Hepatitis B

موضوع: Hepatitis B الأربعاء سبتمبر 07, 2011 9:57 am

Hepatitis B is an infectious hepatitis caused by the hepatitis B virus (HBV). This infection has two possible phases; 1) acute and 2) chronic.
Acute hepatitis B refers to newly acquired infections. Affected individuals notice symptoms approximately 1 to 4 months after exposure to the virus. In most people with acute hepatitis, symptoms resolve over weeks to months and they are cured of the infection. However, a small number of people develop a very severe, life-threatening form of acute hepatitis called fulminant hepatitis.

Chronic hepatitis B is an infection with HBV that lasts longer than 6 months. Once the infection becomes chronic, it may never go away completely.

Approximately 90% to 95% of infected adults are able to fight off the virus so their infection is cured. Only about 5% to 10% of adults infected with HBV go on to develop chronic infection. Children are at much higher risk for chronic infection. Up to 90% of infected young children will fail to clear the virus from their bodies and go on to develop chronic infection.

About two-thirds of people with chronic HBV infection are chronic carriers. These people do not develop symptoms, even though they harbor the virus and can transmit it to other people. The remaining one third develop "active" hepatitis, a disease of the liver that can be very serious.
The liver is an important organ that filters toxins out of the blood, stores energy for later use, helps with digestion, and makes substances that fight infections and control bleeding.

The liver has an incredible ability to heal itself, but long-term inflammation caused by HBV can result in permanent damage.

Scarring of the liver is called cirrhosis, a condition traditionally associated with alcoholism but one that is also caused by chronic active hepatitis B infection. When this occurs, the liver can no longer carry out its normal functions and may fail completely. The only treatment for liver failure is liver transplant.

Chronic hepatitis B also can lead to a type of liver cancer known as hepatocellular carcinoma.

Any of these conditions can be fatal. About 15% to 25% percent of people with chronic hepatitis B die of liver disease.

Hepatitis B is the most common serious liver infection in the world. Worldwide, about 350 million people are chronic carriers of HBV, of whom, more than 620,000 die from liver-related disease each year.

In the United States, hepatitis B is largely a disease of young adults aged 20-50 years. About 800,000 to 1.4 million Americans are chronic hepatitis B virus carriers, and the disease causes about 3, 000 deaths each year.

The good news is that infection with HBV is usually preventable because there is an effective vaccine. Use of the vaccine has resulted in an 82% decrease in the number of new infections reported in the United States each year.

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 of it. The infection may be entirely asymptomatic and may go unrecognized.[14]

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).

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, re-use of contaminated needles & syringes, and vertical transmission from mother to child 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.[21][22] However, at least 30% of reported hepatitis B among adults cannot be associated with an
identifiable risk factor

Diagnosis

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.[13]

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 named as the 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).[11] 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.[37] 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.[38]

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.[39] Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy

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, 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.[40]

The risk of vertical transmission to the newborn can be drastically reduced from 20%-90% 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 1-2 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. [41]

Following vaccination, hepatitis B surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia.[42] The vaccine is administered in either two-, three-, or four-dose schedules into infants and adults, which provides protection for 85–90% of individuals.[43] 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.[44]

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.[45]

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, 200–400 IU per month),[46][47] 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),[48][49] effectively and safely prevent HBV intrauterine transmission, which provide new insight into prevention of HBV at the earliest stage

Treatment

Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously.[50] 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.[51]

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.[52] 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).[53]

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%.[54] This treatment allows a mother to safely breastfeed her child.

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 25–30% in types C and D.[55]

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.[56]

Treatment lasts from 6 months to a year, depending on medication and genotype..

موضوع: رد: Hepatitis B الأربعاء سبتمبر 07, 2011 6:13 pm

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موضوع: رد: Hepatitis B السبت سبتمبر 10, 2011 6:42 pm

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