乙型病毒性肝炎 (Viral Hepatitis Type B)，亦簡稱B肝、B肝，是一種由B型肝炎病毒引起的疾病。B型肝炎病毒會引起肝臟病變。目前中國人口中約有十分之一是B肝病毒攜帶者。

B型肝炎是全球死亡原因的第10位，全世界約有3.5～4億人感染B肝病毒，人數高達愛滋病感染者的八倍以上。

治療方法包括口服藥拉米夫定 (Lamivudine)、阿德福韋酯 (Adefovir)、Entecavir，和注射

[編輯] 基本病理變化

] 肝炎種類

B肝檢驗

B肝的臨床檢驗最常見的方法是進行「B型肝炎抗原二對半」驗血體檢。二對半（兩對半）包括5項內容：B肝表面抗原，B肝表面抗體、B肝e抗原、B肝e抗體、B肝核心抗體。每項檢測結果可能分別是陽性或陰性。

檢測	英文名稱	代碼	「小三陽」	「大三陽」	有免疫力的人	尚未接觸過B肝病毒的人	注釋
B肝表面抗原	hepatitis B surface antigen	HBsAg	+	+	-	-	檢驗B肝感染的最直接指標，但在感染初期和在病毒被清除之後很可能檢測不到（陰性）。連續6個月以上陽性表示慢性肝炎或B肝病毒攜帶者。這個指標陽性表示有傳染性。另外在注射B肝疫苗72小時之內呈陽性。
B肝e抗原	hepatitis B e antigen	HBeAg	-	+	-	-	檢驗治療進展的檢驗。通常在表面抗原出現後不久就出現（陽性），表示B肝病毒在大量複製，傳染性強。但有些種類的B肝病毒並不產生e抗原。
B肝e抗體	antibodies to the hepatitis B e antigen	anti-HBe，HBeAb	+	-	-	-	在e抗原出現後如果身體可以自動清除病毒則e抗體會出現（陽性），通常表示身體正在大量殺死病毒。通常和e抗原不會同時陽性。但也有由於病毒基因變異而出現e抗體，這種情況下e抗體陽性比不表明病毒正在減少，即「假小三陽」。
B肝表面抗體	antibodies to the hepatitis B surface antigen	anti-HBs，HBsAb	-	-	+	-	如果病毒被清除，表面抗原會變得檢測不到（陰性），而表面抗體出現（陽性）。表面抗原陰性而表面抗體陽性表示或者這個人從前被B肝病毒侵入過並已經痊癒，或者是他/她曾注射過B肝疫苗。
B肝核心抗體（抗核抗體）	IgM antibodies to the hepatitis B core antigen	anti-HBc IGM，抗HBc	+	+	-	-	和表面抗原一樣是表明B肝病毒存在的依據。由於這一檢測相對費用較高，在B肝病患較少的國家和地區只用於有理由懷疑被檢測人處在感染後不久表面抗原已經檢測不到（陰性）而表面抗體尚未出現的幾周內。

通常講，「大三陽」表示B肝病毒在大量複製，傳染性強，可出現在慢性肝炎及B肝病毒攜帶者。「小三陽」表示身體的免疫系統正在殺死病毒。但由於有的病毒會造成「假小三陽」，故有人說有的「小三陽」比「大三陽」危險。在這種情況下，肝功能、B超、HBV（B肝病毒）DNA檢測是確定是否需要使用藥物治療的必要手段。^[1] 在很多時候，肝臟是否受損、多大程度上受損比能否將「大三陽」轉成「小三陽」更重要。

根據美國權威組織American Gastroenterological Association (AGA)的報告指出, 檢驗B肝病毒基因量是最有效的臨床檢驗方法。2006年的報告指出, 如果B肝病毒基因在每毫升的血液含量超過4log10, 病人就應該展開治療。

目前已有多種針對B肝患者或病毒攜帶者的藥物，比如拉米夫定(Lamivudine)、阿德福韋酯(Adefovir)和干擾病毒繁殖的干擾素(PEG Interferon)等。它們不是可以直接殺死病毒以根治, 而是幫助患者自己的免疫系統抵抗和清除病毒。這些藥物在病人身上的效果因人而異，有的能有效控制病情。以往為人詬病的抗藥性副作用, 在一些新藥已可減至10%或以下。而號稱可以保證「大三陽」轉陰的藥物廣告則是不可信的。

預防

參見

外部連結

參考文獻

許祖德陳增良主編《病理學》復旦大學出版社 ISBN 7-309-03470-8 王德林著《B肝五項及其32種組合模式》（北京）科學普及出版社 ISBN 7-110-05484-5

頁面分類: 醫學 | 傳染病 | 消化系統疾病

Hepatitis B

From Wikipedia, the free encyclopedia

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“HBV” redirects here. For other uses, see HBV (disambiguation).

