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)

A randomised clinical trial was undertaken to compare the value of a factor II, IX, and X concentrate (Prothromplex) with intravenous vitamin K1 (2-5 mg) in reversing an overdose of oral anticoagulants. Rapid partial correction of the prothrombin time, partial thromboplastin time, and the clotting factor assays were observed with the concentrate, but these changes were not always sustained. In contrast vitamin K1 did not show any great effect at two hours but at 24 hours there was always over-correction despite the conservative dosage, prothrombin times being shorter than the therapeutic range. The prothrombin complex concentrate provides a quicker, more controlled but less sustained method of reversing the coumarin defect than vitamin K1. But there remains a significant risk of hepatitis even with a preparation for which strenuous efforts have been made to minimise this risk by screening for hepatitis B virus. The risk should be carefully considered before such concentrates are infused in non-urgent conditions.
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PMID:Comparison of prothrombin complex concentrate and vitamin K1 in oral anticoagulant reversal. 77 48

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

Liver dysfunction and exposure to the hepatitis B antigen were assessed by serum transaminase (SGPT and SGOT) levels and HBsAg and anti-HBs during a three year period in a group of 118 patients with factor VIII or factor IX deficiency. The 107 HBsAg negative patients were divided into four groups according to their mode of therapy. Persistently abnormal transaminase values were present in 51 per cent of patients with a large exposure to factor VIII concentrates, in 43 per cent with a small factor VIII exposure and in 37 per cent exposed to prothrombin complexes. This was contrasted with abnormalities in 8 per cent of patients treated only with cryoprecipitate. The incidence and degree of serum transaminase abnormality appeared independent of a past history of jaundice. All patients without persistent antigenemia who had been treated with pooled plasma products showed antibodies to HBsAg. High titer anti-HBs prior to initial fraction therapy appeared protective against jaundice. The eleven patients with persistent antigenemia had significantly higher transaminase levels than the HBsAg negative group.
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PMID:Chronic liver dysfunction in multitransfused hemophiliacs. 91 Feb 67

Because of the inhomogeneous prognosis in fulminant hepatic failure, prognostic criteria are required which help to establish the indication for liver transplantation as a successful therapeutic procedure. In our study of 33 patients with fulminant hepatic failure (94% viral hepatitis, 67% hepatitis B), serum bilirubin > 320 or < 160 mumol/L, serum creatinine > 110 mumol/L, prothrombin time < 15% of the normal value and duration of jaundice until onset of encephalopathy > 7 days indicated a fatal outcome. When criteria described by O'Grady et al. were used, only limited predictability was achieved. This, as well as the frequently contradictory results of the few prognostic studies published so far, is probably due to the regional differences in the etiology and the different clinical courses of fulminant hepatic failure.
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PMID:Prognostic indicators in fulminant hepatic failure. 144 4

Twelve cases of childhood fulminant hepatitis seen over a 4-year period are described. Six had hepatitis A, five hepatitis B and one non-A non-B hepatitis. Encephalopathy, the cardinal feature of fulminant hepatitis, was usually evident within 2 weeks of onset of illness, and the median duration of illness in fatal cases was 19 days. Deep jaundice, prolongation of the prothrombin time and raised serum ammonia were invariable. Eight children died and the four survivors were critically ill before recovering. Acute viral hepatitis is generally a benign illness in childhood. Although infrequently recorded, fulminant hepatitis may, however, ensue and is associated with a high mortality.
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PMID:Fulminant hepatitis in children: report of 12 cases. 171 18

The implications of hepatitis B virus (HBV) reinfection after liver transplantation were studied in 29 patients followed for 1.7-15 years. Of 20 patients with HBV infection alone, nine were HBeAg and HBV DNA seronegative and 11 had evidence of HBV replication as measured by HBeAg or HBV DNA seropositivity. Nine patients had co-existing HBV and delta virus (HDV) infection. Five patients became HBsAg seronegative after transplantation (four immediately and one after an hepatitic episode). Of the 20 patients with HBV infection alone, 17 had evidence of viral replication after transplantation with markedly increased HBV DNA levels. Five patients with HDV infection had HBV DNA in serum, but in significantly lower amounts than in those with HBV infection alone. Twenty-five episodes of graft dysfunction attributed to recurrent HBV infection occurred in 19 patients (65.5%). Thirteen episodes (in 12 patients) were self-resolving acute hepatitic illnesses. Six patients had a rapidly progressive illness leading to graft loss within 6 weeks, with the distinctive histological features termed fibrosing cholestatic hepatitis (FCH). Liver function tests in these patients showed markedly abnormal serum bilirubin and prothrombin times, but only modest increases in serum transaminase levels. An additional six patients lost their graft as a consequence of HBV recurrence through various pathogenetic mechanisms including possible (but unproven) FCH, chronic active hepatitis or late-onset hepatic failure. Co-existing HDV infection appeared to confer some medium-term protection from graft loss.
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PMID:Hepatitis B virus reinfection after orthotopic liver transplantation. Serological and clinical implications. 173 10

