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activated protein c resistance/phospholipid
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Pagina 1 a partire dal 76 risultati
Studies on phospholipid antibodies, APC-resistance and associated mutation in the coagulation factor V gene.
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The influence of antibodies against phospholipids (PLa) on APC response was investigated in 155 women with a history of thromboembolism and/or repeated foetal losses. PLa were determined as antibodies against cardiolipin (CLa) and phosphatidyl serine (PSa) and as lupus anticoagulant (LA) tested by
Combination of activated protein C resistance and antibodies to phospholipids in the development of thrombosis.
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An insufficient response to activated protein C (APC) resistance and antibodies against phospholipids (PLa) are frequent laboratory findings associated with thrombosis. Studies investigating the coexistance of these two factors in thrombophilic patients and in patients with autoimmune disorders are
Effect of platelet phospholipid exposure on activated protein C resistance: implications for thrombophilia screening.
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The effect of platelet contamination and freeze-thawing on the activated protein C sensitivity ratio (APCsr) was determined. With increasing platelet count there was a progressive reduction in the ratio. Filtration of samples through a 0.2 microm filter before or after freeze-thawing abolished the
False positive activated protein C resistance test due to anti-phospholipid antibodies is corrected by platelet extract.
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Phospholipid antibodies and resistance to activated protein C in women with thrombophilia.
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Seventy-eight women with a history of thromboembolism were studied for cardiolipin antibodies (CLa), lupus anticoagulant activity (LA) and resistance to activated protein C (APC-resistance). Elevated CLa were found in 15 (19%) and LA in 15 women (19%), respectively. Twenty-six patients (33%) were
A new variant of interaction between phospholipid antibodies and the protein C system.
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The influence of 38 IgG fractions with either cardiolipin antibodies only (CLa) or both CLa and lupus anticoagulant activity (LA) on the response to activated protein C (APC) and on the snake venom activation of protein C were investigated. Five of eight IgG fractions with LA activity showed a
Production of phospholipid antibodies in selected thrombophilic women differing in genotype at the 506 site of factor V.
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The composition of antibodies against phospholipids (PLa) was analysed in 54 PLa-positive thrombophilic women, different in the factor V genotype (Arg506-Gln mutation carriers, n=23; and noncarriers, n=31). The presence of antibodies against prothrombin was also studied. The incidence of cardiolipin
Molecular mechanisms of activated protein C resistance. Properties of factor V isolated from an individual with homozygosity for the Arg506 to Gln mutation in the factor V gene.
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Resistance to activated protein C (APC), which is the most prevalent pathogenetic risk factor of thrombosis, is linked to a single point-mutation in the factor V (FV) gene, which predicts replacement of Arg (R) at position 506 with a Gln (Q). This mutation modifies one of three APC-cleavage sites in
Acquired activated protein C resistance is associated with the co-existence of anti-prothrombin antibodies and lupus anticoagulant activity in patients with systemic lupus erythematosus.
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Venous thromboembolism (VTE) is one of the common manifestations in the anti-phospholipid (aPL) syndrome. We examined the levels of IgG antibodies (Abs) to beta2-glycoprotein I (beta2-GP I) and prothrombin, lupus anticoagulant (LA) activity, activated protein C resistance (APC-R), and factor V
Acquired activated protein C resistance associated with IgG antibodies against beta2-glycoprotein I and prothrombin as a strong risk factor for venous thromboembolism.
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BACKGROUND
Venous thromboembolic events such as deep vein thrombosis and pulmonary embolism are common manifestations of antiphospholipid syndrome. Our aim was to clarify the roles of anti-phospholipid (aPL) antibodies in the pathogenesis of venous thromboembolism (VTE) in patients with systemic
Determination of activated protein C resistance in anticoagulated and lupus positive patients.
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Clotting-based activated protein C (APC) assays have limitations when testing patients on oral anticoagulant (OA) therapy or with a lupus anticoagulant (LA). Predilution in factor V (FV)-deficient plasma and testing with phospholipid-rich Russell Viper venom (RVV)-based methods have been shown to be
A comparison between two activated protein C resistance methods as routine diagnostic tests for factor V Leiden mutation.
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The most common commercially available test measuring activated protein C (APC) resistance relies on the the anticoagulant response to added APC in an activated partial thromboplastin time (APTT) based method. Another method is a Russell Viper venom time (RVVT) based system. To improve the
Effects of (pre-)analytical variables on activated protein C resistance determined via a thrombin generation-based assay.
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The normalized activated protein C sensitivity ratio (nAPC-sr) determined with an assay that quantifies the effect of APC on thrombin formation initiated via the extrinsic coagulation pathway identifies hereditary and acquired defects of the protein C system. We investigated the influence of assay
Use of modified functional assays for activated protein C resistance in patients with basally prolonged aPTT.
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Inherited resistance to activated protein C (APCr) is currently recognized as the most prevalent cause underlying venous thrombophilia, with an estimated prevalence around 20% in thrombotic patients and around 1.8-7% in the general population. A correct laboratory diagnosis of APCr is therefore
The use of two different APC resistance assay systems provides optimal sensitivity and specificity for diagnosing genetic APC resistance.
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We compared the performance characteristics of a commercial dilute Russell's viper venom (DRVV)-based APC resistance assay (Gradipore PC Impedance Test) to a routinely utilized commercial APTT based assay (Coatest APC Resistance Assay). The DRVV based assay offers improved sensitivity and
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