worldwide.<ref name="pmid16271543"/> | HAV infection produces a self-limited disease that does not result in chronic infection or chronic liver disease. However, 10–15% of patients might experience a relapse of symptoms during the 6 months after acute illness. Acute liver failure from Hepatitis A is rare (overall case-fatality rate: 0.5%). The risk for symptomatic infection is directly related to age, with >80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infection.<ref name="pmid10683554">{{cite journal |doi=10.1016/S0264-410X(99)00470-3 |author=Ciocca M. |title=Clinical course and consequences of hepatitis A infection |journal=Vaccine |volume=18 |pages=71–4 |year=2000 |pmid=10683554}}</ref> Antibody produced in response to HAV infection persists for life and confers protection against reinfection. The disease can be prevented by [[vaccination]], and [[hepatitis A vaccine]] has been proven effective in controlling outbreaks worldwide.<ref name="pmid16271543"/> | ||
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==Historical Perspective== | |||
[[Hepatitis A virus]] was first identified in 1973. It was classified as a separate disease from other types of [[hepatitis]] during World War II. However, its true [[prevalence]] and route of [[transmission]] would only be recognized later.<ref name="pmid7876643 [">{{cite journal| author=Melnick JL| title=History and epidemiology of hepatitis A virus. | journal=J Infect Dis | year= 1995 | volume= 171 Suppl 1 | issue= | pages= S2-8 | pmid=7876643 [ | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7876643 }} </ref> During 1995-1996, the Food and Drug Administration (FDA) approved the inactivated hepatitis A vaccines. Consequently, [[hepatitis A]] became a disease that was not only common but also vaccine-preventable. | |||
==Pathophysiology== | |||
[[Hepatitis A]] is a [[liver]] disease caused by the [[hepatitis A virus]] (HAV). HAV has fecal-oral transmission and its [[infectivity]] peaks about 2-weeks before the onset of [[jaundice]]. Gross observation of the [[liver]] may show an enlarged and [[erythematous]] [[liver]], while microscopically it may reveal [[lymphocyte]] infiltration and [[inflammation]] of the portal tracts. | |||
==Causes== | |||
[[Hepatitis A]] is a [[liver]] disease caused by the [[hepatitis A virus]] (HAV). HAV has fecal-oral transmission and its [[infectivity]] peaks about 2-weeks before the onset of [[jaundice]]. Gross observation of the [[liver]] may show an enlarged and [[erythematous]] [[liver]], while microscopically it may reveal [[lymphocyte]] infiltration and [[inflammation]] of the portal tracts. | |||
==Differential Diagnosis== | |||
[[Hepatitis A]] must be differentiated from other diseases that cause [[fever]], [[nausea]], [[vomiting]], [[jaundice]], [[hepatomegaly]], icteric [[sclera]], elevated [[ALT]], [[AST]], and [[PCR]] such as other [[viral hepatitis]], [[alcoholic hepatitis]], and [[autoimmune hepatitis]]. | |||
==Epidemiology and Demographics== | |||
The [[incidence]] of [[hepatitis A]] varies among eras, countries and even cities within the same country. In recent years it has been noted a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. In the United States, the [[incidence]] of [[hepatitis A]] in 2011 was 0.4 cases per 100,000 population. In recent years, the rates of [[hepatitis A]] have been similar among all age groups. After the introduction of the HAV [[vaccine]], historic differences in rates of hepatitis A among racial/ethnic populations have also narrowed. In developed countries, elimination of historic geographic differences in [[incidence]] rates has also occurred. In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) are [[infected]] with the [[hepatitis A virus]] before the age of 10. | |||
==Risk Factors== | |||
Subjects who are not immunized against hepatitis A virus (HAV) and who travel to endemic areas where there is poor sanitation and lack of safe water are at increased risk of contracting HAV infection. Additional risk factors for HAV include [[intravenous drug injection]], living in a household with an infected person, having a sexual partner with acute HAV infection, and attending childcare centers. | |||
==Screening== | |||
The detection of [[hepatitis A virus]] (HAV) [[antibodies]] in the blood is used to screen for [[hepatitis A]]. Anti-[[HAV]] [[IgG]] remains elevated after acute disease.<ref name=CDC>{{cite web | title = Hepatitis A Screening | url = http://www.ncbi.nlm.nih.gov/books/NBK92029/ }}</ref> | |||
==Natural History, Complications and Prognosis== | |||
[[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]].<ref name=MMWR>Sexually Transmitted Diseases Treatment Guidelines, 2010. Centers for Disease Control and Prevention. Recommendations and Reports December 17, 2010 / 59(RR12);1-110 [http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5912a1.htm?s_cid=rr5912a1_e]</ref> 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. | |||
