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 etiology of 72 episodes of liver disease that developed in 62 of 162 renal-transplant recipients was evaluated. Infection with hepatitis B virus was a minor problem, and none of our patients had evidence of infection with hepatitis A. Cytomegalovirus infection was ubiquitous in the population and probably accounted for many episodes of acute liver disease. This agent's role in causing chronic hepatitis is less secure. Infections with other viruses including Epstein-Barr virus, adenovirus, and the herpes viruses were only rarely associated with hepatic disease. Azathioprine was responsible for some episodes of acute cholestasis but could not be incriminated as a direct cause of chronic disease. A cause could be identified for the majority of episodes of acute hepatic dysfunction, but the cause of most of the chronic hepatitis remains undetermined. It is likely that infection with non-A, non-B hepatitis virus accounts for much of this serious, often fatal, complication of renal transplantation.
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PMID:Etiology of liver disease in renal-transplant patients. 22 42

Genetic study of acute and chronic mouse hepatitis virus type 3 disease was carried out in segregating generations of a cross involving a susceptible (C57BL/6) and a resistant (A/J) mouse strain. The data obtained indicate that one or two recessive genes may be involved in resistance of acute and chronic diseases but suggest that the genes involved in both diseases are different. In this cross, no correlation was observed between H-2 and acute or chronic disease. In mice of congenic lines, however, A/Sn (H-2a), A.SW (H-2s), A.BY (H-2b), and A.CA (H-2f), it appeared that the presence of the H-2f allele conferred to heterozygote as well as to homozygote animals the capacity to resist the development of chronic disease. It seems, therefore, that MHV3 sensitivity in mice is under the influence of at least two major genes: one for the acute disease and the other, H-2 linked, for the chronic disease.
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PMID:Genetic study of mouse sensitivity to MHV3 infection: influence of the H-2 complex. 44 93

The following tests were performed in 15 cases of chronic aggressive hepatitis (CAH), 12 of cirrhosis, and 8 of other forms of chronic disease: liver function, thromboelastogram, prothrombin time (PT), partial thromboplastin time (PTT), determination of factors I, II, V, X and XIII, euglobulin and FDP lysis, and platelet count, shape and agglutinability. At least one haemostasis alteration was observed in nearly every case, the most common being in the thromboelastogram, PTT, prothrombin, and platelet shape and agglutinability. Defects were most marked in cirrhosis and comparison with CAH was significant in the case of PT and factor V. Fibrinolysis was increased in 60% of the CAH group and rarely elsewhere. Haemorrhage was noted in 7 cases of cirrhosis and 1 of CAH. On each occasion, it was more dependent on the serious nature of the disease, rather than defective haemostasis.
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PMID:[Hemostatic changes in the course of different chronic hepatopathies]. 111 9

We treated four cases of acute unresolving non-A, non-B hepatitis, and eleven cases of chronic non-A, non-B hepatitis with recombinant interferon alpha-2a for up to one year. The dose of interferon was initially 3 million units daily, and was gradually decreased to 1 million units three times weekly. The overall response rate was 80 percent (twelve out of fifteen cases) at the end of treatment. Relapse occurred after the cessation of treatment in seven of the eight cases of chronic disease responding to interferon therapy. In contrast, three of the four cases of acute unresolving hepatitis became (sero)negative for antibody to hepatitis C virus, and in three completely normal serum aminotransferase levels persisted for more than one year after therapy. It is urged that early recognition of non-A, non-B hepatitis should be striven for, because interferon therapy may lead to an improved prognosis of the disease, particularly in cases of possible transitional phase from acute to chronic disease.
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PMID:Interferon therapy for non-A, non-B hepatitis: a pilot study and review of the literature. 133 37

28 patients with posttransfusion non-A, non-B (NANB) hepatitis in Stockholm, Sweden, were studied for seroconversion to hepatitis C virus antibodies (anti-HCV) and time lag to seroconversion by first and second generation tests. 15/28 patients (54%) seroconverted to anti-HCV with a first generation anti-HCV ELISA using C100-3 from the nonstructural (NS) region 4 of the HCV genome and 23 (82%) with a second generation anti-HCV ELISA including also antigens from the core and NS3 regions of the HCV genome. The mean time from onset of hepatitis to seroconversion was 6.1 weeks (0-18 weeks) with the first generation test and 2.3 weeks (0-7 weeks) with the second generation test. Development of chronic hepatitis was noticed in 14/23 (61%) patients who seroconverted to anti-HCV with the second generation ELISA and in none of 5 patients with posttransfusion NANB hepatitis who did not seroconvert. The inclusion of antigens from the core and NS3 regions of the HCV genome has increased the sensitivity of the second generation anti-HCV ELISA as compared to the first generation ELISA and also shortened the time lag to seroconversion in patients with posttransfusion hepatitis C. Patients with posttransfusion NANB hepatitis seroconverting seem more prone to develop chronic disease than patients not seroconverting.
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PMID:Seroconversion to hepatitis C virus antibodies in patients with acute posttransfusion non-A, non-B hepatitis in Sweden with a second generation test. 137 90

