Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic hepatitis is defined as chronic liver disease of at least 6 months' duration. Liver biopsy is essential for diagnosis and allows classification into chronic persistent hepatitis and chronic active hepatitis. Chronic persistent hepatitis is associated with hepatitis B infection or with infection with the non A non B viruses. The prognosis is good and it requires no treatment. Autoimmune chronic active hepatitis presents a very active clinical, biochemical and immunological picture. Prednisolone therapy is of benefit in prolonging life. Steroid therapy is disappointing in hepatitis B related chronic active hepatitis. Superinfection with delta agent may affect HBsAg positive patients: it appears to cause activation of disease and progression towards cirrhosis. Hepatocarcinoma is another complication of chronic B infection. Chronic active non A non B hepatitis is diagnosed by elimination since there is no specific diagnostic test.
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PMID:[Value of puncture biopsy of the liver during diagnostic and follow-up examinations (clinical aspects, immunological markers, images) in chronic hepatitis]. 242 1

Chronic hepatitis (CH) may be defined as persistence of an inflammatory reaction in the liver for greater than 4 months. Different immune mechanisms of liver damage are operative in children with the three common types of CH. In autoimmune CH the cytotoxic effect is mostly confined to the non-T cell lymphocyte fraction. Autoimmune CH is steroid responsive and has a generally favorable prognosis. In hepatitis B virus (HBV) hepatitis both T and non-T lymphocytes are responsible for the cytotoxic reaction. Steroid or interferon treatment is controversial and the prognosis is less favorable. Hepatitis delta virus (HDV) hepatitis only occurs in children with HBV hepatitis as either a co-infection or superinfection. As a co-infection the HBV is usually eliminated and CH does not ensue. Superinfection with HDV, however, frequently leads to rapidly progressive liver damage and a more serious prognosis. Non-A, non-B (NANB) hepatitis is a diagnosis of exclusion. In NANB hepatitis, the cytotoxic effect is predominantly T cell. NANB hepatitis generally runs a mild course, and no treatment is usually recommended.
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PMID:Living with chronic hepatitis. 248 25

Superinfection by hepatitis delta virus (HDV) in hepatitis B virus chronic carriers is normally associated with a progressive liver injury. For this reason, the aim of the present study was to determine the efficacy of recombinant interferon alpha (rIFN-alpha) treatment of chronic delta hepatitis, by giving high doses of rIFN-alpha 2c during a prolonged period. A total of 20 HBsAg, anti-HD carriers with a chronic active hepatitis were randomly allocated in two groups: (I) n = 10, control and (II) n = 10, treated with 10 MU/m2 body surface of rIFN-alpha, twice weekly, intramuscularly (im) during 6 months. Basally, all patients presented HDAg in the liver and serum IgM anti-HD. Serum HDV-RNA was positive in 8 and 7 patients from groups I and II, respectively. The interferon therapy was well tolerated and all patients finished the treatment period. During the first 6 months, a decrease in ALT levels among treated patients (255 +/- 98 vs. 193 +/- 117) was observed. In addition, a transient drop in HDV-RNA levels was also observed. No changes in anti-HD titer, IgM anti-HD and HBsAg concentration were detected. At the end of the follow-up period (15 months) two treated patients had lost IgM anti-HD. In addition, another two patients were HDV-RNA negative. In conclusion, no permanent antiviral effects of rIFN-alpha 2c in chronic delta hepatitis, using this schedule, was achieved.
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PMID:Treatment of chronic delta infection with recombinant human interferon alpha 2c at high doses. 269 69

