The impact of oral anticoagulant therapy, factor VIII level and quality of factor V-deficient plasma on three commercial methods for activated protein C resistance

2001 ◽  
Vol 12 (3) ◽  
pp. 179-186 ◽  
Author(s):  
A. Chitolie ◽  
A. S. Lawrie ◽  
I. J. Mackie ◽  
P. Harrison ◽  
S. J. Machin
Keyword(s):  
Oral Anticoagulant ◽  
Protein C ◽  
Oral Anticoagulant Therapy ◽  
Activated Protein C ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor Viii Level ◽  
Viii Level ◽  
The Impact

Coagulation Factor V Leiden Mutation Was Detected in the Patients with Activated Protein C Resistance in Thailand

1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Coagulation Factor ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor V Leiden Mutation ◽  
Coagulation Factor V

The Diagnosis and Clinical Manifestations of Activated Protein C Resistance: A Case Report and Review of the Literature

1996 ◽  
Vol 1 (4) ◽  
pp. 275-280 ◽  
Author(s):  
Howard Daniel Hoerl ◽  
Aldo Tabares ◽  
Kandice Kottke-Marchant
Keyword(s):  
Case Report ◽  
Protein C ◽  
Activated Protein C ◽  
Clinical Manifestations ◽  
Factor V Leiden ◽  
Laboratory Diagnosis ◽  
Factor V ◽  
Review Of The Literature ◽  
Activated Protein C Resistance ◽  
Genetic Anomaly

Activated protein C resistance (APCR) is a recently discovered, medically important cause of venous thrombosis. More than 95% of cases are due to factor V Leiden (FVL), a mutated form of factor V that is resistant to degradation by activated protein C. The prevalence of this disorder, which is inherited in an autosomal dominant fashion, is approximately 5% among asymptomatic people of European heritage. In addition, 20 to 60% of patient cohorts with previous thrombosis demonstrate APCR, making it the most common known genetic cause of abnormal thrombophilia. Current laboratory techniques available for diagnosis include functional assays, such as the APC ratio, as well as DNA-based tests that detect the specific genetic anomaly responsible for FVL. A case report is presented, along with a review of the literature highlighting epidemiology, pathogenesis, clinical features and methods for laboratory diagnosis.

scholarly journals Improved Distinction of Factor V Wild-Type and Factor V Leiden Using a Novel Prothrombin-Based Activated Protein C Resistance Assay

2004 ◽  
Vol 122 (6) ◽  
pp. 836-842 ◽  
Author(s):  
Marianne Wilmer ◽  
Christoph Stocker ◽  
Beatrice Bühler ◽  
Brigitte Conell ◽  
Andreas Calatzis
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Factor V ◽  
Wild Type ◽  
Activated Protein C Resistance

Inhibition of Activated Protein C Anticoagulant Activity by Prothrombin

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3839-3846 ◽  
Author(s):  
Mikhail D. Smirnov ◽  
Omid Safa ◽  
Naomi L. Esmon ◽  
Charles T. Esmon
Keyword(s):  
Anticoagulant Therapy ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Anticoagulant Activity ◽  
Oral Anticoagulant Therapy ◽  
Membrane Surface ◽  
Activated Protein C ◽  
Significant Risk ◽  
Thrombotic Risk ◽  
Factor Va

Abstract In this study, we test the hypothesis that prothrombin levels may modulate activated protein C (APC) anticoagulant activity. Prothrombin in purified systems or plasma dramatically inhibited the ability of APC to inactivate factor Va and to anticoagulate plasma. This was not due solely to competition for binding to the membrane surface, as prothrombin also inhibited factor Va inactivation by APC in the absence of a membrane surface. Compared with normal factor Va, inactivation of factor Va Leiden by APC was much less sensitive to prothrombin inhibition. This may account for the observation that the Leiden mutation has less of an effect on plasma-based clotting assays than would be predicted from the purified system. Reduction of protein C levels to 20% of normal constitutes a significant risk of thrombosis, yet these levels are observed in neonates and patients on oral anticoagulant therapy. In both situations, the correspondingly low prothrombin levels would result in an increased effectiveness of the remaining functional APC of ≈5-fold. Thus, while the protein C activation system is impaired by the reduction in protein C levels, the APC that is formed is a more effective anticoagulant, allowing protein C levels to be reduced without significant thrombotic risk. In situations where prothrombin is high and protein C levels are low, as in early stages of oral anticoagulant therapy, the reduction in protein C would result only in impaired function of the anticoagulant system, possibly explaining the tendency for warfarin-induced skin necrosis.

scholarly journals Activated Protein C Resistance and Factor V Leiden in Mexico

2007 ◽  
Vol 14 (4) ◽  
pp. 428-437 ◽  
Author(s):  
Abraham Majluf-Cruz ◽  
Manuel Moreno-Hernández ◽  
Adriana Ruiz-de-Chávez-Ochoa ◽  
Rosario Monroy-García ◽  
Karim Majluf-Cruz ◽  
...  
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor V Leiden Mutation ◽  
Common Cause ◽  
Factor V Gene ◽  
V Gene ◽  
Low Prevalence

A common cause of hereditary thrombophilia is activated protein C resistance (APCR), and most cases result from factor V Leiden mutation. An APCR phenotype without association with factor V Leiden has been described. This transversal, observational, nonrandomized study evaluated these 2 phenomena in healthy indigenous and mestizo Mexican subjects (n = 4345), including 600 Mexican natives. No indigenous subjects had APCR, but 82 mestizo subjects did. After retesting, 50 subjects had a negative test. The remaining 32 subjects had factor V Leiden, giving a 0.85% prevalence of factor V Leiden in the mestizo Mexican population. Only 31% of APCR carriers had factor V Leiden. These results show a very low prevalence of APCR and factor V Leiden in Mexico. Except for factor V Leiden, there are no other mutations in the factor V gene responsible for the APCR phenotype. Acquired APCR is nearly twice as prevalent as the inherited variant.

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