Hepatitis B virus

Micrograph showing hepatitis B virions

Virus classification

Group:	Group VII (dsDNA-RT)
Family:	Hepadnaviridae
Genus:	Orthohepadnavirus
Species:	Hepatitis B virus

Hepatitis B is a disease of the liver and is caused by the Hepatitis B virus (HBV), a member of the Hepadnavirus family^[1] and one of hundreds of unrelated viral species which cause viral hepatitis. It was originally known as "serum hepatitis" and has caused current epidemics in parts of Asia and Africa.^[2] Hepatitis B is recognized as endemic in China and various other parts of Asia.^[3] The proportion of the world's population currently infected with the virus is 3 to 6%, but up to a third have been exposed. Symptoms of the acute illness caused by the virus include liver inflammation, vomiting, jaundice, and rarely, death. Chronic hepatitis B may cause liver cirrhosis which may then lead to liver cancer.

[hide]

1 Structure
2 Replication
3 Transmission
4 Immunopathogenesis
5 Symptoms and complications
6 Diagnosis
7 Treatment
8 Prevention
9 See also
10 References
11 External links

[edit] Structure

Virions consist of an outer lipid envelope and an icosahedral nucleocapsid core, the latter being composed of both protein and DNA. The outer envelope contains embedded proteins which are involved in viral binding of, and release into, susceptible cells. Virion shape is generally spherical with a diameter of 40 - 48 nanometers (nm) but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These "subviral" particles are not infectious.

The DNA genome is not segmented but rather partially double-stranded, containing a long and short segment which overlap approximately 240 nucleotides to form an open circle. The longer strand is 3020-3320 nucleotides long, and the shorter is 1700-2800 nucleotides long.^[4] The virus can be divided into four major serotypes (adr, adw, ayr, ayw) based on antigenic epitopes present on its envelope proteins, and into eight genotypes (A-H) according to overall nucleotide sequence variation of the genome. Different genotypes have distinct geographic distributions. For example, genotypes B and C are prevalent in China and neighboring countries.

[edit] Replication

Hepatitis B is one of a few known non-retroviral viruses which employ reverse transcription as a part of its replication process. (HIV, a completely unrelated virus, also uses reverse transcription.) Hepatitis B's genome is DNA, and reverse transcription is one of the later steps in making new viral particles. (Because HIV has an RNA genome, reverse transcription is one of the first steps in replication).

Upon entry into a host cell, the virus' double-stranded DNA genome is relocated to the cell's nucleus and converted to covalently closed circular DNA form, from which viral mRNAs are transcribed. These transcripts are exported to cytoplasm for translation of the envelope proteins (also known as hepatitis B surface antigen, or HBsAg), hepatitis B e antigen (HBeAg), and the X protein, whose function is still under debate.^[1] A fourth pre-genomic RNA is transcribed, which translates the viral polymerase and core proteins. Polymerase and pre-genomic RNA are encapsidated in the assembling core particles, where reverse transcription of the pre-genomic RNA to genomic DNA occurs by the Reverse Transcriptase (RT) protein. The mature core particle then exits the cell via normal secretory pathway, acquiring an envelope along the way.

[edit] Transmission

Hepatitis B is largely transmitted through exposure to bodily fluids containing the virus. This includes unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, vertical transmission from mother to child during childbirth, and so on. The primary method of transmission depends on the prevalence of the disease in a given area. In low prevalence areas, such as the continental United States, injection drug abuse and unprotected sex are the primary methods. In moderate prevalence areas, the disease is predominantly spread among children. In high prevalence areas, such as South East Asia, vertical transmission is most common. Without intervention, a mother who is positive for the hepatitis B surface antigen confers a 20% risk of passing the infection to her offspring at the time of birth. This risk is as high as 90% if the mother is also positive for the hepatitis B e antigen.

Roughly 16-40% of unimmunized sexual partners of individuals with hepatitis B will be infected through sexual contact. The risk of transmission is closely related to the rate of viral replication in the infected individual at the time of exposure.

[edit] Immunopathogenesis

During HBV infection the host immune response is responsible for both hepatocellular damage and viral clearance. While the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to nearly all of the liver injury associated with HBV infection. By killing infected cells and by producing antiviral cytokines capable of purging HBV from viable hepatocytes, CTLs also eliminate the virus.^[5] Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology and platelets may facilitate the accumulation of CTLs into the liver.^[6]

[edit] Symptoms and complications

Hepatitis B virus infection may either be acute (self-limited) or chronic (long-standing). Persons with self-limited infection clear the infection spontaneously within weeks to months.