Of 377 cases of fulminant hepatitis in persons positive for hepatitis B surface antigen (HBsAg) in Greece, Italy, the United States, the United Kingdom, the Central African Republic, Taiwan, Egypt, and India, only 52% could be attributed to infection with hepatitis B virus, which was defined as the presence of the IgM antibody to the hepatitis B core antigen (IgM anti-HBc) and the absence of serum markers of infection by extraneous viruses. Thirty percent of cases were caused by coinfection with hepatitis B virus and hepatitis delta virus or by infection with hepatitis delta virus superimposed on carriers of chronic HBsAg. In 18.5% of the patients, the absence of IgM anti-HBc indicated that they were not known to carry HBsAg, but no obvious superimposed factor of hepatitis could be identified. The cause of fulminant hepatitis is complex, and major risk factors are a pre-existing HBsAg state and hepatitis delta virus infection. Superinfection of HBsAg carriers by non-A, non-B viruses seems to be the cause in a consistent proportion of cases.
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PMID:Serologic markers with fulminant hepatitis in persons positive for hepatitis B surface antigen. A worldwide epidemiologic and clinical survey. 334 75

delta-virus, first described by Rizzetto, is a defective virus dependent on hepatitis B virus as helper-virus. Superinfection of inactive hepatitis B with delta-virus leads to chronic active or even fulminant hepatitis. It can be detected by RIA or ELISA and its distribution is world-wide. Also in Austria, 4 sera with antibodies to delta-virus have been found among 138 HBsAg-positive sera. No therapy is known, but vaccination against HB virus also prevents the propagation of delta-virus.
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PMID:[Delta virus: now also detected in Austria. A defective virus as a pathogenic agent]. 401 41

The hepatitis delta virus (Delta) is a defective RNA pathogen dependent for replication on obligatory helper functions provided by the hepatitis B virus (HBV). The virion is a particle of 35-37 nm, which encloses within a HBsAg coat the RNA genome and the Delta antigen, the specific immunologic expression of the new pathogen. Infection is diagnosed by the presence of Delta antigen in liver and the finding of antibody to Delta in serum. The virus is infectious for primates but can also adapt to non-primates. Distribution is world-wide with peak prevalence in the Mediterranean basin, the Middle East and areas of Africa. Transmission occurs by direct parenteral inoculation and by non-parenteral routes linked to close body contacts. Delta is highly pathogenic and a cause or an aggravating factor of HBsAg-positive liver disease. Infection superimposed on acute HBV hepatitis may induce a fulminant illness. Superinfection of carriers of HBsAg may convert a previously asymptomatic carrier in a carrier with chronic hepatitis, or accelerate the downward clinical course of chronic underlying HBV disease. Carriers of HBsAg probably represent the reservoir of the virus.
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PMID:Delta hepatitis--present status. 405 44

The aetiological agents responsible for, and the outcome of, acute liver failure were investigated prospectively in 44 children (29 males, 15 females) attending a tertiary health care facility in India. The children were between the ages of 2 months and 13 years. Studies for viral infections and other etiologies could be carried out in 40 patients. Specific aetiological labels were possible in 35 (87.5%) patients. Thirty (75%) had evidence of acute viral hepatitis. Acute hepatitis E virus (HEV) infection was found in a total of 18 children, with hepatitis A (HAV) in 16, hepatitis B in 5, and C in 1. Seven had isolated infection with hepatitis E, five with A, and four with B. Nine had both E and A infection. Superinfection of HEV was observed in a child with Indian childhood cirrhosis (ICC). Acute HEV infection was confirmed by immunoblot assay in all the patients and in eight of these, HEV-RNA was also detected in the serum. HAV was involved in 37.5% of cases with isolated infection in 10% (4 of 40). The aetiological factors associated with acute liver failure, apart from HAV and HEV, were other hepatotropic viruses (22.5%), Wilson's disease (5%), ICC (5%), and hepatotoxic drugs (7.5%). In five patients, no serological evidence of acute viral hepatitis could be found, neither did the metabolic screen yield any result. It was observed that enterically transmitted hepatitis viruses (HAV and HEV) were associated with 60% of acute hepatic failure in children. Mixed infection of HAV and HEV formed the single largest aetiological subgroup. In developing countries, where hepatitis A and E infections are endemic, severe complications can arise in the case of mixed infection. This may contribute to most of the mortality from acute liver failure during childhood.
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PMID:Acute viral hepatitis types E, A, and B singly and in combination in acute liver failure in children in north India. 880 Dec 80

