Hepatitis B What is hepatitis? Hepatitis means inflammation of the liver.

Hepatitis can be cause by medications, herbal remedies, chemicals, toxins, alcohol, autoimmune diseases, and viruses. What is Hepatitis B? Hepatitis B is a liver disease caused by a specific type of virus called hepatitis B virus (HBV). Diagnosis and Monitoring There are several blood tests that are use to find out if someone has been exposed to HBV. These tests can either indicate if someone has been recently infected referring to a short term (acute infection) or long term (chronic infection). Other type of tests called liver function tests are used to evaluate how the virus (HBV) is affecting the liver. HBsAg. This test identifies the hepatitis B surface antigen (HbsAg), a part of the outer coat of the virus. This test determines if someone has been exposed to HBV. HbeAg. This test identifies the hepatitis B e antigen (HbeAg), another part of the virus. If this antigen is found, it means the patient is contagious and can pass the virus on to someone else. Antibody tests. These tests can identify several different antibodies, including the hepatitis B surface

antibody (HBsAb), the hepatitis B core antibody (HBcAb) and the hepatitis B e antibody (HBeAb). If these antibodies are found, it means that the immune system was able to fight off the virus and clear the infection either because the person has been vaccinated against HBV or because the body has recovered from Hepatitis B infection. Monitoring liver enzyme Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are liver enzymes that are normally present in the blood. A higher-than-normal amount of these enzymes in a sample of blood can be a sign of liver damage. Symptoms Once someone is exposed to the hepatitis B virus, there are two possible outcome: first hepatitis B infection has a short-term phase called acute infection. The onset of symptoms ranges from 45 to 180 days (average 60-90 days). Up to 30% of people have no symptoms at all. Other people may have flu-like symptoms such as; chills, fever, fatigue, aching joints and muscles and fatigue, loss of appetite, nausea and vomiting, diarrhea, weight loss. A few people may develop jaundice - a condition in which the skin and the whites of the eyes turn yellow. Most adults, 90 to 9 percent, will recover from the acute infection without too much problems and they will have life long antibody protection (immunity) against future exposure to hepatitis B virus (HBV). Chronic Hepatitis B

The progression from acute to chronic infection is largely influence by the age of the person who becomes in contact with the virus. The chronic phase of the disease is determine when someone immune system is not able to clear the virus six months later after initial exposure to HBV. Newborns and infants are at higher risk to carry the infection beyond the acute stage of the infection. Up to 90% of infants and up to 50% of young children of 5 years of age infected with hepatitis B are not able to get rid of the virus and will develop a chronic hepatitis B infection. A smaller number of infected adults, 5 to 10 percent, will also progress to the chronic stage of hepatitis B infection. Often individuals with chronic HBV infection have no symptoms beside bouts of fatigue, loss of appetite and nausea. Chronic hepatitis B is a serious lifelong disease that can lead to scarring tissue of the liver called cirrhosis, and liver cancer, liver failure and death. . Treatment The goal of treatment for chronic hepatitis B infection is to shut down the virus replication, slow down liver progression from fibrosis to cirrhosis. The decision to start treatment is base on a careful evaluation of physical health, blood tests, and liver biopsy. Be sure you see a liver specialist called hepatologist or gastroenterologist for the most current information on hepatitis B therapies. Studies have show that people with signs of active liver disease tend to respond better to current treatments. Individuals with elevated liver enzymes (ALT), elevated levels of

hepatitis B virus (HBV DNA), positive blood tests for hepatitis B virus surface antigen (HBsAg) and hepatitis B e-antigen (HBeAg) tend to have a better antiviral response to treatment and a better outcome. Currently Interfereon alpha (Intron), Lamivudine (Epivir-HBV), and Adefovir dipivoxil (Hepsera) are three drugs licensed for the treatment of chronic hepatitis B. Interferon (Intron) Interferon-alpha is a cytokine, a protein messenger produced by the immune system in response to viral infections. Interferon-alpha-2b known as Intron A works by slowing down HBV replication and by improving the immune system response to fight off the hepatitis B virus. Interferon-alpha is taken as subcutaneous (under the skin) injection. The recommended dose for adults is 5 million units (MU) daily or 10 million units (MU) three times a week for four to six months. The most common side effects are flu-like symptoms, including fevers, chills, nausea and vomiting, shaking, hair thinning, fatigue and depression. These side effects may last for four to ten hours after the injection. Acetaminophen in small amount (1000 mg) and rest may help to alleviate flu like symptoms. Interferon therapy is not for everyone. The presence of other medical conditions may affect the use of interferon alpha. Make sure you tell your doctor if you have any other medical problems, especially you have the one of the following conditions: bleeding problems, Convulsions (seizures), history of mental problems (depression), diabetes, heart disease, kidney disease, lack of blood supply to any part of the body, lung

disease, thyroid disease, autoimmune disease (problems with overactive immune system). Your doctor will perform blood work al least once a month to monitor any abnormalities within the white blood cells, the platelets, and the red blood cells. Also, Interferon should not be use by pregnant women. Unfortunately, less than 35% of people with chronic hepatitis B are eligible to receive interferon therapy. Epivir-HBV (Lamivudine. 3TC) In December 1998, the FDA approved Epivir-HBV for the treatment of chronic hepatitis B. Epivir-HBV is an antiviral medication that belongs to a class of drugs called nucleoside analog reverse transcriptase inhibitors (NRTI). Epivir works by blocking the production of the reverse transcriptase enzyme that HBV need to reproduce. Epivir-HBV have shown to lower the amount of HBV in blood and reduce inflammation of the liver. Epivir is a tablet taken by mouth with or without food. It's also available as an oral liquid for children. The dosage is 100 mg taken once day. In general, Epivir is well tolerated. The most common side effects are headache, fatigue, upset stomach, nausea, vomiting, sleeping problems (insomnia), stuffy nose. In addition, studies have implicated all nucleoside analogues including Epivir, have shown to induce liver enlargement and increase lactic acid in the blood, a condition called lactic acidosis. If you experience any

