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)

Plasma or serum from 4 patients with acute or chronic non-A, non-B post-transfusion hepatitis (P.T.H.) and from a blood-donor implicated in two cases of P.T.H. was inoculated into 5 chimpanzees. Biochemical and histological evidence of hepatitis developed in these 5 chimpanzees but not in a control animal. The mean incubation period in the chimpanzees was 13.4 weeks, compared with 7.7 weeks in the 4 patients with P.T.H. The peak alanine aminotransferase (A.L.T.) levels in the 5 chimpanzees were 265, 212, 219, 70, and 62 I.U./l. Histological changes ranged from mild to conspicuous hepatitis and generally correlated with the degree of A.L.T. elevation. There was no evidence of clinical disease and all animals went on to biochemical and histological recovery. There was no serological evidence of type A or type B hepatitis. Hepatitis was transmitted by serum derived from patients with chronic as well as acute hepatitis, strongly suggesting a chronic carrier state for the agent responsible for non-A, non-B hepatitis. Non-A, non-B hepatitis thus seems to be due to a transmissible agent which can persist and remain infectious for long periods.
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PMID:Transmissible agent in non-A, non-B hepatitis. 7 17

Non-A, non-B hepatitis was transmitted to four colony-born chimpanzees by intravenous inoculation of human sera. Two chimpanzees were inoculated with serum from a patient with a clinical and serological diagnosis of chronic non-A, non-B hepatitis whose blood appeared to transmit this disease to a nurse following accidental needle-stick, and the other two chimpanzees were inoculated with serum from either of two former blood-donors whose HBsAg-negative blood appeared to transmit clinically recognisable hepatitis, and who were found to have raised serum-aminotransferase levels 1 1/2 and 5 years later. Serum-aminotransferase levels rose in all four chimpanzees, beginning 2--4 weeks after inoculation: peak alanine-aminotransferase values were 210 to 328 I.U./l. Evidence of hepatitis was present in liver biopsy specimens from all four chimpanzees, beginning 8--10 weeks after inoculation. None showed serological evidence of infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus.
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PMID:Transmission of non-A, non-B hepatitis from man to chimpanzee. 7 18

Evidence for a new hepatitis-specific antigen has been obtained from double immunodiffusion assays between acute and convalescent sera obtained from patients with non-A, non-B post-transfusion hepatitis. The designation hepatitis C (HC) antigen is proposed. HC was found in the acute-phase sera of all 13 non-A, non-B post-transfusion hepatitis patients with longer incubation and duration periods (type 2) tested, but only transiently in 4 out of 10 acutephase sera obtained from patients with type 1 non-A, non-B hepatitis, with shorter incubation and duration periods. The antigen was also detected in 2 out of 16 single specimens obtained during the acute phase from acute hepatitis patients who had not received a blood-transfusion. This suggests presence of a carrier state. No patients with alcoholic hepatitis and no healthy blood-donor carried HC antigen. The antigen seems distinct from those of hepatitis A and B (surface and core). It migrated in the serum beta-globulin region and had a buoyant density of 1.30 and a molecular weight between 100 000 and 300 000. Antibodies against HC antigen were found in only 30% of the type-2 non-A, non-B post-transfusion hepatitis patients and did not persist for long. However, these antibodies were directed specifically against HC antigen and moved in a manner similar to 7S globulin on rate-zonal centrifugation.
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PMID:Hepatitis "C" antigen in non-A, non-B post-transfusion hepatitis. 8 9

Liver dysfunction was observed in 33% of patients treated by hemodialysis and kidney transplantation. Fifty-eight percent of these cases of hepatitis occurred in patients with past or present HBs antigenemia, and 77% of HBsAg-positive patients showed evidence of LD. However, during the course of a program conducted from 1969 to 1976 and involving 267 patients, the decrease in the prevalence of HBs antigenemia observed during the last two years did not lead to any reduction in LD incidence. In a small number of patients, potentially hepatotoxic drugs could be incriminated, but in our experience azathioprine never appeared to be involved. In a few patients, LD was due to granulomatous disease of the liver, such as tuberculosis and schistosomiasis. Twenty-one (7%) of the 267 patients at risk developed chronic hepatitis, which contributed to death in nine patients. In 12 cases (three deaths), this form of hepatitis occurred in HBsAg-positive patients, and in nine cases (six deaths), in HBsAg-negative patients. In three of these latter individuals, cytomegalovirus could be incriminated. Routine monthly screening for CMV in kidney recipients confirmed the high incidence of this viral infection in such patients. Studies on murine CMV infection have demonstrated that this infection can be enhanced by histoincompatible graft or by cyclophosphamide in a model that is very close to the kidney recipient. As in mice, CMV infection in kidney recipients apparently results from reactivation of a latent infection. It seems to play a major role in the LD observed and could apparently lead to chronic hepatitis and even to cirrhosis of the liver. Finally, the occurrence of LD in HBsAg-, anti-HBs- and antiCMV-negative patients would suggest the responsibility of other viruses for the pathogenesis of liver disease in patients treated by hemodialysis and kidney transplantation. Besides Epstein-Barr virus, other viruses, such as hepatitis C virus, should be thoroughly scrutinized.
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PMID:Liver disease in patients undergoing hemodialysis and kidney transplantation. 11 44