==Diagnosis== | ==Diagnosis== | ||
Revision as of 02:16, 30 July 2014
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Hepatitis A |
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Hepatitis A overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Hepatitis A (formerly known as infectious hepatitis and epidemical virus) is an acute infectious disease of the liver caused by the hepatitis A virus (Hep A),[1] an RNA virus, usually spread the fecal-oral route; transmitted person-to-person by ingestion of contaminated food or water or through direct contact with an infectious person. Tens of millions of individuals worldwide are estimated to become infected with Hep A each year.[2] The time between infection and the appearance of the symptoms (the incubation period) is between two and six weeks and the average incubation period is 28 days.[3]
In developing countries, and in regions with poor hygiene standards, the incidence of infection with this virus is high[4] and the illness is usually contracted in early childhood. As incomes rise and access to clean water increases, the incidence of HAV decreases.[5] Hepatitis A infection causes no clinical signs and symptoms in over 90% of infected children and since the infection confers lifelong immunity, the disease is of no special significance to those infected early in life. In Europe, the United States and other industrialized countries, on the other hand, the infection is contracted primarily by susceptible young adults, most of whom are infected with the virus during trips to countries with a high incidence of the disease[3] or through contact with infectious persons.
HAV infection produces a self-limited disease that does not result in chronic infection or chronic liver disease. However, 10–15% of patients might experience a relapse of symptoms during the 6 months after acute illness. Acute liver failure from Hepatitis A is rare (overall case-fatality rate: 0.5%). The risk for symptomatic infection is directly related to age, with >80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infection.[6] Antibody produced in response to HAV infection persists for life and confers protection against reinfection. The disease can be prevented by vaccination, and hepatitis A vaccine has been proven effective in controlling outbreaks worldwide.[3]
Historical Perspective
Hepatitis A virus was first identified in 1973. It was classified as a separate disease from other types of hepatitis during World War II. However, its true prevalence and route of transmission would only be recognized later.[7] During 1995-1996, the Food and Drug Administration (FDA) approved the inactivated hepatitis A vaccines. Consequently, hepatitis A became a disease that was not only common but also vaccine-preventable.
Pathophysiology
Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.
Causes
Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.
Differential Diagnosis
Hepatitis A must be differentiated from other diseases that cause fever, nausea, vomiting, jaundice, hepatomegaly, icteric sclera, elevated ALT, AST, and PCR such as other viral hepatitis, alcoholic hepatitis, and autoimmune hepatitis.
Epidemiology and Demographics
The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noted a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. In the United States, the incidence of hepatitis A in 2011 was 0.4 cases per 100,000 population. In recent years, the rates of hepatitis A have been similar among all age groups. After the introduction of the HAV vaccine, historic differences in rates of hepatitis A among racial/ethnic populations have also narrowed. In developed countries, elimination of historic geographic differences in incidence rates has also occurred. In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) are infected with the hepatitis A virus before the age of 10.
Risk Factors
Subjects who are not immunized against hepatitis A virus (HAV) and who travel to endemic areas where there is poor sanitation and lack of safe water are at increased risk of contracting HAV infection. Additional risk factors for HAV include intravenous drug injection, living in a household with an infected person, having a sexual partner with acute HAV infection, and attending childcare centers.
Screening
The detection of hepatitis A virus (HAV) antibodies in the blood is used to screen for hepatitis A. Anti-HAV IgG remains elevated after acute disease.[8]
Natural History, Complications and Prognosis
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.[9] 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.