of the following symptoms, upset stomach, loss of appetite, excessive tiredness, weakness, dark yellow or brown urine, unusual bleeding or bruising, flu-like symptoms, yellowing of the skin or eyes, and pain in the upper right part of your stomach call your doctor. It's not clear how long the treatment for HBV with Epivir should last for best results. Studies have shown that the lost of HbeAg (seroconversion rate) increases to 27% after 2 years, 40% after 3 years, and 47% after 4 years of treatment in individuals with low viral load (less than 100 pg/mL). When Epivir is stopped, levels of virus (HBV) in the blood often rise again, signs of liver inflammation (elevated levels of liver enzymes) reappear and symptoms can occur again. In addition, when 3TC is used by itself as monotherapy, viral resistance can develop, and causes the drug to stop working. Studies have shown that resistance occurs approximately in 15-30% of individuals after 12 months of treatment, and approximately 50% after 3 years of treatment. Even though of the emergence of 3TC resistance, continued treatment has been associated with lower levels of the virus (H BV DNA), less liver enzymes (ALT) activity, and an improvement in liver scarring tissue. Discontinuation of Epivir is often associated by a reversion to a wild type of Hepatitis B virus and a flare of the hepatitis B symptoms. Hepsera September 2002, the FDA has approved a new treatment for chronic hepatitis B called

Hepsera. Hepsera is oral drug that is approved for the treatment of chronic hepatitis B in adults with active HBV replication and either with persistent elevated liver enzymes (ALT or AST) or active liver inflammation. Hepsera (adeforvir dipivoxil) is a new class of antiviral drugs called nucleotide reverse transcriptae inhibitor that works by blocking the hepatitis B virus (HBV) enzyme polymerase involved in the replication of HBV. The dosage is 10mg once a day. The most common side effects are weakness, headaches, abdominal pain, nausea, flatulence, diarrhea, elevated liver enzymes, and disturbed digestion. Studies have shown that Hepsera is effective in individuals who had Epivir resistant virus. Transmission HBV and HIV share similar routes of transmission. HBV transmission occurs when blood or body fluids from an infected person enters the body of another person. HBV can be spread through unprotected sex with an infected person, sharing needles or "works" when "shooting" drugs, through needle sticks, and from an infected mother to her baby during birth. Vaccine The good news is that hepatitis B is preventable. Hepatitis B vaccines are available for all age groups to prevent the spread of the hepatitis B virus. The vaccine enables the body to produce antibodies against Hepatitis B infection The FDA has approved two vaccines, one

called Engerix-B and the other one Recombivax HB. The vaccines are given as a series of three (3) injections to achieve maximal protection. Make sure that you receive the 3 shots: a first dose, the second dose after one month, and the third dose six months after first dose. The vaccine is generally well tolerated. Health care professionals that get infected through needle stick injury have access to a preventative vaccine that involves hepatitis B immune globulin (HBIG), hepatitis B vaccine, or a combination of both. Who should be vaccinated? People with HIV, hepatitis C or other chronic liver disease, individuals who have multiple sexual partners, newborns & children up to age 19, health care professionals exposed to blood work, Injection drug users and people living in the same household with a chronically infected individual. Prevention Individuals should practice safe sex, use condom, not share personal care items that might have blood on them (razors, toothbrushes), consider the risks if you are thinking about getting a tattoo or body piercing, dont share needles, syringes, water, or "works" with other people. Liver health If it is not already done, get vaccinated against hepatitis A and hepatitis B Dink lots of water (at least 6 to 8 glasses a day) If you have chronic liver disease, drinking alcohol can worsen your liver condition.

Alcohol can greatly increase the risk of alcoholic and hepatitis C cirrhosis Be aware of drugs, herbal remedies, over-the- counter medications, recreational or street drugs that can be harsh for your liver. If you have advance liver disease, make sure you see your doctor regularly and you may have to consider to make a few changes into your dietary intake; protein, fats, salt, iron, etc. You may want to meet with a dietitian to review your nutrition needs. Written by Bertrand Toulouse for NATAP

Hepatitis B is an infectious illness caused by hepatitis B virus (HBV) which infects the liver of hominoidea, including humans, and causes an inflammation called hepatitis. Originally known as "serum hepatitis",[1] the disease has caused epidemics in parts of Asia and Africa, and it is endemic in China.[2] More than 2 billion people have been infected with the hepatitis B virus[3], and this includes 350 million chronic carriers of the virus.[4] Transmission of hepatitis B virus results from exposure to infectious blood or body fluids such as semen and vaginal fluids, while viral DNA has been detected in the saliva, tears, and urine of chronic carriers with high titer DNA in serum. Perinatal infection is a major route of infection in endemic (mainly developing) countries.[5] Other risk factors for developing HBV infection include working in a health care setting, transfusions, and dialysis, acupuncture, tattooing, extended overseas travel and residence in an institution. [6] [3][7] However, Hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding.[8][9] The acute illness causes liver inflammation, vomiting, jaundice, and (rarely) death. Chronic hepatitis B may eventually cause cirrhosis and liver cancera fatal disease with very poor response to current chemotherapy.[10] The infection is preventable by vaccination.[11] Hepatitis B virus is an hepadnavirushepa from hepatotrophic and dna because it is a DNA virus[12]and it has a circular genome composed of partially double-stranded DNA. The viruses replicate through an RNA intermediate form by reverse transcription, and in this respect they are similar to retroviruses.[13] Although replication takes place in the liver, the virus spreads to the blood where virus-specific proteins and their corresponding antibodies are found in infected people. Blood tests for these proteins and antibodies are used to diagnose the infection.[14]

Contents
[hide]

