Hepatitis B is caused by a DNA virus that is transmitted parenterally frequently. It causes the typical symptoms of viral hepatitis, including anorexia, nausea and jaundice. Fulminant hepatitis and death may occur. Chronic infections can lead to liver cirrhosis and (or hepatocellular carcinoma. The diagnosis is carried out serologically. The treatment is symptomatic. The vaccine is protective and use of hepatitis B immune globulin after exposure can prevent clinical disease or weaken.
See also causes of hepatitis, Overview of the acute viral hepatitis, and chronic hepatitis B.)
Hepatitis B is caused by a DNA virus that is transmitted parenterally frequently. It causes the typical symptoms of viral hepatitis, including anorexia, nausea and jaundice. Fulminant hepatitis and death may occur. Chronic infection can lead to cirrhosis and (or hepatocellular carcinoma. The diagnosis is made serologically. The treatment is symptomatic. The vaccine is protective and the use of hepatitis B immune globulin after exposure may prevent clinical disease or weaken. See also causes hepatitis, Overview of the acute viral hepatitis, and chronic hepatitis B.) the hepatitis B virus (HBV) is the most studied and most complex hepatitis virus. The infectious particles consist of a core (core) and a superficial sheath. The core contains a circular double stranded DNA and DNA polymerase. The virus replicates in the nuclei of infected hepatocytes. A surface protein is released into the cytoplasm and formed for reasons still unknown in excess. The HBV represents the second most common cause of acute viral hepatitis A subclinical extending infection is often, however, less common than that in the hepatitis A virus. In the US B infection is berichtet- a decline from the 25,000 annual cases prior to use of the hepatitis B vaccine annually by about 3,000 cases of acute hepatitis. However, since many cases are not recognized or not reported by those who appreciate the Centers for Disease Control and Prevention (CDC) that the actual number of new infections per year is close at 20,000 (see CDC Hepatitis B FAQs). For unknown reasons, the HBV is associated with more than one primary extrahepatic manifestations such. B. with polyarteritis nodosa and other connective tissue diseases, membranous glomerulonephritis, and the essential mixed cryoglobulinemia. The pathogenic role of HBV in these diseases is unclear, it is suspected autoimmune mechanisms. Transmission of Hepatitis B HBV is usually transmitted parenterally, typically by contaminated blood or blood products. The routine screening of blood donors for hepatitis B surface antigen (HBsAg) which used common posttransfusion transmission has virtually eliminated, however, is the transmission by contaminated needles during i.v. Drug addicts frequently. The risk of HBV infection is increased in patients in dialysis and oncology wards and staff at medical facilities. Children of an infected mother have to buy 70 to 90iges risk a hepatitis B during birth (neonatal hepatitis B virus infection), unless the newborn is treated with hepatitis B immune globulin (HBIG) and is seeded immediately after birth , Earlier placental transfer is also possible, but is rare. The virus can spread through contact with grinding skins and other body fluids (eg., Between intimate partners, both heterosexual and homosexual, and in closed institutions such as mental hospitals and prisons). However, the infectivity is lower than for the hepatitis A virus and the transmission paths often remain in the dark. The role of insect bites in transmission is unclear, many cases of acute hepatitis B occur sporadically and with no known source of infection. Chronic HBV carriers provide a worldwide reservoir of infection. The prevalence varies depending on various factors such as geographic differences (z. B. <0.5% in North America and northern Europe,> 10% in some regions in the Far East and Africa). Symptoms and signs Hepatitis B infection can cause a wide range of liver diseases, to severe hepatitis or aktutem liver failure from subclinical carrier state (fulminant hepatitis,) especially in the elderly, where the mortality can be 10-15%. Most patients have typical manifestations of viral hepatitis on, including anorexia, malaise, fever, nausea and vomiting, followed by jaundice. Symptoms hold for a few weeks to up to 3-6 months. 