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)

An outbreak of jaundice associated with three out of four batches of a commercial brand of freeze-dried factor-VIII concentrate occurred at the Bournemouth haemophilia centre between April and June, 1974. Seven cases of non-B hepatitis and four of hepatitis B occurred within 6 months of the first use of this product. Two patients contracted both types of hepatitis; thus nine patients became ill out of a total of twenty regularly seen at the centre, eighteen of whom received commercial factor-VIII concentrate.
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PMID:An outbreak of hepatitis associated with intravenous injection of factor-VIII concentrate. 5 75

Systematic screening of forty-seven haemophiliacs in Sheffield revealed abnormal liver-function tests in thirty-six (77%), with a tendency for these abnormalities to persist. To assess the importance of these abnormalities, percutaneous liver biopsy was carried out on eight symptom-free patients under factor-VIII cover. A wide spectrum of chronic liver disease was demonstrated, including chronic aggressive hepatitis and cirrhosis. The liver pathology bore no relation to clinical history or to biochemical findings. Hepatitis-B-virus markers were common, but evidence suggests that this is not the only factor contributing to the development of liver disease. The high incidence of chronic liver disease seems to be a recent development and is probably related to factor-concentrate replacement therapy.
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PMID:Percutaneous liver biopsy and chronic liver disease in haemophiliacs. 8 May 24

Deoxyschisandrin (VIII) and five new lignans, named schisantherin A, B, C, D, and E, were isolated from the active fraction of the fruits of Schisandra sphenanthera Rehd. et Wils. Their configurations and conformations were established by exhaustive spectral analysis as well as chemical degradations as shown in Ia, Ib; IIa, IIb; IIIa, IIIb; IVa, IVb, and Va, Vb respectively, and their absolute configurations at biphenyl, at C6, C7, and C8 were all assigned to be S form. The position of the methylenedioxyl group in the structures of gamma-schisandrin and Wuweizisu C (as described in the literature), isolated from Schisandra chinensis, must be corrected as shown in VI and VII respectively. In pharmacologica studies and preliminary clinical trials, schisantherin A, B, C, and D showed good effect in lowering the serum glutamic-pyruvic transaminase level of the patients suffering from chronic virus hepatitis. Schisantherin E and deoxyschisandrin were not effective.
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PMID:Studies on the active principles of Schisandra sphenanthera Rehd. et Wils. The structures of schisantherin A, B, C, D, E, and the related compounds. 23 22

Modifications of Factor VIII related antigen (F, VIII R. A.) were investigated in three hemophilic patients during the course of post transfusion hepatitis. F. VIII R. A. was found to be elevated and correlated with the increase of the S.G.P.T. During the acute phase of the disease the Factor VIII related protein was tested for its ristocetin cofactor activity, its electrophoretic mobility on crossed antigen-antibody electrophoresis and its elution pattern on Sepharose 4B columns; all these properties proved to be abnormal. Liver function tests and F. VIII R. A. were measured in 36 multitransfused hemophiliacs. There was a significant increase of the F. VIII R. A. in the plasma of patients with abnormal liver function tests. Only a few of the multitransfused hemophiliacs had clinical symptoms of hepatitis, although 72% had elevated transaminase levels.
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PMID:Modifications of factor VIII related antigen in hemophiliacs with acute hepatitis and sub-clinical liver disease. 26 93

The relationship of chronic hepatitis B and/or liver dysfunction to treatment in 113 hemophiliacs was evaluated by the enzyme tests, SGOT and SGPT, and by the presence of circulating hepatis B surface antigen (HbsAg) or antibody (anti-Hbs). The hemophiliacs were divided into three groups according to treatment pattern. Individuals who had received multiple doses of plasma fractions, derived from four or more commercial lots were placed in tgroup I "large Exposure". Group II "Small Exposure" had been treated with fractions from three or fewer lots and Group III "Cryo" had never received commercial fractions, but had been treated with cryoprecipitate. Abnormal liver function tests (LFT's) were found in 87% of Group I and 76% of Group II, but in only 16% of the "Cryo" group. Differences in LFT's were not great between treated VIII and IX deficient patients. All patients treated with 100,000 units or more showed either persistent or intermittent abnormalities. In the high exposure group, this history of past, overt hepatitis had no influence on observed LFT's. The sera of all patients in the high exposure and all, except one, in the low exposure groups were positive for HbsAg or anti-Hbs by RIA. Splenomegaly was found in 13% of fraction-treated patients. We conclude that there is biochemical evidence of liver disease following large exposure to commercial VIII or IX fractions, which should temper the physician's decision to start treatment with these fractions. On the other hand, evidence that their continued use produces mounting liver dysfunction is insufficient to withdraw this very effective and life-changing treatment from these individuals.
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PMID:Chronic hepatitis in hemophilia. 26 94

