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)

19 (51%) of 37 hemophiliac children and adolescents regularly treated with factor VIII and IX concentrates were positive for HTLV III antibodies. The prevalence of HTLV III antibodies was higher in patients with severe hemophilia (64%) requiring frequent administration of concentrates than in patients with mild hemophilia (17%). No patient showed signs of AIDS or AIDS related complex. Immunologic alterations (inverse ratio of helper- and suppressor lymphocytes, elevated immunoglobulins, and elevated total serum proteins) were more often observed in patients requiring frequent administration of concentrates than in patients requiring relatively infrequent administration of concentrates. Since in patients frequently treated with concentrates the prevalence of HTLV III antibodies was also higher, it was not possible to draw any conclusions whether the observed immunologic alterations are due to the HTLV III infection alone or are also induced by the frequent administration of coagulation factor concentrates. No HTLV III positive person was detected in 45 relatives of 18 HTLV III positive hemophiliac children living together in 16 households and actively participating in the care of those children. In contrast, 6 (11%) of 55 relatives living in 21 households with 23 hepatitis-B-positive hemophiliac children were positive for hepatitis B. Our results support the general impression, that the risk to contract hepatitis B seems to be greater than to contract HTLV III from seropositive patients, and should help to facilitate the social integration of HTLV III positive hemophiliac children.
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PMID:[HTLV-III antibodies and immunologic changes in hemophilic children. Prevalence of HTLV-III antibodies in hemophilic children and their relatives living in the same household]. 310 27

Factor VIII deficient plasma was made from pooled, HIV antibody and hepatitis B antigen screened, normal human plasma by cryoprecipitation and immuno-depletion, using three different monoclonal antibodies bound to Sepharose columns, in series. These monoclonal antibodies are specific respectively for von Willebrand factor, factor VIII heavy chain and factor VIII light chain. The immunodepleted plasma contained less than 0.002 u/ml factor VIII coagulation activity (VIII:C) less than 0.0001 u/ml von Willebrand factor antigen and 1-2 g/l fibrinogen, while the levels of other clotting factors were unchanged. This immunodepleted plasma was compared with commercial factor VIII deficient plasma obtained from a severe haemophilia A patient as substrate in the one-stage factor VIII assay. Plasmas obtained from 20 normal subjects and 28 patients with von Willebrand's disease or haemophilia A were assayed for VIII:C using the two substrates. The results were very highly correlated (r = 0.96). The columns have high capacity and can be regenerated at least 10 times. Large-scale production of a substrate for factor VIII assays free of virus contamination is now feasible.
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PMID:Production of factor VIII deficient plasma by immunodepletion using three monoclonal antibodies. 311 89

A factor VIII concentrate prepared from large plasma pools and then exposed to hot vapour to inactivate blood-borne viruses was evaluated in 28 factor-VIII deficient patients (14 vaccinated against the hepatitis B virus, HBV) who had not been treated with any blood product and hence were highly susceptible to the development of post-transfusion hepatitis. Tests for aminotransferases and HBV markers were made every 2 weeks in the first 4 months and at 5, 6 and 12 months. Twenty-four patients were considered not to have developed hepatitis, either because they had no elevations of aminotransferases or did not become seropositive for HBV markers. The four remaining unvaccinated patients (three treated with the same batch and the fourth with a different one) developed HBV infection 8-24 weeks after the first concentrate infusion. Hence, this method of viral inactivation did not afford complete protection from hepatitis B.
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PMID:Prospective study of hepatitis after factor VIII concentrate exposed to hot vapour. 313 99