Superinfection by hepatitis D virus (HDV) leads to acute hepatitis and causes progression to liver cirrhosis in a significant proportion of hepatitis B surface antigen (HBsAg) carriers. Current regimens (interferon) to treat hepatitis D patients has only transient but no lasting effects. New approaches are, therefore, warranted. Recently, several laboratory studies have discovered interesting properties of HDV that may become targets for antiviral chemicals. Viral replication requires the small hepatitis delta antigen (s-HDAg). The s-HDAg is a nuclear phosphoprotein. There is evidence indicating that phosphorylation is important for HDV replication. A second step of replication requires HDV-RNA self-cleavage and self-ligation. Interestingly, one group of antibiotics, the aminoglycosides, exerts strong suppression effects on HDV ribozyme activities. In the following stage of viral assembly, two post-translational modifications, namely isoprenylation of large HDAg and glycosylation of HBsAg are involved. Agents capable of blocking the two modifications should reduce viral production. These four possible targets are reviewed. For prevention, effective vaccines are not yet available. Two novel approaches are discussed. The first demonstrates the immunogenicity of a nucleic acid vaccine in mice. The second approach assembled an empty HDV particle in yeast. Advances on such laboratory investigations may provide new methods for the control of hepatitis D in the future.
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PMID:Molecular biology of hepatitis D virus: research and potential for application. 940 37

Superinfection of hepatitis D virus (HDV) among hepatitis B virus (HBV) carriers is mainly through heterosexual contact in Taiwan. This study investigated the change of HDV endemicity and its associated contributory factors. Seventy-seven patients with acute HDV superinfection among 527 consecutive exacerbating hepatitis B surface antigen (HBsAg) carriers were identified over the past 12 years. The prevalence decreased significantly by each 3-year period from June 1983 to May 1995 (23.7, 15.5, 13.1 and 4.2%, respectively, P < 0.001). This trend was more significant in the hepatitis B e antigen (HBeAg)-negative group (P < 0.001) than in the HBeAg-positive group (P = 0.073). Subjects with a history of paid sex and prostitutes were also recruited for analysis both in 1989 and 1996. Although not statistically significant, there was a trend showing a decrease in the prevalence of serum antibody against HDV (anti-HDV) in each risk group: it was lower in 1996 among HBsAg-positive brothel-goers (10.3 vs 6.9%), licensed prostitutes (54.5 vs 50%) and unlicensed prostitutes (36.1 vs 30.8%). Accumulation of anti-HDV-positive subjects in risk groups may mask the actual decrease of new HDV-infected cases. The prevalence of the HBsAg carrier rate among all prostitutes has significantly decreased (18.3 vs 12.2%, P = 0.015). The efficacy of each preventive strategy was examined and mapped with the trend. It was concluded that active preventive measures directed against promiscuity and sexually transmitted disease and the promotion of disposable needles may have contributed to the decrease in HDV endemicity.
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PMID:Decreasing hepatitis D virus infection in Taiwan: an analysis of contributory factors. 943 40

Two hundred and forty-eight blood specimens collected from patients of sporadic acute viral hepatitis were serotyped with enzyme immunoassay (EIA), to study its pathogenic components during non-epidemic seasons of hepatitis A (HA). Results showed that HA accounted for 61.3% of the total sporadic acute hepatitis cases during its non-epidemic seasons, occurred mainly in youngsters and decreased with increase of their age. Hepatitis B (HB) ranked the second and accounted for 26.2%, occurred mainly in the middle-aged and the elderly and its prevalence increased with age. Hepatitis C (HC) accounted for 9.9% and hepatitis E (HE) 22.2% of the total cases, without obvious age difference. Prevalence of hepatitis D (HD) was 12.7%, with a positive rate of hepatitis D antigen (HDAg) of 12%. Superinfection accounted for 18.9%, and the viral hepatitis markers were all negative in 0.8% of the total cases. There was very significant difference in prevalence of HCV-IgG and HEV-IgG between sporadic acute hepatitis patients and blood donors during the same periods. Icterus occurred in 68% of the total cases, 86.8% in HA. Patients of HB complicated with HD were liable to chronicity.
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PMID:[Studies on serotyping of sporadic acute viral hepatitis]. 981 91


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