5-10% of all patients with HBV develop chronic hepatitis or become inactive carriers. The younger the age when an acute infection occurs, the greater the risk of developing chronic infections: For infants: 90% For children aged 1 to 5 years: 25 to 50% of adults: About 5% Liver cirrhosis can develop , Hepatocellular carcinoma can arise eventually from chronic HBV infection, even without prior cirrhosis. Diagnosis Serological tests should Therefore, in the early diagnosis of acute hepatitis, viral hepatitis are the differential diagnosis, distinguished from other diseases that cause jaundice (Simplified diagnostic approach to potential acute viral hepatitis.). If an acute viral hepatitis is suspected, the following tests to screen for hepatitis viruses A, B and C are carried out: IgM antibody to HAV (IgM anti-HAV) hepatitis B surface antigen (HBsAg) IgM antibody to hepatitis B core (anti-HBc IgM) antibody to hepatitis C virus (anti-HCV) positive hepatitis B test results further serological tests for differentiation of acute displayed by a past or chronic infection (are see table: hepatitis B serology * . When a suspect for HBV infection serology are used for hepatitis B e antigen (HBeAg) and anti-HBe tested to determine the prognosis of the disease and establish an antiviral treatment. If the serologically diagnosed HBV infection is severe , antibodies of the hepatitis D virus (HDV nti-) should be determined. In hepatitis B, there are at least three different antigen-antibody systems that can be tested: HBsAg hepatitis B core antigen (HBcAg) HBeAg HBsAg characteristically occurs during the incubation on, usually 1-6 weeks before emergence of clinical symptoms and increase in biochemical tests and shows infectivity blood on. It disappears into the recovery phase. Occasionally, HBsAg transiently. The corresponding protective antibody (anti-HBs) appears weeks or months later after clinical convalescence and persists lifelong generally. Therefore, its detection is an indication of an elapsed HBV infection and the existence of a relative immunity. In 5-10% of patients HBsAg persists, and corresponding antibodies do not develop; these patients are asymptomatic carriers of the virus or develop chronic hepatitis. HBcAg corresponds to the core protein of the virus. It can be detected in the infected liver cells but not in serum except by special techniques. Antibodies to HBcAg (anti-HBc) occur usually at the beginning of the clinical disease. After that, the titer over the years and throughout life gradually drop. His presence, along with the anti-HBs antibodies indicates a past HBV infection. Anti-HBc antibodies consist in chronic HBsAg carriers who do not develop anti-HBs antibodies. During the acute infection of the anti-HBc antibody has almost exclusively the IgM isotype, however, is chronic infection mainly of the IgG isotype ago. IgM anti-HBc is a sensitive marker for the diagnosis of acute hepatitis B infection, and occasionally the only marker of just past infection in the so-called phase of the open window between the disappearance of HBs antigen and the appearance of anti-HBs. HBeAg is a protein derived from the core protein (it must not be confused with the HEV). It occurs only in HBsAg-positive serum and then an indication of a more active viral replication and greater infectivity. In contrast, the presence of the corresponding antibody (anti-HBe) point to lower infectivity. The e antigen markers are therefore useful in determining the prognosis than in diagnosis. Chronic liver diseases develop common in patients with HBe antigen, less frequent in patients with anti-HBe. HBV DNA can be detected in the serum of patients with active HBV infection. Hepatitis B serology markers * Acute HBV infection Chronic HBV infection previous HBV infection HBsAg + + – Anti-HBs – – + Anti-HBc IgM + – – IgG anti-HBc – + ± ± ± HBeAg – Anti-HBe – ± ± HBV DNA + + – * antibodies against Hepatitis D virus (anti-HDV) levels should be measured when serological tests have confirmed HBV and the infection is severe. Patients had HBV infection and have recovered. Anti-HBs also be regarded as the sole serological markers for HBV vaccination. Anti-HBc = antibody against hepatitis B core, anti-HBe antibodies against HBeAg =, Anti-HBs Antibodies to HBsAg =; HBeAg = hepatitis B e antigen; HBsAg = hepatitis B surface antigen; HBV = hepatitis B virus. Other function tests Liver function tests be determined if that has not happened before. These include serum transaminases (ALT and AST), alkaline phosphatase and bilirubin. Other tests should be performed to assess the severity of the disease; they include serum albumin, platelet count and PT / INR. Therapy Supportive treatment In fulminant hepatitis B, antiviral medications and liver transplant No specific treatment softens the course of acute hepatitis, including hepatitis, alcohol should be avoided because it increases the liver damage. Restrictions in diet or physical activity incl. The often prescribed bed rest have no scientific basis. When fulminant hepatitis occurs, treatment with oral nucleoside or nucleotide analogues can improve the likelihood of survival. On the other hand, only liver transplantation the most promising treatment option. Adults survive such a course rarely without