hemophilia a/protease

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A moderate form of hemophilia B is caused by a novel mutation in the protease domain of factor IXVancouver.

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A genomic phage library was constructed using lymphocyte DNA from a patient with cross-reacting material-positive, moderately severe hemophilia B. The library was screened by using a full-length factor IX cDNA as a hybridization probe. DNA sequence analysis of the factor IX exons and intron/exon

Plasma concentration of protein Z and protein Z-dependent protease inhibitor in patients with haemophilia A.

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The potential role of alterations in protein Z (PZ) concentrations in the pathogenesis of coagulation has been investigated in several studies which, however, yielded conflicting results. Protein Z deficiency may induce bleeding as well as prothrombotic tendencies and it might occur as an inherited

Hemophilia B caused by five different nondeletion mutations in the protease domain of factor IX.

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Factor IX is a multidomain protein and is the proenzyme of a serine protease, factor IXa, essential for hemostasis. In this report, we describe the molecular basis of hemophilia B (deficiency of factor IX activity) in five patients who have neither deletions nor rearrangements of the factor IX gene.

Successful use of protease inhibitors in HIV-infected haemophilia patients.

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The haemophilias are a group of inherited haemostatic disorders that require regular clotting factor replacement therapy in the severe and moderately severe subgroups. Prior to the introduction of adequate viral inactivation methods in 1985, haemophilia patients were at exceptionally high risk of

Targeting Protease Nexin-1, a natural anticoagulant serpin, to control bleeding and improve hemostasis in hemophilia.

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Hemophilia A and B, diseases caused by the lack of factor VIII (FVIII) and factor IX (FIX) respectively, lead to insufficient thrombin production, and therefore to bleeding. New therapeutic strategies for hemophilia treatment that do not rely on clotting factor replacement, but imply the

Engineering a protein Z-dependent protease inhibitor (ZPI) mutant as a novel antagonist of ZPI anticoagulant function for hemophilia treatment.

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Protein Z-dependent protease inhibitor (ZPI), is an important anticoagulant protein in plasma that functions in complex with its cofactor, protein Z (PZ) to rapidly inhibit activated factor X (FXa) on a procoagulant membrane surface. Recent studies suggest that the ZPI-PZ anticoagulant

Region of factor IXa protease domain that interacts with factor VIIIa: analysis of select hemophilia B mutants.

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Essential to hemostasis is the interaction of factor IXa with factor VIIIa. Recent studies indicate that helix-330 in the protease domain of factor IXa provides a critical binding site for factor VIIIa. Although weaker interactions cannot be ruled out, a primary role of the EGF1 domain of factor IXa

Haemophilia and the protease inhibitor in peanuts.

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Does protease inhibitor treatment induce increased bleeding tendency in haemophilia?

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Monitoring but no drug-regimen changes advised for hemophilia patients taking protease inhibitors.

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HIV protease inhibitors and increased bleeding in hemophilia?

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Characterisation of factor IX with a glycine-to-valine missense mutation at residue 190 in a patient with severe haemophilia B.

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A patient with severe haemophilia B with a glycine-to-valine missense mutation at residue 190 (c25, chymotrypsin numbering) in factor IX (FIX; FIX-G190V or FIX-FuChou) had <1% of normal FIX clotting activity and 36% of normal FIX antigen levels (cross-reacting material- reduced, CRMr). Residue 190

Bleeding episodes in HIV-positive patients taking HIV protease inhibitors: a case series.

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In July 1996 the Food and Drug Administration (FDA) alerted healthcare providers about 15 case reports of spontaneous bleeding episodes in HIV-positive haemophiliacs taking HIV protease inhibitors. In order to characterize the bleeding associated with HIV protease inhibitor therapy, the FDA's

Increased bleeding in HIV-positive haemophiliacs treated with antiretroviral protease inhibitors.

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Seventeen HIV-positive patients with congenital haemophilia, one with von Willebrand's disease, and one with acquired haemophilia in remission, were treated with antiretroviral protease inhibitors. Clear increases in the frequency of bleeds or changes in the bleeding pattern were documented in 10

A mutation adjacent to the beta cleavage site of factor IX (valine 182 to leucine) results in mild haemophilia Bm.

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The genetic basis of a mild form of haemophilia Bm has been investigated. The patient under investigation has a mild bleeding disorder and has never experienced spontaneous bleeds. Factor IX coagulant activity (FIX:C) was 0.15 units/ml and factor IX antigen (FIX:Ag) 1.32 units/ml. The prothrombin

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