A modification of the APC resistance test and its application to the study of patients on coumarin therapy

A modification of the APC resistance test and its application to the study of patients on coumarin therapy

APC resistance appears to be caused, predominantly, by a mutation in coagulation factor V (nucleotide 1691: G to A). This phenomenon is usually studied by performing APTTs in the absence and presence of added APC. We studied a modification of the assay involving dilution of the test plasma in factor...

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Bibliographic Details
Published in:Thrombosis research Vol. 82; no. 3; pp. 217 - 224
Main Authors: Jorquera, Juan I, Aznar, Justo, Fernández, M Angeles, Montoro, JoséManuel, Curats, Rafael, Casaña, Pilar
Format: Journal Article
Language:English
Published: New York, NY Elsevier Ltd 01-05-1996
Elsevier Science
Subjects:
Adult
Aged
Aged, 80 and over
Anticoagulants - therapeutic use
APC resistance
Biological and medical sciences
Blood coagulation
Case-Control Studies
coumarin therapy
Coumarins - therapeutic use
Drug Resistance - genetics
Factor V Deficiency - blood
Factor V Deficiency - genetics
factor V Leiden
Humans
Investigative techniques, diagnostic techniques (general aspects)
Medical sciences
Middle Aged
Mutation
Protein C - agonists
Thrombophlebitis - blood
Thrombophlebitis - drug therapy
factor V Leiden
coumarin therapy
APC resistance
Activated state
Human
Factor V
Resistance
Chemotherapy
Treatment
Coumarine derivatives
Laboratory investigations
Protein C
In vitro
Blood plasma
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Summary:APC resistance appears to be caused, predominantly, by a mutation in coagulation factor V (nucleotide 1691: G to A). This phenomenon is usually studied by performing APTTs in the absence and presence of added APC. We studied a modification of the assay involving dilution of the test plasma in factor V deficient plasma, to render the assay more factor V specific. This modification was applied to 76 patients with venous thrombosis on coumarin treatment and to 45 controls. Two out of 45 controls (4.4%) showed abnormal results with the modified test. They also showed loss of factor V exon 10 Mnl I restriction site, associated to APC resistance. All remaining controls, with normal functional results by the modified assay, showed normal restriction profile. We detected 9 affected patients (11.8%), one of them homozygous or double heterozygous. In conclusion, the modified assay is very sensitive for factor V dependent APC resistance, and can successfully be applied to patients on coumarin therapy.
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ISSN:0049-3848
1879-2472
DOI:10.1016/0049-3848(96)00068-0