In contrast to the type of bleeding encountered in congenital hemophilia with inhibitors, the diathesis toward bleeding exhibited by patients with spontaneously acquired factor VIII (FVIII) inhibitors often is severe and life threatening. Large hematomas and retropharyngeal or central nervous system hemorrhage may appear suddenly. Thus, a high premium is placed on rapid therapeutic intervention. Several treatment options are at the physician's disposal. The role of factor IX (FIX) complex concentrates, both standard and purposely activated, is discussed. The FIX products are also known as prothrombin complex concentrates (PCCs). Prudent choice of any treatment modality requires weighing its benefits and shortcomings. Advantages of PCCs--particularly the activated products--include availability, ease of reconstitution and administration, and at least partial efficacy; control of bleeding episodes can be achieved with PCCs in many (but not all) instances. One salient disadvantage of therapy with FIX complex concentrates is that they are not subjected to such rigorous viral-attenuation processes as are most of the currently marketed FVIII products. Therefore, a small but definite risk of infection with hepatitis B or C (HBV, HCV) remains. An assay that detects antibodies against HCV has been licensed and is being used to screen blood donors. Nevertheless, up to the present time the U.S. Food and Drug Administration (FDA) has ruled that HCV screening of plasmapheresis donors should not be performed for plasma collections destined to be pooled for fractionation and that units of HCV-positive source plasma (e.g., that provided by American Red Cross donors) found to be HCV positive be sent for fractionation. The starting plasma from which FIX complex concentrates and human FVIII concentrates are made thus contains some HCV and may also contain some HBV. Because nonhemophiliacs with acquired antibodies against FVIII are unlikely to have had prior exposure to blood products and are unlikely to have been vaccinated against HBV, they are at risk of viral hepatitis and its sequelae when treated with FIX complex concentrates. Furthermore, therapy with FIX complex concentrates is not always effective in controlling bleeding in persons with FVIII inhibitors, its mechanism of action in bypassing the need for FVIII remains unclear, very large doses are required, and it has an attendant risk of several adverse effects when used in large, repeated doses. These include disseminated intravascular coagulation, thromboembolism, and acute myocardial infarction. Thus, FIX complex concentrates may play a useful role in the treatment of bleeding in nonhemophiliacs with acquired inhibitors against FVIII, but one must carefully consider their disadvantages profile.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Perspectives on the use of factor IX complex concentrates in the treatment of bleeding in persons with acquired factor VIII inhibition. 174 94

One hundred hemophilia A and 30 hemophilia B patients who had been treated with non-heated and heated factor VIII or prothrombin complex concentrates were examined by immunological tests including Clq-bearing immune complexes assay. Antibodies to human immunodeficiency virus type 1 (HIV-1), hepatitis B virus (HBV), hepatitis C virus (HCV) and human parvovirus B19 (B19) were analyzed by Western blotting, enzyme immunoassay, passive hemagglutination or radio-immunoassay. Clq-bearing immune complexes were assayed by a monoclonal anti-Clq ELISA system (Immunomedics). Seropositivity to HIV-1, HBV, HCV, and B19 was 56.9%, 87.7%, 79.2% and 100% respectively. Clq-bearing immune complexes were positive in 109 of the 130 patients (83.8%). The positivity and the levels were extremely higher than those in normal individuals. Clq-bearing immune complex levels in patient positive for HIV-1, HCV, or HBV were higher than those in the negative group (HIV: P less than 0.001, HCV: P less than 0.005, HBV: P less than 0.05). When the patients were divided into four groups according to seropositivity to HIV-1 and/or HCV, Clq-bearing immune complex levels were the highest in the group positive for both antibodies, and the lowest in the group negative for both antibodies. These results suggested that each viral infection influences the formation of immune complexes and repeated viral infection increased the level of Clq-bearing immune complexes in these patients.
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PMID:[Elevated Clq-bearing immune complexes in hemophiliacs with viral infections]. 177 53

The risk of infection after application of vapour heated prothrombin complex concentrate PROTHROMPLEX S-TIM 4 (PCC) was investigated in patients undergoing cardiovascular surgery. The study was conducted according to the recommendations of the International Committee on Thrombosis and Hemostasis (ICTH) with the exception that most patients required other blood products in addition to PCC. Twenty-One patients were eligible to test for the risk of acquiring hepatitis NANB (ALT-levels) and samples from 12 patients were available that could be screened for anti-HCV. Twenty patients qualified for evaluation of the risk of developing hepatitis B, and 67 patients qualified to test for HIV-1-Infection. None of these patients showed any signs of infection. Vapour heating of prothrombin complex concentrate seems to lower the risk of transmitting viral diseases considerably.
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PMID:Safety of vapour heated prothrombin complex concentrate (PCC) Prothromplex S-TIM 4. 178 Aug 9


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