1 Signs and symptoms 2 Mechanisms

2.1 Pathogenesis 2.2 Transmission

3 Virology

3.1 Structure 3.2 Genome 3.3 Replication 3.4 Serotypes and genotypes

4 Diagnosis 5 Prevention 6 Treatment 7 Prognosis

7.1 Reactivation

8 Epidemiology 9 History 10 See also 11 References 12 External links

[edit] Signs and symptoms

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, body aches, mild fever, dark urine, and then progresses to development of jaundice. It has been noted that itchy skin 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 affected people. A few patients may have more severe liver disease (fulminant hepatic failure), and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.[15] 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 hepatocellular carcinoma (liver cancer). Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. Hepatitis B virus has been linked to the development of Membranous glomerulonephritis (MGN).[16] Extrahepatic manifestations of hepatitis B are present in 110% of HBV-infected patients and include serum-sicknesslike syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti-Crosti syndrome).[17][18] The serum-sicknesslike syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice.[19] The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B.[20] About 3050% of patients with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers.[21] HBV-associated nephropathy has been described in adults but is more common in children.[22][23] Membranous glomerulonephritis is the

most common form.[20] Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.[20]

[edit] Mechanisms
[edit] Pathogenesis
Hepatitis B virus primarily interferes with the functions of the liver by replicating in liver cells, known as hepatocytes. The receptor is not yet known, though there is evidence that the receptor in the closely related duck hepatitis B virus is carboxypeptidase D.[24][25] HBV virions (DANE particle) bind to the host cell via the preS domain of the viral surface antigen and are subsequently internalized by endocytosis. PreS and IgA receptors are accused of this interaction. HBV-preS specific receptors are primarily expressed on hepatocytes; however, viral DNA and proteins have also been detected in extrahepatic sites, suggesting that cellular receptors for HBV may also exist on extrahepatic cells.[26] During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. Although 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 most of the liver injury associated with HBV infection. CTLs eliminate HBV infection by killing infected cells and producing antiviral cytokines, which are then used to purge HBV from viable hepatocytes.[27] Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver.[28]

[edit] Transmission
Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood. Possible forms of transmission include sexual contact, blood transfusions, reuse of contaminated needles & syringes, and vertical transmission from mother to child (MTCT) during childbirth. Without intervention, a mother who is positive for HBsAg 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 HBeAg. HBV can be transmitted between family members within households, possibly by contact of nonintact skin or mucous membrane with secretions or saliva containing HBV.[29][30] However, at least 30% of reported hepatitis B among adults cannot be associated with an identifiable risk factor.[31] And Shi et al. showed that breastfeeding after proper immunoprophylaxis did not contribute to MTCT of HBV.[32]

[edit] Virology
Main article: Hepatitis B virus

[edit] Structure

The genome organisation of HBV. The genes overlap.

Hepatitis B virus replication. Hepatitis B virus (HBV) is a member of the Hepadnavirus family.[12] The virus particle, (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity.[13] The outer envelope contains embedded proteins which are involved in viral binding of, and entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses, with a virion diameter of 42 nm, but pleomorphic forms exist, including filamentous and spherical bodies lacking a core. These particles are not infectious and are composed of the lipid and protein that forms part of the surface of the virion, which is called the surface antigen (HBsAg), and is produced in excess during the life cycle of the virus.[33]

[edit] Genome
The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase. The genome is 30203320 nucleotides long (for the full-length strand) and 17002800 nucleotides long (for the short length-strand).[34] The negative-sense, (non-coding), is complementary to the viral mRNA. The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the (+) sense strand and removal of a protein molecule from the (-) sense strand and a short sequence of RNA from the (+) sense strand. Non-coding bases are removed from the ends of the (-) sense strand and the ends are rejoined. There are four known genes encoded by the genome, called C, X, P, and S.

The core protein is coded for by gene C (HBcAg), and its start codon is preceded by an upstream in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen (HBsAg). The HBsAg gene is one long open reading frame but contains three in frame "start" (ATG) codons that divide the gene into three sections, pre-S1, pre-S2, and S. Because of the multiple start codons, polypeptides of three different sizes called large, middle, and small (pre-S1 + pre-S2 + S, pre-S2 + S, or S) are produced.[35] The function of the protein coded for by gene X is not fully understood but it is associated with the development of liver cancer. It stimulates genes that promote cell growth and inactivates growth regulating molecules.[36]

[edit] Replication
The life cycle of hepatitis B virus is complex. Hepatitis B is one of a few known non-retroviral viruses which use reverse transcription as a part of its replication process. The virus gains entry into the cell by binding to an unknown receptor on the surface of the cell and enters it by endocytosis. Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus by host proteins called chaperones. The partially double stranded viral DNA is then made fully double stranded and transformed into covalently closed circular DNA (cccDNA) that serves as a template for transcription of four viral mRNAs. The largest mRNA, (which is longer than the viral genome), is used to make the new copies of the genome and to make the capsid core protein and the viral DNA polymerase. These four viral transcripts undergo additional processing and go on to form progeny virions which are released from the cell or returned to the nucleus and re-cycled to produce even more copies.[35][37] The long mRNA is then transported back to the cytoplasm where the virion P protein synthesizes DNA via its reverse transcriptase activity.

[edit] Serotypes and genotypes

The virus is divided into four major serotypes (adr, adw, ayr, ayw) based on antigenic epitopes presented on its envelope proteins, and into eight genotypes (A-H) according to overall nucleotide sequence variation of the genome. The genotypes have a distinct geographical distribution and are used in tracing the evolution and transmission of the virus. Differences between genotypes affect the disease severity, course and likelihood of complications, and response to treatment and possibly vaccination.[38][39] Genotypes differ by at least 8% of their sequence and were first reported in 1988 when six were initially described (A-F).[40] Two further types have since been described (G and H).[41] Most genotypes are now divided into subgenotypes with distinct properties.[42] Genotype A is most commonly found in the Americas, Africa, India and Western Europe. Genotype B is most commonly found in Asia and the United States. Genotype B1 dominates in Japan, B2 in China and Vietnam while B3 confined to Indonesia. B4 is confined to Vietnam. All these strains specify the serotype ayw1. B5 is most common in the Philippines. Genotype C is most common in Asia and the United States. Subgenotype C1 is common in Japan, Korea and China. C2 is common in China, South-East Asia and Bangladesh and C3 in Oceania. All these strains specify the serotype adrq. C4 specifying ayw3 is found in Aborigines from Australia.[43] Genotype D is most commonly found in Southern Europe, India and the United States and has been divided into 8 subtypes (D1D8). In Turkey genotype D is also the most common type. A pattern of defined geographical distribution is less evident with D1D4 where these subgenotypes are widely spread within Europe, Africa and Asia. This may be due to their divergence having occurred before than of genotypes B and C. D4 appears to be the oldest split