transplantation, children tend to have a more favorable course. Most patients can resume safe to work after the jaundice has subsided, even if the transaminases are still increased. In the cholestatic hepatitis, the administration of cholestyramine can be 8 g p.o. 1 to 2 times reduce the itching daily. The presence of a viral hepatitis is reportable. Prevention Patients should be counseled that they avoid high-risk behavior (eg sharing needles to inject drugs;. Multiple sexual partners). Blood and other body fluids (eg. As saliva, semen) are considered infectious. Leaks should be cleaned with diluted bleach. Protective measures are recommended, but isolation of patients is not of value. The risk of post-transfusion hepatitis is minimized by avoiding unnecessary transfusions and all blood donors are tested for HBsAg and anti-HCV. This screening has reduced the incidence of post-transfusion hepatitis to about 1: reduced 100,000 units of transfused blood components. Vaccinations Hepatitis B Impfungin endemic areas has considerably reduced the local prevalence. A Präexpositionsimmunprophylaxe will have long recommended for high-risk individuals. On the other hand, the selective vaccination of high-risk groups in the US and in other Nichtendemiegebieten has reduced the incidence of HBV infection is not substantial, therefore vaccination is now recommended for all US citizens by birth or at <18 years of age (see table: Recommended vaccination plan for the age of 0-6 years) .. A universal worldwide vaccination is desirable but not possible for reasons of cost. Adults with a high risk for HBV infection should be tested and vaccinated if they are not already immune or infected (see Adult Immunization Schedule). These high-risk groups include men who have sex with men, persons with sexually transmitted disease. Patients who had> 1 sexual partner within the last 6 months health care workers and public safety that may be exposed to blood or other infectious body fluids People who have diabetes and <60 years (or ? 60 years if their risk of HBV to acquire, is considered to be increased) people with end-stage kidney disease, HIV or chronic liver disease household contacts and sex partners of people who are HBsAg-positive clients and staff of institutions and commercial day care centers for people with intellectual disabilities people in prisons or institutions for treatment for substance abuse and prevention provide International travelers in regions with high or intermediate HBV endemicity Two recombinant vaccines are available. Both are safe, even during pregnancy. Three injections in the deltoid be given as a primary series at time 0, after 1 month and 6 months. Children receive lower, immunosuppressed and those on hemodialysis higher doses of the vaccine. After the vaccination is formed with the anti-HBs levels in immunocompetent patients in 80-90% of cases for 5 years and in 60-80% of cases for 10 years of protection. Booster doses are recommended for patients on dialysis, and immunocompromised patients, the anti-HBs <10 mIU / ml liegen.Postexpositionsprophylaxe In the hepatitis B post-exposure immunoprophylaxis the active vaccination is coadministered with hepatitis B immunoglobulin (HBIG), a high-titer anti-HBs product. The HBIG can probably an infection does not prevent, but it prevents or mitigates the clinical picture. Newborns from HBsAg positive mothers, an initial dose of the vaccine combined with 0.5 ml of HBIG i.m. administered into the thigh immediately after birth. All those who have sexual contact with HBsAg-positive persons or percutaneous or mucosal exposure to HBsAg-positive blood had 0.06 ml / kg HBIG is i.m. administered within days together with the vaccine. All previously vaccinated patients who are exposed to a percutaneous HBsAg positive exposure are tested for anti-HBs; if the titers are <10 mI.E./ml, a booster dose is needed. Important points hepatitis B is often transmitted through parenteral contact with infected blood, but can also result from mucosal contact with other body fluids. For infants whose mothers are infected with the hepatitis B virus, there is a 70 to 90% chance that they acquire the infection during delivery unless the infants are infected with hepatitis B immune globulin (HBIG) treated and vaccinated after delivery. A chronic infection develops in 5 to 10% of patients with acute hepatitis B, and often leads to cirrhosis and / or hepatocellular carcinoma. Diagnosis is made by testing for hepatitis B surface antigen and other serological markers. Treatment is supportive. Routine vaccination at birth beginning, is recommended for all. A "post exposure prophylaxis" consists of HBIG and vaccination. HBIG can probably an infection does not prevent, but it prevents or mitigates the clinical hepatitis. For more information CDC Hepatitis B FAQs