Classical sex-linked hemophilia (Hemophilia A) has been described as due to deficiency in the synthesis of Factor VIII procoagulant activity (VIII:C). The availability of immunological techniques provided the means of identifying Factor VIII-Related Antigen(VI-IIR:Ag) detectable by rabbit antibodies to F VIII, which is distinct from VIII:C detected by human anti-F VIII available from multitransfused patients. Hemophilia A is lacking in VIII:C but not VIIIR:Ag. Recently, a third function of the F VIII "complex" was discovered with the help of ristocetin (von Willebrand's Factor, VIIIR: RCo). This activity is reduced in von Willebrand's syndrome. Estimation of the titers of VIII:C and VIIIR:Ag provides a method for more accurate detection of hemophilic carriers. Newly available chromogenic substrates perhaps will give rise to more simplified assays of VIII:C. The development of cryoprecipitates and stable lyophilized concentrates of F VIII has greatly simplified and intensified maintenance therapy, and has opened a new era in treatment. Prophylactic therapy has been shown to be very helpful in certain "high risk" cases. The impact and benefits of home care and self-administration has been tremendous. However, the varying quality of cryoprecipitates and the high cost of more purified concentrates are still stumbling blocks in treatment regimes. Other problems exist. Spontaneous bleeding, especially central nervous system bleeding, account for the majority deaths by haemorrhage. Inhibitor kinetics have been well characterized. It is clear that there exists "low" and "high" responders. For the "high" responders, plasmapheresis, immunosuppressives and the infusion of Factor IX concentrates have been utilized with varying success. The prevention of hemophilic arthropathy and its progression by maintenance therapy seems to be still inadequate. The results of trials with more vigorous regimes are awaited. The complications of therapy still remain to be solved. Apart from the well-known complications wuch as hepatitis, haemolytic disease and F VIII inhibitors, the existence of previously unnoticed complications as splenomegaly, hypertension, renal disease and paradoxal bleeding have been recently realized. The role of altered fibrinogen, fibrin degradation products (FDP) and unclassified fibrinogen derivatives (UFD) present in cryoprecipitates and F VIII concentrates in the above complications needs to be further clarified. In conclusion, tremendous progress in various aspects of hemophilia has been achieved in developed countries. Comprehensive care can now be carried out in various centers. On the other hand, developing countries still face a number of basic problems. The concept that hemophilia is a "manageable" disease and that chronic crippling and death from exsanguination can be prevented, should be disseminated widely by various means...
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PMID:Recent advances in hemophilia. 52 46

In a six year old boy with severe hemophilia prophylactic substitution of factor VIII was started in 1973 in order to prevent early invalidity due to series of bleeding in the right anklejoint. A substitution of factor VIII over 8 months with 21 resp. 30 U/kg body-weight did not lead to a significant improvement. But since the factor VIII in a dosage of 18 U/kg body-weight is given three times a week no bleeding occurred during the treatment time of 14 months and also the ability to walk improved to an excellent degree.--So far no signs of hepatitis or an factor-VIII-antibody could be detected.--Some results from the prophylactic treatment of severe hemophilia and Christmas disease are cited from the literature.
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PMID:[Prophylactic replacement therapy in hemophilia. A case report (author's transl)]. 96 9

We recently observed a increase in factor-VIII clot promoting activity as measured by a one-stage assay (VIII AHF) in a haemophiliac with hepatitis. However, VIII AHF as measured by a two-stage assay (VIII AHF) was 0.013 u/ml at a time when VIII AHF measured 0.38 u/ml. We then studied seven non-haemophiliacs with liver disease, and attempted to correlate the lvels of VIII AHF and VIII AHF with factor VIII-like antigen (VIII AGN) as measured by quantitative immunoelectrophoresis. In four of the seven patients, disproportionate elevations of VIII AHF compared to VIII AHF were found. Furthermore, VIII AHF values correlated well with VIII AGN vales . No such discrepancy was apparent in four normal control subjects. These findings emphasize the necessity for performing two-stage assays in haemophiliacs as well as non-haemophiliacs with liver disease to assess factor-VIII levels. In addition, they suggest that confirmation of the diagnosis of haemophilia may not be possible in the haemophiliac with hepatitis unless VIII AHF determinations are performed. The reason for the disparity between VIII ahf and VIII AHF levels is not apparent. However, the correlation of VIII AGN and VIII AHF levels in the non-haemophiliacs with liver disease provides further support for the concept that VIII AGN and VIII AHF are closely related or identical molecular entities.
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PMID:Relationship of factor VIII-like antigen (VIII AGN) and clot promoting acitivty (VIII AHF) as measured by one- and two-stage assays in patients with liver disease. 99 Jan 95

A prothrombin complex concentrate was used in attempts to control life-threatening hemorrhage in 4 patients with chronic liver disease. The population manifested profuse bleeding from varices and/or hemorrhagic gastritis; 3 had Laennec's cirrhosis and 1 had postnecrotic cirrhosis from childhood hepatitis. In all patients the complex was given in amounts needed to raise the prothrombin (factor II) level to approximately 100% of normal. In all 4 cases the prothrombin time and prothrombin complex factors approached normal within 1-2 hr after beginning the infusion. In all patients bleeding ceased with correction of the clotting status. One patient rebled several hours after completing the infusion. In several patients, increases in factors V and VIII were noted following infusion of the concentrate. A further unexpected finding was a spontaneous increase in factors II and IX at 3 days postinfusion. Prothrombin complex concentrate appears to be useful in controlling the hemorrhage of chronic liver disease when used alone or in combination with other modalities to correct specific hemostatic defects; however, patients may be expected to rebleed when the effect of the concentrate wears off. Its use, therefore, should probably be restricted to those patients who are to undergo corrective surgery of the bleeding point once hemostasis is achieved.
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PMID:Prothrombin complex concentrate: use in controlling the hemorrhagic diathesis of chronic liver disease. 108 Mar 55

A 51-year-old patient with haemophilia since childhood (usual factor VIII level 14%) developed acute viral hepatitis type B two months after an operation which had been covered by cryoprecipitate. The course of the hepatitis following admission was severe with encephalopathy and ascites. Evidence of intravascular coagulation with an increased radioactive fibrinogen turnover was also present. The factor VIII level measured by a one-stage clotting factor assay rose rapidly to 200% of normal and remained at this level for two weeks, and factor-VIII-related antigen as measured by electroimmunoassay also became greatly elevated (900% of normal). The possible mechanisms underlying those surprising changes are discussed.
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PMID:Factor VIII levels during the course of acute hepatitis in a haemophiliac. 120 22


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