The risk of hepatitis B infections has been reduced by screening of blood donors for hepatitis B surface antigen (HBsAg). However, recipients remain at significant risk of developing post-transfusion hepatitis. Studies have shown that non-A, non-B hepatitis virus(es) are responsible for the majority of post-transfusion hepatitis infections. In spite of many efforts, these non-A, non-B hepatitis viruses have not yet been identified. Epidemiological studies, however, suggest that non-A, non-B hepatitis shares many features with hepatitis B. Recently, Wands et al [1982] showed, in chimpanzees infected with non-A, non-B hepatitis agents, the presence of antigenemia or viremia by radioimmunoassay with monoclonal antibodies directed toward distinct determinants of HBsAg and by molecular hybridization analysis. They suggested that non-A, non-B hepatitis agents may be related, but distinct variant(s) of hepatitis B virus (HBV). In this study, five chimpanzees were inoculated with three different agents that have been shown to transmit non-A, non-B hepatitis. The following inocula were used (I) a factor VIII preparation kindly provided by D.W. Bradley, (II) acute phase serum from a chimpanzee infected with the F strain kindly provided by A.J. Zuckerman, and (III) a DS-antigen serum previously shown by us to transmit non-A, non-B hepatitis [Duermeyer et al, 1983]. All chimpanzees developed a rise in transaminase levels between 8 and 10 weeks after inoculation. None of the chimpanzees was positive for any markers of HBV infection. No evidence was obtained of infection with hepatitis A, cytomegalovirus, or Epstein-Barr virus. One chimpanzee developed chronic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of detectable hepatitis B virus DNA in sera and liver of chimpanzees with non-A, non-B hepatitis. 392 Mar 54

After a first exposure to factor VIII concentrates, 9/9 British patients treated with U.S.A.-derived commercial products, and 10/12 treated with British volunteer (NHS) products, developed acute non-A, non-B (NANB) hepatitis. Hepatitis following commercial products was more severe, and of shorter incubation. High previous exposure to NHS blood products seemed to prevent NHS but not commercial factor VIII-induced hepatitis; the latter was also not attenuated by administration of U.S.A.-derived commercial immune serum globulin (ISG). After a first exposure to NHS factor IX concentrates without ISG, 4/4 patients developed short incubation NANB hepatitis; one also contracted prolonged incubation hepatitis B. One patient treated with ISG and factor IX of proven infectivity did not develop hepatitis, suggesting protection by ISG. Observed differences between concentrates might be attributable to their content of different NANB agents, but dose-related effects could provide alternative explanations. This data provides a basis for comparative assessment of new products of possible reduced infectivity in only small numbers of patients.
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PMID:High risk of non-A non-B hepatitis after a first exposure to volunteer or commercial clotting factor concentrates: effects of prophylactic immune serum globulin. 392 81

We report here the results of our evaluation of two procedures to eliminate viruses in factor VIII and factor IX coagulation factor concentrates. Both procedures were equally effective in the in vitro destruction of marker viruses. However, in a controlled infectivity test in chimpanzees, treatment at 60 degrees C for 20 hours inactivated greater than 500 and less than 10,000 chimpanzee infectious doses (CID) of hepatitis B virus, while treatment at 98 degrees C for 30 minutes inactivated less than 500 CID. Both methods were successful in preventing infection with an undetermined amount of an indeterminate non-A, non-B hepatitis agent. The 60 degrees C, 20-hour treatment method rendered 5.25 logs of the putative acquired immune deficiency syndrome virus, human T-cell lymphotrophic virus III/lymphadenopathy virus, added to factor VIII or factor IX concentrates, undetectable. Heat-treated factor VIII and factor IX complex concentrates prepared by these methods were tested against corresponding untreated control lots. There was no significant difference in the plasma recovery or plasma half-life of the factor (p greater than 0.05). The treated concentrates were equivalent to the control concentrates with respect to vital signs, clinical laboratory studies, and adverse reactions. The heat-treated concentrates appeared bioequivalent to the untreated concentrates with the additional benefit of inactivation of potentially present infectious viruses.
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PMID:Evaluation of two viral inactivation methods for the preparation of safer factor VIII and factor IX concentrates. 393

243 Australian haemophiliacs have been studied retrospectively over 4 1/2 years to assess the effect of treatment products on liver function and to determine the frequency of hepatitis-B markers in these patients. Commercial blood products are not used in Australia, and the patients were treated with products of blood from unpaid donors screened for hepatitis B surface antigen. Cryoprecipitate was the major treatment product, and only small amounts of factor VIII and IX concentrates were used. Despite the use of blood products obtained from entirely voluntary blood donors and the frequent use of single-donor packs of cryoprecipitate, markers of viral hepatitis were common in these haemophiliacs. Antibody to hepatitis B surface antigen was detected in 63% of the patients, and there were 66 cases of non-A, non-B hepatitis during the study. 29 of these episodes persisted for longer than 6 months. 13 patients (5.4%) had hepatitis B during the study; 2 patients remained HBsAg-positive for longer than 6 months. Abnormal serum aminotransferase levels were found in 34% of the patients; in 8% of patients these abnormalities persisted for more than 6 months.
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PMID:Hepatitis and haemophilia therapy in Australia. 612 51