The frequency of non-A, non-B hepatitis (n = 325) was determined among all cases (n = 1368) of acute viral hepatitis observed in the Hannover are abetwen 1975 and 1978. Hepatitis A was excluded by demonstration of anti-HAV-IgM, hepatitis B by demonstration of HBs antigen or an isolated occurrence of anti-HBc at the beginning of the disease. Non-A, non-B hepatitis occurred predominantly in adults and showed no seasonal variability. As a consequence of results of followup investigations in 174 hepatitis patients 2 years after the onset of the disease it can be assumed that non-A, non-B hepatitis tends to lead to chronic courses more frequently than hepatitis B.
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PMID:[Epidemiology and prognosis of non-A, non-B hepatitis (author's transl)]. 11 67

Hepatitis B virus-like particles (including DANE particles) with DNA polymerase activity but negative for HBs Ag have been identified in NON-A, NON-B hepatitis sera positive for HC Ag. Although specifically associated with the particles, HC Ag is not a surface antigen of the hepatitis C virus identified here for the first time. The relationship of this agent with HBV seems obvious, and deserves further study.
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PMID:[Identification of a virus similar to hepatitis B virus in non-A non-B hepatitis]. 12 Jul 82

One hundred patients on chronic haemodialysis were studied prospectively over one year for evidence of hepatitis and of infection with hepatitis A or B virus. Five patients developed transient elevations of SGPT, accompanied by a consistent pattern of clinical manifestations, including low-grade fever, anorexia, nausea, hepatomegaly, and hypotension during dialysis. None of these patients had a positive test for A or B virus infection. Non-A non-B hepatitis appears to cause a specific syndrome in uraemic patients, and its transmission in a dialysis unit seems unrelated to blood transfusions.
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PMID:Non-A, non-B hepatitis: a new syndrome in uraemic patients. 12 59

Some species of marmosets are susceptible, not only by parenteral inoculation but also by oral exposure, to human hepatitis A virus present in sera or feces. The stools of animals inoculated parenterally or orally contained fecal antigen during certain times of the incubation period and the early, acute phase of the disease; viruslike particles were present in feces of orally infected animals and such feces were infectious when inoculated into marmosets. The fecal antigen crossreacted both with the fecal virus particles and the immune-adherence antigen (see also papers by Purcell et al and Hilleman et al). The MS-1 and CR-326 strains of hepatitis A appeared antigenically similar or identical whereas the GB strain was antigenically different and may be associated with the recently defined type of hepatitis termed hepatitis C or hepatitis non-A/non-B. On repeated challenge hyperegic responses with diffuse liver cell necrosis occurred in some immune animals and this phenomenon must be taken into account in any future vaccination studies.
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PMID:Hepatitis in marmosets. 17 53

Hbs-Ag, anti-Hbs, anti-Hbc and anti-HA were determined and the concentration of IgM measured in the sera of cases of acute infectious hepatitis which occurred in the Hannover area in 1975. Although there was a high degree of contamination with hepatitis A virus among the population, acute infectious hepatitis A was rare (n = 56). The hepatitis A virus is principally transmitted by contact with infection or while traveling in southern Europe. The greatest part of infectious hepatitis is due to hepatitis virus B (n = 211). Non-A, non-B hepatitis was less frequently observed (n = 62). A high percentage of patients with serum hepatitis and non-A, non-B hepatitis gave a history of parenteral exposure to possibly infectious material.
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PMID:[Seroepidemiology of acute infectious hepatitis (author's transl)]. 30 23

Non-A, non-B hepatitis, previously transmitted to chimpanzees by inoculation of human serum, was serially transmitted through a second and third passage to additional chimpanzees using serum drawn during acute non-A, non-B hepatitis. Sera obtained at weeks 4 and 5 after inoculation from two different chimpanzees, and from one chimpanzee at week 13 after inoculation, were shown to cause elevation of serum aminotransferase levels and abnormal liver biopsies in recipient chimpanzees, with no serologic evidence of hepatitis A or B, cytomegalovirus, or Epstein-Barr virus infection. Serum obtained 3 wk after inoculation did not cause elevation of aminotransferase levels in the recipient chimpanzee, although a single abnormal biopsy was obtained. Thus, the non-A, non-B hepatitis agent was present in serum during acute disease near the time of the first aminotransferase elevation (week 4; perhaps also week 3), and persisted at least until 1 week after the peak aminotransferase level (week 13).
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PMID:Acute non-A, non-B hepatitis. Prolonged presence of the infectious agent in blood. 42 94


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