and is still the dominating subgenotype of D in Oceania. Type E is most commonly found in West and Southern Africa. Type F is most commonly found in Central and South America and has been divided into two subgroups (F1 and F2). Genotype G has an insertion of 36 nucleotides in the core gene and is found in France and the United States.[44] Type H is most commonly found in Central and South America and California in United States. Africa has five genotypes (A-E). Of these the predominant genotypes are A in Kenya, B and D in Egypt, D in Tunisia, A-D in South Africa and E in Nigeria.[43] Genotype H is probably split off from genotype F within the New World.[45]

[edit] Diagnosis

Hepatitis B viral antigens and antibodies detectable in the blood following acute infection.

Hepatitis B viral antigens and antibodies detectable in the blood of a chronically infected person.

Ground glass hepatocytes as seen in a chronic hepatitis B. Liver biopsy. H&E stain. The tests, called 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.[14] The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. 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. 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 serological evidence of disease. Shortly after the appearance of the HBsAg, another antigen called hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the hepatitis B virus do not produce the 'e' antigen, 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 afterwards. 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 IgG antibodies to the hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc IgG).[12] The time between the removal of the HBsAg and the appearance of anti-HBs is called the window period. A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously. Individuals who remain HBsAg positive for at least six months are considered to be hepatitis B carriers.[46] Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase (ALT) levels and inflammation of the liver, as revealed by biopsy. Carriers who have seroconverted to HBeAg negative status, particularly those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.[47] PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. These tests are used to assess a person's infection status and to monitor treatment.[48] Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy.

[edit] Prevention
Main article: Hepatitis B vaccine

HBsAg

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, it is made using a synthetic recombinant DNA technology that does not contain blood products. One cannot be infected with hepatitis B from this vaccine.[49] The risk of vertical transmission to the newborn can be drastically reduced from 2090% to 5 10% by administering to the newborn hepatitis B vaccine (HBV 1) and hepatitis B immune globulin (HBIG) within 12 hours of birth, followed by a second dose of hepatitis B vaccine (HBV 2) at 12 months and a third dose at and no earlier than 6 months (24 weeks). Since 2% of infants vaccinated will not develop immunity after the first three dose series, infants born to hepatitis B positive mothers are tested at 9 months for hepatitis B surface antigen (HBsAg) and the antibody to the hepatitis B surface antigen (anti-HBs); if post-vaccination test results indicate that the child is still susceptible, a second three dose series at (0, 1 and 6 months) is administered. If the child is still susceptible after the second series, a third series is not recommended. [50] Following vaccination, hepatitis B surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia.[51] The vaccine is administered in either two-, three-, or four-dose schedules into infants and adults, which provides protection for 8590% of individuals.[52] Protection has been observed to last 12 years in individuals who show adequate initial response to the primary course of vaccinations, and that immunity is predicted to last at least 25 years.[53] Unlike hepatitis A, hepatitis B does not generally spread through water and food. Instead, it is transmitted through body fluids; prevention is thus the avoidance of such transmission: unprotected sexual contact, blood transfusions, re-use of contaminated needles and syringes, and vertical transmission during child birth. Infants may be vaccinated at birth.[54] Shi, et al. showed that besides the WHO recommended joint immunoprophylaxis starting from the newborn, multiple injections of small doses of hepatitis B immune globulin (HBIg, 200400 IU per month),[55][56] or oral lamivudine (100 mg per day) in HBV carrier mothers with a high degree of infectiousness (>106 copies/ml) in late pregnancy (the last three months of pregnancy), [57][58] effectively and safely prevent HBV intrauterine transmission, which provide new insight into prevention of HBV at the earliest stage.

[edit] Treatment
Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously.[59] Early antiviral treatment may only be required in fewer than 1% of patients, whose infection takes a very aggressive course (fulminant hepatitis) or who are immunocompromised. On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected individuals with persistently elevated serum alanine aminotransferase, a marker of liver damage, and HBV DNA levels are candidates for therapy.[60] Although none of the available drugs can clear the infection, they can stop the virus from replicating, thus minimizing liver damage. Currently, there are seven medications licensed for treatment of hepatitis B infection in the United States. These include antiviral drugs lamivudine (Epivir), adefovir (Hepsera), tenofovir (Viread), telbivudine (Tyzeka) and entecavir (Baraclude) and the two immune system modulators interferon alpha-2a and PEGylated interferon alpha-2a

(Pegasys). The use of interferon, which requires injections daily or thrice weekly, has been supplanted by long-acting PEGylated interferon, which is injected only once weekly.[61] However, some individuals are much more likely to respond than others and this might be because of the genotype of the infecting virus or the patient's heredity. The treatment reduces viral replication in the liver, thereby reducing the viral load (the amount of virus particles as measured in the blood).[62] Infants born to mothers known to carry hepatitis B can be treated with antibodies to the hepatitis B virus (HBIg). When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis B is reduced 90%.[63] Response to treatment differs between the genotypes. Interferon treatment may produce an e antigen seroconversion rate of 37% in genotype A but only a 6% seroconversion in type D. Genotype B has similar seroconversion rates to type A while type C seroconverts only in 15% of cases. Sustained e antigen loss after treatment is ~45% in types A and B but only 2530% in types C and D.[64] In July 2005, researchers identified an association between a host-derived DNA-binding protein and the amount of HBV replication in the liver. Controlling the level of production of this protein could be used to treat hepatitis B.[65] Treatment lasts from 6 months to a year, depending on medication and genotype.[66]

[edit] Prognosis
Hepatitis B virus infection may either be 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.[67] This population has a 40% lifetime risk of death from cirrhosis or hepatocellular carcinoma.[61] Of those infected between the age of one to six, 70% will clear the infection.[68] Hepatitis D (HDV) can only occur with a concomitant hepatitis B infection, because HDV uses the HBV surface antigen to form a capsid.[69] Co-infection with hepatitis D increases the risk of liver cirrhosis and liver cancer.[70] Polyarteritis nodosa is more common in people with hepatitis B infection.

