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, and 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 people 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.
Chronic infection with hepatitis B virus either may be 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).
Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti-Crosti syndrome).
The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice.
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.
About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form.
Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.
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 people who had long-standing hepatitis B virus infection.
However, 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.
The risk of transmission from mother to newborn can be 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.
Following vaccination, hepatitis B surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia.
The vaccine is administered in either two-, three-, or four-dose schedules into infants and adults, which provides protection for 85–90% of individuals.
For Hepatitis A, 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; similar long-term effects are expected for Hepatitis B.
Unlike hepatitis A, hepatitis B does not generally spread through water and food. Instead, it is transmitted through body fluids; thus, prevention is 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.
Besides the WHO-recommended joint immunoprophylaxis starting from the newborn, multiple injections of small doses of hepatitis B immune globulin, or oral lamivudine in HBV carrier mothers with a high degree of infectiousness (>106 copies/ml) in late pregnancy (the last three months of pregnancy), effectively and safely prevent HBV intrauterine transmission, which provide new insight into prevention of HBV at the earliest stage.
Treatment
The hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously.
Early antiviral treatment may be required in fewer than 1% of people, 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.
Treatment lasts from six months to a year, depending on medication and genotype.
Although none of the available drugs can clear the infection, they can stop the virus from replicating, thus minimizing liver damage.
As of 2008, 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.
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 person'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). 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.
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, and dark urine, and then progresses to development of jaundice.
The illness lasts for a few weeks and then gradually improves in most affected people. A few people 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.
Chronic infection with hepatitis B virus either may be 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).
Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti-Crosti syndrome).
The serum-sickness–like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice.
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.
About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form.
Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia.
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 people who had long-standing hepatitis B virus infection.
However, 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.
The risk of transmission from mother to newborn can be 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.
Following vaccination, hepatitis B surface antigen may be detected in serum for several days; this is known as vaccine antigenaemia.
The vaccine is administered in either two-, three-, or four-dose schedules into infants and adults, which provides protection for 85–90% of individuals.
For Hepatitis A, 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; similar long-term effects are expected for Hepatitis B.
Unlike hepatitis A, hepatitis B does not generally spread through water and food. Instead, it is transmitted through body fluids; thus, prevention is 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.
Besides the WHO-recommended joint immunoprophylaxis starting from the newborn, multiple injections of small doses of hepatitis B immune globulin, or oral lamivudine in HBV carrier mothers with a high degree of infectiousness (>106 copies/ml) in late pregnancy (the last three months of pregnancy), effectively and safely prevent HBV intrauterine transmission, which provide new insight into prevention of HBV at the earliest stage.
Treatment
The hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously.
Early antiviral treatment may be required in fewer than 1% of people, 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.
Treatment lasts from six months to a year, depending on medication and genotype.
Although none of the available drugs can clear the infection, they can stop the virus from replicating, thus minimizing liver damage.
As of 2008, 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.
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 person'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). 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.
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