The greater a person's age at the time of infection, the greater the chance their body will 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, only 5% of new-borns that acquire the infection from their mother at birth will clear the infection. Of those infected between the age of one to six, 70% will clear the infection. When the infection is not cleared, one becomes a chronic carrier of the virus.

Acute infection with hepatitis B virus is associated with acute viral hepatitis - an illness that begins with general ill-health, loss of appetite, nausea, vomiting, bodyaches, mild fever, dark urine, and then progresses to development of jaundice. It has also been noted that itchy skin all over the body, has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most of the affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result of it. The infection may also be entirely asymptomatic and may go unrecognized.

Chronic infection with hepatitis B virus may be either asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of liver cancer. Hepatitis D infection requires a concomitant infection with hepatitis B. Co-infection with hepatitis D increases the risk of liver cirrhosis and subsequently, liver cancer.

Polyarteritis nodosa is more common in people with hepatitis B infection.

[edit] Diagnosis

The original assays for detection of hepatitis B virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex. The table below is organized chronologically, from top to bottom:

Antigens	Antibodies
The hepatitis B surface antigen (HBsAg^[7]) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection with this virus; however, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host.	-
The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen, or HBcAg^[8]	During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IGM) may be the only serologic evidence of disease.
Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg^[9]) will appear.^[2] Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication; however, some variants of the hepatitis B virus do not produce the 'e' antigen at all, so this rule does not always hold true.	During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will arise immediately afterward. This conversion is usually associated with a dramatic decline in viral replication.
-	If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by antibodies to the hepatitis B surface antigen (anti-HBs).^[1]

A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously. A number of persons who are positive for HBsAg may have very little viral multiplication, and hence may be at little risk of long-term complications or of transmitting infection to others.

More recently, PCR tests have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These tests are useful to assess a person's infection status and to monitor treatment.

Treatment:

There are currently several treatments for chronic hepatitis B that can increase a person's chance of clearing the infection. Treatments are available in the form of antivirals such as lamivudine and adefovir and immune system modulators such as interferon alpha (Uniferon). There are several other antivirals under investigation. Roughly, all of the currently available treatments, when used alone, are about equally efficacious. However, some individuals are much more likely to respond than others. It does not appear that combination therapy offers any advantages.^[10] In general, each works by reducing the viral load by several orders of magnitude thus helping a body's immune system clear the infection. Treatment strategies should be individualized by a doctor and patient. Considerations include the risks associated with each treatment, a person's likelihood of clearing the virus with treatment, a person's risk for developing complications of persistent infection, and development of viral resistance with some of the treatments.

On March 29, 2005, the US Food and Drug Administration (FDA) approved Entecavir for the treatment of hepatitis B.

On February 25, 2005, the EU Commission approved PEGASYS for the treatment of hepatitis B making it the first pegylated interferon to be approved for hepatitis B.

On October 27, 2006 telbivudine gained FDA approval for chronic treatment of chronic hepatitis B. Its side effects profile is generally less than that of other anti-virals in comparison, especially lamivudine. It is marketed under the brand name Tyzeka in the US and Sebivo outside the US. It is already approved in Switzerland [1].

Chronic carriers should be strongly encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and hepatocellular carcinoma (liver cancer).

Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (hepatitis B immune globulin or HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 95%. This treatment also allows a mother to safely breastfeed her child.

An individual exposed to the virus who has never been vaccinated may be treated with HBIg immediately following the exposure. For instance, a health care worker accidentally stuck by a needle used in a hepatitis B carrier would qualify. Treatment must be soon after exposure, however.

[edit] Prevention

Several vaccines have been developed for the prevention of hepatitis B virus infection. These rely on the use of one of the viral envelope proteins (hepatitis B surface antigen or HBsAg). The vaccine was originally prepared from plasma obtained from patients who had long-standing hepatitis B virus infection. However, currently, these are more often made using recombinant DNA technology, though plasma-derived vaccines continue to be used; the two types of vaccines are equally effective and safe.

Many countries now routinely vaccinate infants against hepatitis B. Babies born to HBeAg positive mothers are strongly recommended to be vaccinated and injected with immune globulin immediately after birth, so as to prevent transmission of infection. In many areas, vaccination against hepatitis B is also required for all health-care workers. Some college campus housing units now require proof of vaccination as a prerequisite. Booster doses are not needed for low-risk general population. Some recommend such doses every five to ten years for health-care workers, though the evidence supporting such doses is quite limited.