[edit] Reactivation
Hepatitis B virus DNA persists in the body after infection and in some people the disease recurs. [71] Although rare, reactivation is seen most often in people with impaired immunity.[72] HBV goes through cycles of replication and non-replication. Approximately 50% of patients experience acute reactivation. Male patients with baseline ALT of 200 UL/L are three times more likely to develop a reactivation than patients with lower levels. Patients 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.[73]

[edit] Epidemiology
According to the World Health Organization, hepatitis B virus (HBV) is an important risk factor for liver cancer and cirrhosis. Currently, two billion people are infected with HBV, and 350 million people have long-term effects resulting from the virus. For example, approximately one

quarter of adults that were infected with HBV as children ultimately die from liver cancer and cirrhosis. An effective method to prevent HBV infection and its subsequent long-term health effects is through immunization with the hepatitis B vaccine.[74].

2002 estimate of disability-adjusted life year for hepatitis B per 100,000 inhabitants.[75] no data 80100 10 100120 1020 120150 2030 150200 3040 200500 4050 500 5080 In 2004, an estimated 350 million individuals were infected worldwide. National and regional prevalence ranges from over 10% in Asia to under 0.5% in the United States and northern Europe. Routes of infection include vertical transmission (such as through childbirth), early life horizontal transmission (bites, lesions, and sanitary habits), and adult horizontal transmission (sexual contact, intravenous drug use).[76] The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, injection drug abuse and unprotected sex are the primary methods, although other factors may also be important.[77] In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 27% of the population is chronically infected, the disease is predominantly spread among children. In high prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor.[78] The prevalence of chronic HBV infection in areas of high endemicity is at least 8%. As of 2010, China has 120 million infected people, followed by India and Indonesia with 40 million and 12 million respectively. According to WHO, an estimated 600,000 people die every year related to the infection.[79]

[edit] History
The earliest record of an epidemic caused by hepatitis B virus was made by Lurman in 1885.[80] An outbreak of smallpox occurred in Bremen in 1883 and 1,289 shipyard employees were vaccinated with lymph from other people. After several weeks, and up to eight months later, 191 of the vaccinated workers became ill with jaundice and were diagnosed as suffering from serum hepatitis. Other employees who had been inoculated with different batches of lymph remained healthy. Lurman's paper, now regarded as a classical example of an epidemiological study, proved that contaminated lymph was the source of the outbreak. Later, numerous similar outbreaks were reported following the introduction, in 1909, of hypodermic needles that were used, and more importantly reused, for administering Salvarsan for the treatment of syphilis. The virus was not discovered until 1965 when Baruch Blumberg, then working at the National Institutes of Health (NIH), discovered the Australia antigen (later known to be hepatitis B

surface antigen, or HBsAg) in the blood of Australian aboriginal people.[81] Although a virus had been suspected since the research published by MacCallum in 1947,[82] D.S. Dane and others discovered the virus particle in 1970 by electron microscopy.[83] By the early 1980s the genome of the virus had been sequenced,[84] and the first vaccines were being tested.[85]

[edit] See also

Hepatitis B in China World Hepatitis Day

1. ^ Barker, L. F. et al. (1996). "Transmission of serum hepatitis. 1970". Journal of the American Medical
Association 276 (10): 841844. doi:10.1001/jama.276.10.841. PMID 8769597. doi:10.1002/hep.21347. PMID 16941687.
edit edit

[edit] References
2. ^ Williams, R. (2006). "Global challenges in liver disease". Hepatology (Baltimore, Md.) 44 (3): 521526. 3. ^ a b "Hepatitis B". World Health Organization.
http://www.who.int/mediacentre/factsheets/fs204/en/index.html. Retrieved 2009-09-19.

4. ^ "FAQ about Hepatitis B". Stanford School of Medicine. 2008-07-10.

http://liver.stanford.edu/Education/faq.html. Retrieved 2009-09-19.

5. ^ Coopstead, Lee-Ellen C. (2010). Pathophysiology. Missouri: Saunders. pp. 886887. ISBN 978-1-41605543-3.

6. ^ Sleisenger, MH; Feldman M, Friedman LS (2006). Fordtran's gastrointestinal and liver disease:
pathophysiology, diagnosis, management (8th ed.). Philadelphia: Saunders.

7. ^ Kidd-Ljunggren K, Holmberg A, Blckberg J, Lindqvist B (December 2006). "High levels of hepatitis B

virus DNA in body fluids from chronic carriers". The Journal of Hospital Infection 64 (4): 3527. doi:10.1016/j.jhin.2006.06.029. PMID 17046105.

8. ^ "Hepatitis B". National Institute of Health. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001324.

Retrieved 2010-11-23.

9. ^ "Hepatitis B FAQ Transmission". U.S. Centers for Disease Control and Prevention.
http://www.cdc.gov/hepatitis/B/bFAQ.htm#transmission. Retrieved 2011-11-29.