A screening assay for the detection of antibodies to hepatitis C virus (HCV); ORTHO HCV ELISA Test System, Second Generation, was compared with the currently licensed c100-3 based test (ORTHO HCV ELISA Test System). The second generation ELISA differs from the c100-3 based assay in that it detects circulating antibodies to both structural (nucleocapsid) and non-structural (NS3/NS4) HCV proteins. Specimens tested consisted of a cohort of 35 patients diagnosed with non-A, non-B hepatitis (NANBH) and 3971 presumably healthy volunteer blood donors. Second generation ELISA demonstrated significantly greater clinical sensitivity in patients with acute phase NANBH (80% vs. 60%) as well as chronic disease (88% vs. 72%). Additional specimens reactive only in second generation ELISA, demonstrated reactivity to HCV antigens c33c and/or c22-3 in supplemental testing by the Chiron HCV RIBA Assay System. The second generation ELISA also detected additional RIBA reactive volunteer blood donors (0.18% of the population tested) that were nonreactive in first generation ELISA. This data indicated that second generation ELISA would detect approximately 2 additional anti-HCV reactive donors per 1,000 screened. Specificities obtained with this low risk population were 99.6% for first generation and 99.7% for second generation ELISA.
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PMID:Improved detection of antibodies to hepatitis C virus using a second generation ELISA. 138 Nov 39

Hepatitis C virus (HCV) is the primary agent of posttransfusion non-A, non-B hepatitis. HCV RNA was detected in peripheral blood mononuclear cells (PBMC) by polymerase chain reaction in 17 of 24 HCV-infected patients with chronic hepatitis with or without cirrhosis. One of 5 patients whose PBMC contained HCV RNA also had negative-stranded HCV RNA in the PBMC. In 3 of 11 patients whose PBMC contained HCV RNA, flow cytometry with a murine monoclonal antibody to HCV core epitope revealed cytoplasmic staining of peripheral blood monocytes. The monocyte surface and the peripheral blood lymphocytes did not stain for HCV core epitopes. No correlation could be made between the presence of HCV RNA or antigen in PBMC and any serologic markers of HCV infection. These results indicate that monocyte uptake of HCV by either phagocytosis or infection may be part of the pathophysiology of this chronic disease.
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PMID:Hepatitis C virus is detected in a monocyte/macrophage subpopulation of peripheral blood mononuclear cells of infected patients. 138 47

Overall 180 children aged 3 months to 12 years with acute and chronic hepatitis B and delta were examined for macrophagal function. Chemotaxis, saturation with esterase, the content of nuclear RNA were estimated, antigens of HB virus in these cells were identified as well. The data obtained attest to the correlation between the degree of macrophagal function disorders and the gravity of acute virus hepatitis. The chronic disease is characterized by stable depression of mononuclear cells with a tendency toward deeper depression of their function in patients with virus hepatitis delta as well as a higher rate of HBsAg and HBeAg demonstration in these cells. The authors provide evidence for advisability of the use of BCG vaccine and tactivin in patients with the chronic disease, since they improve macrophagal function, promote the inhibition of HB-virus replication and the onset of a stable remission in patients with chronic hepatitis B and delta.
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PMID:[The pathogenetic significance of disorders in macrophage function in viral hepatitis B and delta in children]. 147 35

An established chimpanzee model of parenterally-transmitted non-A, non-B hepatitis was used to define virus-specific immune response patterns in acutely and persistently infected animals. Serial bleedings were obtained from 23 chimpanzees that had been experimentally infected with an isolate of hepatitis C virus, originally recovered from contaminated lots of factor VIII (antihemophilic) materials. Sera were assayed for the presence of antihepatitis C virus by a newly developed radioimmunoassay procedure that incorporated recombinant DNA-expressed viral antigen as a reagent. Twenty-one of 23 hepatitis C virus infected animals were shown to acquire antihepatitis C virus, most within 2-8 weeks after the major peak of alanine aminotransferase activity. All chimpanzees with biochemical, electron microscopic, and histological evidence of chronic disease clearly acquired antibody; 14 of 16 animals observed through the acute phase of disease were also shown to acquire antibody. A booster effect or anamnestic response was noted in two chimpanzees (one of which was negative for antihepatitis C virus following the acute phase of disease) after challenge with hepatitis C virus. Antihepatitis C virus was not neutralizing, because some animals with high levels of antibody were also shown to have high titers of circulating hepatitis C virus. The development and maintenance of anti-hepatitis C virus appears to reflect concomitant virus replication and high potential for infectivity.
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PMID:Parenterally transmitted non-A, non-B hepatitis: virus-specific antibody response patterns in hepatitis C virus-infected chimpanzees. 169 46

We investigated 17 patients (12 males and 5 females, ages 2 to 57 years old) with posttransfusion non-A, non-B hepatitis to determine relationships between clinical courses and hepatitis C virus (HCV) markers. The patients were grouped according to time course of abnormal serum alanine aminotransferase (ALT) levels into three categories (chronic biochemical disease, biochemically resolved chronic disease, and acute disease). Latest serum samples (1.3 to 10.8 years after blood transfusion) were used to detect antibodies against C100-3 antigen (anti-HCV) by enzyme-linked immunosorbent assay and HCV sequences by polymerase chain reaction (PCR) assay. Of the 17 patients, 13 patients (76.5%) were anti-HCV positive and 8 patients (47.1%), including one anti-HCV negative case, were positive for HCV RNA. In total, 14 patients (82.4%) were positive for either HCV markers. With respect to clinical course, HCV RNA was detected in six of eight patients (75%) with chronic biochemical disease, and in two of five patients (40%) with biochemically resolved chronic disease. HCV RNA was not detectable in convalescent sera from four patients with acute disease. These results show that there is a relationship between clinical status and HCV viremia, but that normal liver function tests do not always represent the clearance of the virus. Viremia in two patients with normal ALT level suggests that hepatitis is not only caused by viral cytopathic effects, but also by immunologic reactions against virus-infected cells. Thus, PCR is useful in determining the persistence of HCV infection as well as to diagnose anti-HCV negative HCV infection.
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PMID:Serum hepatitis C virus sequences in posttransfusion non-A, non-B hepatitis. 170 30


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