Diagnosis
Laboratory Findings
Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. In most persons, IgM anti-HAV becomes detectable 5-10 days before the onset of symptoms and can persist for up to 6 months after infection. [10][11] Immunoglobulin G (IgG) anti-HAV, which appears early in the course of infection, remains detectable for the person's lifetime and confers lifelong protection against the disease. [12] Commercial diagnostic tests are available for the detection of IgM and total (IgM and IgG) anti-HAV in serum.
HAV RNA can be detected in the blood and stool of most persons during the acute phase of infection by using nucleic acid amplification methods, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates. [13] However, these methods, available in only a limited number of research laboratories, generally are not used for diagnostic purposes.
CT
CT scan is usually not indicated towards diagnosis of hepatitis A. However it may be done to exclude alternative diagnosis.
Ultrasound
Ultrasound of the abdomen may be carried out in patients with hepatitis A to evaluate for any other possible causes of hepatomegaly or chronic liver disease.
Treatment
Surgery
Patients who develop fulminant hepatitis may require aggressive supportive therapy, and be transferred to a center capable of performing liver transplantation.
References
- ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 541–4. ISBN 0838585299.
- ↑ Wasley A, Fiore A, Bell BP (2006). "Hepatitis A in the era of vaccination". Epidemiol Rev. 28: 101–11. doi:10.1093/epirev/mxj012. PMID 16775039.
- ↑ 3.0 3.1 3.2 Connor BA (2005). "Hepatitis A vaccine in the last-minute traveler". Am. J. Med. 118 (Suppl 10A): 58S–62S. doi:10.1016/j.amjmed.2005.07.018. PMID 16271543.
- ↑ Steffen R (2005). "Changing travel-related global epidemiology of hepatitis A". Am. J. Med. 118 (10): 46S–49S. doi:10.1016/j.amjmed.2005.07.016. PMID 16271541. Retrieved 2008-12-20. Unknown parameter
|month=ignored (help) - ↑ Jacobsen KH, Koopman JS (2005). "The effects of socioeconomic development on worldwide hepatitis A virus seroprevalence patterns". Int J Epidemiol. 34 (3): 600–9. doi:10.1093/ije/dyi062. PMID 15831565.
- ↑ Ciocca M. (2000). "Clinical course and consequences of hepatitis A infection". Vaccine. 18: 71–4. doi:10.1016/S0264-410X(99)00470-3. PMID 10683554.
- ↑ Melnick JL (1995). "History and epidemiology of hepatitis A virus". J Infect Dis. 171 Suppl 1: S2–8. PMID [ 7876643 [ Check
|pmid=value (help). - ↑ "Hepatitis A Screening".
- ↑ Sexually Transmitted Diseases Treatment Guidelines, 2010. Centers for Disease Control and Prevention. Recommendations and Reports December 17, 2010 / 59(RR12);1-110 [1]
- ↑ Bower WA, Nainan OV, Margolis HS. Duration of viremia in naturally-acquired hepatitis A viral infections. [Abstract 103] In: Abstracts of the Infectious Diseases Society of America 35th Annual Meeting. Alexandria, VA: Infectious Diseases Society of America, 1997.
- ↑ Liaw YF, Yang CY, Chu CM, Huang MJ (1986). "Appearance and persistence of hepatitis A IgM antibody in acute clinical hepatitis A observed in an outbreak". Infection. 14 (4): 156–8. PMID 3759243.
|access-date=requires|url=(help) - ↑ Stapleton JT (1995). "Host immune response to hepatitis A virus". The Journal of Infectious Diseases. 171 Suppl 1: S9–14. PMID 7876654. Retrieved 2012-02-28. Unknown parameter
|month=ignored (help) - ↑ Hutin YJ, Pool V, Cramer EH, Nainan OV, Weth J, Williams IT, Goldstein ST, Gensheimer KF, Bell BP, Shapiro CN, Alter MJ, Margolis HS (1999). "A multistate, foodborne outbreak of hepatitis A. National Hepatitis A Investigation Team". The New England Journal of Medicine. 340 (8): 595–602. doi:10.1056/NEJM199902253400802. PMID 10029643. Retrieved 2012-02-28. Unknown parameter
|month=ignored (help)
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