10. ^ Chang, M. (2007). "Hepatitis B virus infection". Seminars in fetal & neonatal medicine 12 (3): 160167.
doi:10.1016/j.siny.2007.01.013. PMID 17336170.
edit

11. ^ Pungpapong, S.; Kim, W.; Poterucha, J. (2007). "Natural History of Hepatitis B Virus Infection: an
Update for Clinicians". Mayo Clinic Proceedings 82 (8): 967975. doi:10.4065/82.8.967. PMID 17673066. edit

12. ^ a b c Zuckerman AJ (1996). "Hepatitis Viruses". In Baron S, et al. Baron's Medical Microbiology (4th ed.).
University of Texas Medical Branch. ISBN 0-9631172-1-1. http://www.ncbi.nlm.nih.gov/books/bv.fcgi? rid=mmed.section.3738.

13. ^ a b Locarnini, S. (2004). "Molecular virology of hepatitis B virus". Seminars in liver disease. 24 Suppl 1:
310. doi:10.1055/s-2004-828672. PMID 15192795.
edit

14. ^ a b Bonino, F.; Chiaberge; Maran; Piantino (1987). "Serological markers of HBV infectivity". Annali
dell'Istituto superiore di sanita 24 (2): 217223. PMID 3331068.
edit

15. ^ Terrault N, Roche B, Samuel D (July 2005). "Management of the hepatitis B virus in the liver
transplantation setting: a European and an American perspective". Liver Transpl. 11 (7): 71632. doi:10.1002/lt.20492. PMID 15973718. http://dx.doi.org/10.1002/lt.20492.

16. ^ Gan SI, Devlin SM, Scott-Douglas NW, Burak KW (October 2005). "Lamivudine for the treatment of
membranous glomerulopathy secondary to chronic Hepatitis B infection". Canadian journal of gastroenterology = Journal canadien de gastroenterologie 19 (10): 6259. PMID 16247526.

17. ^ Dienstag JL (February 1981). "Hepatitis B as an immune complex disease". Seminars in Liver Disease 1
(1): 4557. doi:10.1055/s-2008-1063929. PMID 6126007. http://www.thieme-connect.com/DOI/DOI? 10.1055/s-2008-1063929.

18. ^ Trepo C, Guillevin L (May 2001). "Polyarteritis nodosa and extrahepatic manifestations of HBV
infection: the case against

19.

iver

ver is the largest organ in the body. It is found high in the right upper abdomen, behind the ribs. It is a very complex and has many functions. They include: Storing energy in the form of sugar (glucose) Storing vitamins, iron, and other minerals Making proteins, including blood clotting factors, to keep the body healthy and help it grow Processing worn out red blood cells Making bile which is needed for food digestion Metabolizing or breaking down many medications and alcohol Killing germs that enter the body through the intestine

ver shoulders a heavy work load for the body, and almost never complains. It even has a remarkable power to regenerate should not be taken for granted. The liver is subject to illnesses, such as hepatitis B, which may lead to serious liver dam

is Hepatitis?

cells in the body are injured by such things as chemicals or infection, the area that is hurt becomes inflamed. Hepatitis is mation of the liver, which in turn causes damage to individual liver cells. It is most often caused by viral infection. Howeve so be caused by alcohol, certain drugs, chemicals or poisons, or other diseases.

tis may be either acute or chronic. In acute hepatitis the inflammation develops quickly, and lasts only a short period of ti atient usually recovers completely, but it can take up to several months. Occasionally, a person fails to recover fully, and t tis becomes chronic. In other words, it continues at a smoldering pace. Chronic hepatitis can develop over a number of ye ut the patient ever having acute hepatitis or even feeling sick. As the liver repairs itself, fibrous tissue develops, much like orms after a cut or injury to the skin heals. Advanced scarring of the liver is called cirrhosis. Over time, cirrhosis irreversib ges the liver, eventually ending in liver failure.

is Hepatitis B?

tis B is caused by the hepatitis B virus (medically abbreviated as HBV). Current estimates are that over 250,000 people United States contract HBV each year. It is often spread through sexual contact, accounting for about 50% of the ed cases. It is also spread through contact with blood or body fluids from a person carrying HBV. Some groups have a hig becoming infected with HBV. These include: Intravenous drug users Health care workers, funeral workers, police People in an HBV infected person's household People with multiple heterosexual or, especially, homosexual partners Residents of nursing homes Hemophiliac and hemodialysis patients Prisoners and prison workers Travelers to underdeveloped countries

Certain ethnic groups such as Asians, Hispanics, American Indians, Alaskan Natives, or people from developing countries

gnancy, the virus is passed from an infected mother to her child in about 90% of the cases. This usually occurs during del also carried in breast milk. In about 30% of all cases of hepatitis B, however, it is unknown how the patient contracted th

This situation is known as community acquired disease.

much more contagious than the AIDS virus. For example, it can live outside the body on a dry surface for up to 10 days. on gets the virus, it may take from one to six months for the infection and symptoms to develop. One of three things can n -- most patients develop acute Hepatitis B and recover completely; a small percentage become HBV carriers; and some op chronic hepatitis B.

e Hepatitis B

patients with acute hepatitis B have no symptoms, or the symptoms are mild and often mistaken for flu. Their bodies are t the virus off quickly. Some, however, can become quite sick while their bodies are fighting off the virus. The following ar oms of acute hepatitis B: Loss of appetite, nausea, vomiting, fever Aching muscles and sometimes joint pain Tenderness in the right upper abdomen Jaundice (yellowing of skin and eyes) Tea-colored urine; putty-like or white stool

osis of the disease is made by a blood test. It is called the hepatitis B surface antigen test (HBsAg). No specific ment is available or usually necessary for acute hepatitis infection. The physician may recommend supportive measures p the patient maintain strength and avoid taxing the liver while the body's natural defenses are fighting the virus. Acute tis B patients recover completely within six months and develop antibodies that give them a life-long immunity.

patients who become infected, however, do not recover completely. Up to 10% of adults with Hepatitis B and up to 50% o ed children under five years of age are not able to completely fight off the virus within six months. This occurs because the are unable to develop antibodies against hepatitis B. Most of these patients become HBV carriers.

