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)

gamma-Glutamyl transpeptidase (GGTP) is a sensitive but nonspecific index hepatobiliary disease. In infectious mononucleosis (IM) or the mononucleosis-like disease attributable to cytomegalovirus (cytomegalovirus-induced IM), GGTP reverted to normal later than aspartate aminotransferase and alkaline phosphatase. In three cases elevated serum GGTP activity persisted for up to 24 months -- raising the question of persistent 'post-IM' hepatitis. Such prolonged GGTP activity was unusual in other late IM specimens. Possible, but unlikely, causes for such persistent GGTP activity are an unusual degree of hepatic damage during acute IM, excessive induction of microsomal enzyme system activity by drugs, or unusual Epstein-Barr virus carrier state activation that might contribute to ongoing hepatic structural damage. Other markers of chronic hepatocellular disease including aspartate aminotrasferase, alkaline phosphatase, and bilirubin were normal in late specimens from these 3 patients. The cause of their persistent elevated GGTP activities remains unknown.
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PMID:Late persistence of serum gamma-glutamyl transpeptidase activity after mononucleosis. Report of 3 cases. 1 21

Of 108 prospectively followed, multiply transfused, open-heart-surgery patients, 12 (11%) developed hepatitis. Patients received only volunteer donor blood tested for hepatitis-B surface antigen (HBsAg) prior to transfusion by counterelectrophoresis (C.E.P.). 4 of the 12 patients developed hepatitis-B-virus infection. Subsequent testing of donor serums by solid-phase radioimmunoassay (R.I.A.) revealed that an R.I.A.-positive, C.E.P.-negative blood unit was transfused to 3 of the 4 type-B hepatitis cases, but to none of the remaining 104 patients; 3 hepatitis-B cases could probably have been prevented by prescreening of donors by solid-phase R.I.A. 8 hepatitis cases were serologically unrelated to the hepatitis-B virus, the hepatitis-A virus, the cytomegalovirus, or the Epstein-Barr virus. Had R.I.A.-positive donors been excluded, 8 of the 9 residual hepatitis cases (89%) would have represented "non-A, non-B" hepatitis. The existence of previously unrecognised human hepatitis virus(es) is probable.
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PMID:Clinical and serological analysis of transfusion-associated hepatitis. 5 29

Of 279 cardiac-surgery patients receiving a mean of twelve transfusions, 47 had significantly increased transaminase concentrations 14 to 180 days postoperatively and 10 were icteric. Preoperatively, each patient randomly received high-titre HbsAb gamma-globulin, normal gamma-globulin, or placebo and was followed at intervals for 9 months. Only 3 patients had serological evidence of hepatitis-B infection. 3 additional patients had serological evidence of cytomegalovirus infection, while none had evidence of hepatitis-A or Epstein-Barr infection. Less icteric hepatitis occurred in patients receiving the gamma-globulin preparations (P = 0-003), and the overall frequency of hepatitis was significantly reduced when compared with recipients of placebo. The protective effects of the two gamma-globulin preparations were not significantly different. Most post-transfusion hepatitis tody is neither viral hepatitis type B nor type A, and its severity and transmission are reduced by pre-transfusion gamma-globulin.
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PMID:Efficacy of prophylactic gamma-globulin in preventing non-A, non-B post-transfusion hepatitis. 5 38

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

6 cases of non-A non-B hepatitis which followed administration of four different batches of concentrates of coagulation factor IX from commercial and non-commercial sources are described. Of 17 patients who received the concentrate on account of chronic liver disease, 4 developed hepatitis, and in 3 of these the illness proved fatal. The incubation periods ranged from 42 to 103 days (mean 65 days). 3 chimpanzees were inoculated with concentrate from the same batch used on the above patients, a further commercial batch upon which no adverse reactions had been reported, and plasma from a known non-A non-B carrier. All developed hepatitis after 10 weeks' incubation. Liver biopsy when serum-aminotransferase was at its highest level showed features consistent with acute hepatitis. As in the patients, viral markers for hepatitis A and B, cytomegalovirus, and Epstein-Barr virus were unchanged.
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PMID:Transmission of non-A non-B hepatitis to chimpanzees by factor-IX concentrates after fatal complications in patients with chronic liver disease. 8 7