The vaccine is highly effective. In endemic countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer. This was reported in Taiwan where the implementation of a nationwide hepatitis B vaccination program in 1984 was associated with a decline in the incidence of childhood hepatocellular carcinoma.^[11] In that sense, this vaccine can be thought of as an anti-cancer vaccine.

Patients with HIV appear to have inferior antibody responses to hepatitis B vaccination.^[12]

[edit] See also

[edit] References

^ ^a ^b ^c Zuckerman AJ (1996). Hepatitis Viruses. In: Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
^ ^a ^b Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, pp. 544–51. ISBN 0-8385-8529-9.
^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). Molecular Biology of the Cell, 4th, Garland. (via NCBI Bookshelf) ISBN 0-8153-3218-1.
^ Hepadnaviridae characteristics - ICTVdB
^ Iannacone M. et al (2006). "Pathogenetic and antiviral immune responses against hepatitis B virus". Future Virology 1 (2): 189-196.
^ Iannacone M, Sitia G, Isogawa M, Marchese P, Castro M, Lowenstein P, Chisari F, Ruggeri Z, Guidotti L (2005). "Platelets mediate cytotoxic T lymphocyte-induced liver damage". Nat Med 11 (11): 1167-9. PMID 16258538.
^ MeSH HBsAg
^ MeSH HBcAg
^ MeSH HBeAg
^ Lau GKK et al (2005). "Peginterferon Alfa-2a, lamivudine, and the combination for HBeAg-positive chronic hepatitis B". N Engl J Med 352 (26): 2682-95. PMID 15987917.
^ Chang MH, Chen CJ, Lai MS, Hsu HM, Wu TC, Kong MS, Liang DC, Chau WY, Chen DS (1997). "Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children. Taiwan Childhood Hepatoma Study Group". N Engl J Med 336 (26): 1855-9. PMID 9197213.
^ Pasricha N, Datta U, Chawla Y, Singh S, Arora S, Sud A, Minz R, Saikia B, Singh H, James I, Sehgal S (2006). "Immune responses in patients with HIV infection after vaccination with recombinant Hepatitis B virus vaccine". BMC Infect Dis 6: 65. PMID 16571140.

[edit] External links

v • d • e

Sexually transmitted diseases and infections (STD/STI)[hide]

Bacterial	Chancroid (Haemophilus ducreyi) • Chlamydia (Chlamydia trachomatis) • Donovanosis (Granuloma Inguinale) • Lymphogranuloma venereum (LGV) (Chlamydia trachomatis) • Gonorrhoea (Neisseria gonorrhoeae) • Syphilis (Treponema pallidum) • Ureaplasma urealyticum
Protozoal	Trichomoniasis (Trichomonas vaginalis)
Parasitic	Crab louse/crabs • Scabies
Viral	AIDS (HIV-1/HIV-2) • Cervical cancer & Genital warts (condyloma) (Human papillomavirus (HPV)) • Hepatitis B • Herpes simplex virus (HSV1/HSV2) • Molluscum contagiosum (MCV)
Other conditions	Cervicitis • Epididymitis • Ectopic pregnancy • Infertility • Non-gonococcal urethritis (NGU) • Pelvic inflammatory disease (PID) • Premature birth • Proctitis • Prostatitis • Reactive arthritis • Urethritis

Retrieved from "http://en.wikipedia.org/wiki/Hepatitis_B"

Categories: Hepatitis | Viruses

藥物名稱	每月開支 HKD(大約)	16-Feb-2009

1. Lamivudine ( Zeffix )	$ 800 - $ 900

2. Adefovir ( Hepsera )	( 略低於 entecavir )

3. Entecavir ( Baraclude )	$ 1,500


		side effects of Lamivudine
Tell your doctor if any of these symptoms are severe or do not go away:

chills	cough	depression	loss of appetite
diarrhea	dizziness	fatigue	headache	stuffy nose	trouble sleeping
upset stomach	vomiting

From Wikipedia, the free encyclopedia

Mechanism of action:

Contents

Function

Clinical significance: reverse fibrosis and cirrhoses

Elevated levels

目錄

[編輯] 基本病理變化

] 肝炎種類

B肝檢驗

預防

參見

外部連結

參考文獻

Hepatitis B

From Wikipedia, the free encyclopedia

Contents

[edit] Structure

[edit] Replication

[edit] Transmission

[edit] Immunopathogenesis

[edit] Symptoms and complications

[edit] Diagnosis

[edit] Prevention

[edit] See also

[edit] References

[edit] External links