Carriers

arriers recover from the infection completely and feel healthy. They have no ongoing hepatitis or liver damage. However, tests show they still have the virus and have not developed hepatitis B antibodies. Therefore, they can pass on the virus. ed an HBV carrier. Because carriers do not develop symptoms or feel sick, thousands of people who become carriers of HB know it. There may be as many as one million Americans carrying HBV. There is no treatment presently available for this on. Carriers have a responsibility to practice safe lifestyle habits that will prevent their passing the virus on to others. This ally includes protected sex.
Search

Liver

r is the largest organ in the body. It is found high in the right domen, behind the ribs. It is a very complex organ and has nctions. They include:
L Low i Upper er | v GI | e GI r

Storing energy in the form of sugar (glucose)

Storing vitamins, iron, and other minerals

Making proteins, including blood clotting factors, to keep he body healthy and help it grow

rocessing worn out red blood cells

Making bile which is needed for food digestion

Autoimmune Hepatitis Cirrhosis Fatty Liver Hemochromatosis Hepatitis hepatitis B Hepatitis c

Metabolizing or breaking down many medications and alcohol

Killing germs that enter the body through the intestine

r shoulders a heavy work load for the body, and almost never complains. It even has a ble power to regenerate itself. Still it should not be taken for granted. The liver is subject to , such as hepatitis B, which may lead to serious liver damage.

t is Hepatitis?

ells in the body are injured by such things as chemicals or infection, the area that is hurt becomes d. Hepatitis is inflammation of the liver, which in turn causes damage to individual liver cells. It often caused by viral infection. However, it can also be caused by alcohol, certain drugs, ls or poisons, or other diseases.

Primary Biliary Cirrhosi

s may be either acute or chronic. In acute hepatitis the inflammation develops quickly, and lasts hort period of time. The patient usually recovers completely, but it can take up to several months. nally, a person fails to recover fully, and the hepatitis becomes chronic. In other words, it s at a smoldering pace. Chronic hepatitis can develop over a number of years without the patient ing acute hepatitis or even feeling sick. As the liver repairs itself, fibrous tissue develops, much ar forms after a cut or injury to the skin heals. Advanced scarring of the liver is called cirrhosis. me, cirrhosis irreversibly damages the liver, eventually ending in liver failure.

Primary Sclerosing Cho

t is Hepatitis B?

s B is caused by the hepatitis B virus (medically abbreviated ). Current estimates are that over 250,000 people in the States contract HBV each year. It is often spread through ontact, accounting for about 50% of the reported cases. It is ead through contact with blood or body fluids from a person HBV. Some groups have a higher risk of becoming infected V. These include:

ntravenous drug users

Health care workers, funeral workers, police

eople in an HBV infected person's household

eople with multiple heterosexual or, especially, homosexual partners

Residents of nursing homes

Hemophiliac and hemodialysis patients

risoners and prison workers

ravelers to underdeveloped countries

Certain ethnic groups such as Asians, Hispanics, American Indians, Alaskan Natives, or eople from developing countries

ancy, the virus is passed from an infected mother to her child in about 90% of the cases. This occurs during delivery. HBV is also carried in breast milk. In about 30% of all cases of hepatitis ver, it is unknown how the patient contracted the virus. This situation is known as community disease.

much more contagious than the AIDS virus. For example, it can live outside the body on a dry or up to 10 days. Once a person gets the virus, it may take from one to six months for the n and symptoms to develop. One of three things can then happen -- most patients develop acute s B and recover completely; a small percentage become HBV carriers; and some develop chronic B.

e Hepatitis B

atients with acute hepatitis B have no symptoms, or the symptoms are mild and often mistaken Their bodies are able to fight the virus off quickly. Some, however, can become quite sick while dies are fighting off the virus. The following are symptoms of acute hepatitis B:

oss of appetite, nausea, vomiting, fever

Aching muscles and sometimes joint pain

enderness in the right upper abdomen

aundice (yellowing of skin and eyes)

ea-colored urine; putty-like or white stool

is of the disease is made by a blood test. It is called the B surface antigen test (HBsAg). No specific treatment is e or usually necessary for acute hepatitis infection. The

n may recommend supportive measures to help the patient maintain strength and avoid taxing while the body's natural defenses are fighting the virus. Acute hepatitis B patients recover ely within six months and develop antibodies that give them a life-long immunity.

tients who become infected, however, do not recover completely. Up to 10% of adults with s B and up to 50% of infected children under five years of age are not able to completely fight irus within six months. This occurs because their bodies are unable to develop antibodies against B. Most of these patients become HBV carriers.

Carriers

rriers recover from the infection completely and feel healthy. They have no ongoing hepatitis or mage. However, their blood tests show they still have the virus and have not developed hepatitis dies. Therefore, they can pass on the virus. This is called an HBV carrier. Because carriers do lop symptoms or feel sick, thousands of people who become carriers of HBV never know it. ay be as many as one million Americans carrying HBV. There is no treatment presently e for this situation. Carriers have a responsibility to practice safe lifestyle habits that will prevent sing the virus on to others. This especially includes protected sex.

nic Hepatitis B

er percentage of patients who cannot fight off the virus will develop chronic hepatitis B. Like rriers, chronic hepatitis B patients are also able to pass on HBV. However, there is a very nt difference with chronic hepatitis B. These patients will also have ongoing hepatitis and liver A few may have an increased risk for developing cancer of the liver. Once again, blood tests at no antibodies have developed.

with chronic hepatitis B should avoid alcohol because it can cause additional liver damage. edicines and drug combinations may cause liver injury, so patients should review all medications taking with their physicians. Patients should never take over-the-counter drugs without the n's approval. Chronic hepatitis B can now be treated with interferon (trade name: Intron A). tients, however, are not good candidates for interferon therapy. A liver disease specialist is often to determine if the patient should be placed on this therapy. Interferon has been shown to reduce ation and liver damage in about 30% of treated patients. A few go on to apparent complete . In some, however, the disease returns when therapy is stopped, and treatment may have to be . There are bothersome side effects with the drug, and treatment must be evaluated with the n on an individual basis.