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

Twenty-two patients who had an episode of transfusion-associated hepatitis not positive for hepatitis B antigen were examined for development of antibody to heaptitis A and B antigens, cytomegalovirus and Epstein-Barr virus. Antibody response to the 27-nm virus-like hepatitis A antigen was measured by immune electron microscopy. In none of the 22 patients studied did serologic evidence of infection with hepatitis A virus develop during the study period. Nine of the 22 patients had antibody responses to cytomegalovirus, but it was difficult to relate these seroconversions to their hepatitis. In addition, all 22 patients had pre-existing antibody to the Epstein-Barr virus. It seems likely that at least a proportion of such antigen-negative transfusion-associated hepatitis is caused by other infectious agents, not yet identified.
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PMID:Transfusion-associated hepatitis not due to viral hepatitis type A or B. 16 36

Viral contamination is at least as important in hospital laboratories and wards as contamination by bacteria or microscopic fungi, but it is much more insidious and sometimes unrecognized. There are two main types: The first has a purely technical effect and only interest the virologist. This is contamination of reagents, reference strains, cell cultures, etc.., by foreign viral agents. It may be the cause of errors on diagnosis or regrettable errors of interpretation of certain experimental data. It is most difficult to detect, if not to avoid. The second is much more worrying as it is liable to cause disease in man, which may induce severe, and even fatal infections in patients or in the medical, para-medical and technical personnel. This is the case with type B hepatitis virus which tends to invade surgical units using extra-corporeal circulation, hemodialysis units and transplantation units, blood transfusion centres, dental units and even causes victims in routine laboratories. However, type B hepatitis is not the only virus which may lead to severe infections; other viruses include: poxvirus, cytomegalovirus, arbovirus, etc. Finally, other often severe accidents may occur in research laboratories and in the pharmaceutical industry, owing to manipulation of dangerous viruses or by contact with experimental animals, e.g. rodents, or monkeys, which contain the virus in a latent state, e.g. lymphocytic choriomeningitis, Sabin virus, Marburg virus, type A hepatitis virus, etc. With regard to such accidents, we are almost completely powerless from the therapeutic point of view and, even poorly equipped, from the point of view of prophylaxis.
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PMID:[Viral contamination in laboratories and hospital units]. 16 48

The discovery of persistent transmissible agents by veterinarians has led to striking advances in the infectious cause of neuropathies of human beings. There is evidence for persisting infection in congenital rubella and the herpes group of viruses including cytomegalovirus infections. Hepatitis types A and B are candidates for inclusion in the category of persisting viral infections. The rubeola or measles virus is established as a persistent virus which causes elevated antibodies in the serum and cerebrospinal fluid of many patients with severe demyelinating disease such as subacute sclerosing panencephalitis and multiple sclerosis. Elevated antibodies against vaccinia virus have been found in the cerebrospinal fluid of some patients with multiple sclerosis and neuromyelitis optica, a rare form of multiple sclerosis.
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PMID:Persistent or slow viral infections and related diseases. 16 38

Two previously healthy adults with acute granulomatous hepatitis attributable to cytomegalovirus (CMV) monucleosis had prolonged fever, heterophil-negative lymphocytosis with numerous atypical forms, minor alterations in hepatic function, and evidence on biopsy, of a nonspecific acute hepatitis with granulomata. Infection with CMV was corroborated by a rising titer of complement-fixing antibody in case 1 and by a high titer of antibody that later fell in case 2. It is important to exclude CMV ivfection as an etiologic factor in cases of acute granulomatous hepatitis and fever of unknown origin.
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PMID:Acute granulomatous hepatitis. Occurrence in cytomegalovirus mononucleosis. 16 2


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