Classic hemophilia or factor VIII deficiency is a recessive, sex-linked bleeding diathesis. The primary clinical problem is hemorrhage, which can be severe and often life threatening, even in the presence of only minor trauma. In the past this inadequate hemostasis has been treated with transfusions of cryoprecipitate, fresh frozen plasma, or commercially prepared factor VIII concentrate. Unfortunately, such treatment carries with it a number of risks, including the development of hepatitis B or hemolytic anemia and the formation of anti-factor VIII antibodies. Because of hemorrhage severity and the risks of conventional treatment, elective surgery in general and oral surgery in particular have often been neglected in patients with hemophilia. This article reviews a drug, 1-desamino-8-d-arginine (DDAVP), heretofore not discussed in the dental literature, and reports on its use in conjunction with epsilon-aminocaproic acid (EACA), a synthetic antifibrinolytic agent, in the surgical dental treatment of a patient with hemophilia A. The results suggest that certain dental surgical procedures can be performed in the presence of subclinical and mild hemophilia without conventional factor VIII replacement therapy with its associated costs and risks.
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PMID:DDAVP: review of indications for its use in the treatment of factor VIII deficiency and report of a case. 622 10

Recently, Acquired Immune Deficiency Syndrome (AIDS) has been reported in hemophiliacs in the USA, Canada and Spain, and this has caused considerable concern amongst hemophiliacs regarding the use of factor VIII concentrates. The aim of this study was to determine whether hemophiliacs in Australia have T-lymphocyte subpopulation changes similar to those observed in patients with AIDS. Factor VIII produced in Australia is derived from a totally volunteer blood donor system and none of the hemophiliacs in this study had received commercial blood products. For the hemophiliacs, the T-helper cell to T-suppressor cell ratio was 1.1 +/- 0.6 (mean +/- SD) which was significantly less (p less than 0.001) than that of the normal age and sex-matched controls. There was a significant relative (p less than 0.001) and absolute (p less than 0.05) reduction of the helper cell subsets and a significant relative (p less than 0.001) and absolute (p less than 0.05) increase of the suppressor cell subsets, in the hemophiliacs compared to the normal controls. There appears to be no correlation between the amount of factor VIII therapy received during the last three years and the T-cell subset changes. All patients with Christmas disease had T-cell subsets within the normal range. All patients were negative for the hepatitis B virus antigen, but all were positive for the antibody, indicating that there had been exposure to the hepatitis virus in all cases. Cytomegalovirus titres were uniformly low and immunoglobulin levels were normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal T-cell subpopulations in hemophilic patients receiving factor VIII concentrates from voluntary donors. 623 88

A previously healthy patient with classic hemophilia who was on a home infusion program with factor VIII concentrates developed an acquired immunodeficiency syndrome manifested by a dramatic weight loss (47 kg over 12 months), lassitude, transient thrombocytopenia, and opportunistic infections with Varicella zoster, Pneumocystis carinii, and Mycobacterium avium-intracellulare. The patient was not homosexual and had no history of intravenous drug abuse. Immunologic studies showed a persistent lymphopenia with reversal of helper/suppressor-cytotoxic T-lymphocyte ratios, depression of human natural killer cell function, and in-vitro lymphocyte proliferative responses to mitogens and viral antigens. Serum IgA levels were also elevated. Serum antibodies against cytomegalovirus, herpes simplex viruses 1 and 2, Epstein-Barr virus, Varicella zoster, and hepatitis B virus were shown, suggesting previous infection by these agents. Reactivation of cytomegalovirus infection was suggested by a rising titer of antibodies against cytomegalovirus concurrent with pneumocystis pneumonia, and was confirmed by the growth of this virus in a throat culture 2 months later.
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PMID:Acquired immunodeficiency syndrome with Pneumocystis carinii pneumonia and Mycobacterium avium-intracellulare infection in a previously healthy patient with classic hemophilia. Clinical, immunologic, and virologic findings. 629 53


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