Transplantation

nsplantation is a newer and very successful form of therapy for people with a badly damaged those patients with chronic hepatitis B, the new liver usually becomes infected with the virus, transplant medical centers are dealing with this effectively. There are new drugs for chronic B now under investigation. However, at the present time the best defense against HBV is on.

ention and Vaccination

a safe and effective vaccine to protect or immunize a person against hepatitis B. The vaccine offers protection for about 10 years or more. However, it is of no use to those already infected V. Persons who have not been vaccinated and who know they have been exposed to HBV eceive an injection of hepatitis B immune globulin within two weeks of exposure to the virus. alled a passive immunization. It gives immediate short-term protection for 3-6 months. The s B vaccine is active immunization. Active immunization provides long-term (sometimes protection. Therefore, people who are at risk of coming in contact with the virus, and especially infants and sexually active teenagers, should be immunized. In the U.S., pediatricians now end that all children be actively vaccinated.

e other precautions people should take to protect themselves against hepatitis B. Since the virus often spread through sexual contact, it is most important to avoid unprotected sex with those who are likely to have the infection. Precautions must be taken to avoid coming in contact with blood

fluids from an infected individual. For those living in households with infected patients, surfaces ay hold the virus should be cleaned with one part household bleach to 10 parts water. Items such , toothbrushes, IV needles or pierced earrings should never be shared. People should also avoid ctices as tattooing and ear piercing in places where sterile conditions are questionable. Women pregnant should be tested for HBV and follow their physicians' advice to protect their unborn

mary

s B is a serious disease that may result in long-term complications. While most people recover, velop chronic hepatitis. Some people become carriers of HBV without knowing it. For this t is important to prevent spread of the disease by vaccination and by lifestyle practices that avoid with infected blood and body fluids. For acute infections, no therapy is available or usually y. Researchers are continually learning more about hepatitis, and research into new treatments is . Chronic hepatitis B patients who are monitored frequently and follow the advice of their ns have every reason to expect a good quality of life.

ice

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nic Hepatitis B

ller percentage of patients who cannot fight off the virus will develop chronic hepatitis B. Like HBV carriers, chronic hepati ts are also able to pass on HBV. However, there is a very important difference with chronic hepatitis B. These patients wil ongoing hepatitis and liver damage. A few may have an increased risk for developing cancer of the liver. Once again, blood that no antibodies have developed.

ts with chronic hepatitis B should avoid alcohol because it can cause additional liver damage. Some medicines and drug nations may cause liver injury, so patients should review all medications they are taking with their physicians. Patients sh take over-the-counter drugs without the physician's approval. Chronic hepatitis B can now be treated with interferon (trad Intron A). Some patients, however, are not good candidates for interferon therapy. A liver disease specialist is often requ ermine if the patient should be placed on this therapy. Interferon has been shown to reduce inflammation and liver damag 30% of treated patients. A few go on to apparent complete recovery. In some, however, the disease returns when therap ed, and treatment may have to be restarted. There are bothersome side effects with the drug, and treatment must be eva he physician on an individual basis.

Transplantation

ransplantation is a newer and very successful form of therapy for people with a badly damaged liver. In those patients wi c hepatitis B, the new liver usually becomes infected with the virus, but most transplant medical centers are dealing with vely. There are new drugs for chronic hepatitis B now under investigation. However, at the present time the best defense t HBV is prevention.

ention and Vaccination

is a safe and effective vaccine to protect or immunize a person against hepatitis B. The vaccine usually offers protection fo 10 years or more. However, it is of no use to those already infected with HBV. Persons who have not been vaccinated and they have been exposed to HBV should receive an injection of hepatitis B immune globulin within two weeks of exposure t This is called a passive immunization. It gives immediate short-term protection for 3-6 months. The Hepatitis B vaccine is immunization. Active immunization provides long-term (sometimes lifelong) protection. Therefore, people who are at risk g in contact with the virus, and especially newborn infants and sexually active teenagers, should be immunized. In the U.S ricians now recommend that all children be actively vaccinated.

are other precautions people should take to protect themselves against hepatitis B. Since the virus is most often spread gh sexual contact, it is most important to avoid unprotected sex with those who have or are likely to have the infection. utions must be taken to avoid coming in contact with blood or body fluids from an infected individual. For those living in holds with infected patients, surfaces which may hold the virus should be cleaned with one part household bleach to 10 pa Items such as razors, toothbrushes, IV needles or pierced earrings should never be shared. People should also avoid such ces as tattooing and ear piercing in places where sterile conditions are questionable. Women who are pregnant should be t V and follow their physicians' advice to protect their unborn children.

mary

tis B is a serious disease that may result in long-term complications. While most people recover, some develop chronic tis. Some people become carriers of HBV without knowing it. For this reason, it is important to prevent spread of the disea ation and by lifestyle practices that avoid contact with infected blood and body fluids. For acute infections, no therapy is ble or usually necessary. Researchers are continually learning more about hepatitis, and research into new treatments is ng. Chronic hepatitis B patients who are monitored frequently and follow the advice of their physicians have every reason t a good quality of life.

ice

Philosophy | Meet The Providers | Nursing Staff | Administrative Staff | Find Us | Office Hours | Insurance | Patient Satisfactio Surveys | Publications | Newsletters High Fiber | GERD | Gluten Free | Lactose Free | Gastroparesis | [More] Barretts Esophagus | Celiac Disease | Cirrhosis | Prevention of Colon Polyps | Crohn's Disease | Diverticulosis/Diverticulitis | Gastroparesis | GERD | Irritable Bowel Syndrome | Ulcerative Colitis | [More] Endoscopy Images | Upper GI Endoscopy (EGD) | Colonoscopy | Flexible Sigmoidoscopy