Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors followed up for a period of five years 276 convalescents after viral hepatitis B where all remained carriers of HBsAg. The group comprised 108 cases of chronic persisting hepatitis, 134 cases of chronic active hepatitis, 13 cirrhoses of the liver and 21 symptom-free carriers of HBsAg. In the group of chronic active hepatitis at the onset of the investigation 128 were HBeAg positive. In the course of five years in 43 patients seroconversion to HBeAg negativity occurred. Thus an annual index of seroconversion from HBeAg of 6.7% was recorded. In the course of five years in 38 patients of 128 HBeAg positive ones an acute relapse was observed. The causes of the relapse were explained by detailed serological examination. Superinfection with the hepatitis A virus participated three times (7.9%), probable superinfection with the hepatitis non-A non-B virus six times (15.8%), superinfection with the EB virus three times (7.9%), superinfection with cytomegalovirus twice (5.3%), seroconversion HBeAg to anti-HBe 14 times (36.8%), discontinuation of corticotherapy six times (15.8%), superinfection with the delta virus in none of the patients and relapses due to other causes four times (10.5%). Seroconversion of HBeAg to anti-HBe was in cca one third of the patients associated with acute exacerbation of the hepatic process. These relapses were, however, transient and their regression was followed by a further improvement of the chronic inflammation. Also relapses after discontinuation of corticotherapy usually improved spontaneously after a certain time interval. When the cause of the relapse was superinfection with the EB virus or cytomegalovirusas as a rule acceleration and further progress of the inflammatory process occurred.
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PMID:[Basic factors affecting the development of chronic hepatitis B virus infection]. 202 93

Radioimmunoassay of 247 patients revealed in their sera 8 cases of anti-delta agents. On the basis of testing of HBV infection markers the authors revealed three cases of coinfection and five cases of delta superinfection. A fatal case of fulminant hepatitis with development of acute liver dystrophy was observed in one patient with coinfection. In two other patients the course of the disease was severe but ended in recovery. Superinfection with delta agent resulted in a progression of the disease with early formation of chronic active hepatitis. This form chronic disease was characterized by a malignant course and proved resistant to immunosuppressive therapy. The clinical and biochemical signs of coinfection and delta superinfection are discussed.
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PMID:[Delta hepatitis as a mixed infection]. 219 67

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

Superinfection of a silently non-A, non-B (NANB)-infected chimpanzee with hepatitis A virus (HAV) resulted in minimal liver enzyme elevations, lack of detectable HAV in stool, and questionable presence of HAV antigen in liver biopsy specimens obtained during the expected period of virus replication. Our findings indicate that even biochemically silent NANB hepatitis can strongly interfere with infection by at least one other hepatotrophic virus.
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PMID:Biochemically silent posttransfusion non-A, non-B hepatitis interferes with superinfection by hepatitis A virus. 282

Liver biopsy specimens from patients positive for serum HBsAg reveal various expression patterns when properly stained by immunohistochemical techniques for the demonstration of HBsAg, HBcAg and HDAg. A negative staining for these three antigens seems to be associated with two conditions, i.e., self-limiting acute lobular hepatitis (ALH) or low amounts of intrahepatic antigens. The discrepancy between serum positivity and tissue negativity for HBsAg can be explained either by sampling error or by the higher sensitivity of the radioimmunoassay as compared with immunohistochemical methods. The use of amplification systems such as the avidin-biotin-peroxidase complex enhances the sensitivity of immunohistochemical peroxidase-antiperoxidase (PAP) techniques and makes it possible to detect very small amounts of both HBsAg and HBcAg in liver cells from paraffin-embedded tissue sections which had been negative with the conventional PAP technique. In cases with a positive staining for viral antigens, two main expression patterns (non-aggressive and aggressive) can be distinguished. The non-aggressive pattern is reflected in the HBcAg-free HBsAg-positive type (HBsAg carrier) or the generalized type of nuclear core (HBcAg carrier), while the aggressive pattern is reflected in the presence of HDAg, the presence of HDAg and HBcAg, the focal type of nuclear core or the cytoplasmic HBcAg. Superinfection of HBsAg carriers or switching from generalized to focal core, with or without cytoplasmic expression of HBcAg, results in transition from non-aggressive to aggressive pattern. The aggressive pattern occurs in association with histological features of chronic active hepatitis (CAH). When it occurs in ALH cases or in milder forms of chronic hepatitis, an evolution into CAH has to be expected. Features of severe CAH, eventually with cirrhosis, are found in association with two new expression patterns: the cytoplasmic core and the simultaneous presence of HBcAg and HDAg. When features of CAH are observed in liver tissue specimens with HBcAg-free HBsAg-positive type, the liver disease may be due to viral superinfection or to non-viral etiology, e.g., alpha 1-antitrypsin deficiency.
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PMID:Immunohistochemical techniques for the demonstration of viral antigens in liver tissue. 306 47

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


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