Rivaroxaban dose-dependently caused false high protein C activity in clotting assays (r=0.695, p<0.001), whereas chromogenic assays were unaffected by any tested direct oral anticoagulants.
Observational (n=90)
No
Does the type of direct oral anticoagulant affect the measurement of Protein C activity using clotting versus chromogenic assays in patients with AF or VTE?
In patients taking DOACs, particularly rivaroxaban, Protein C activity should be measured using chromogenic substrate assays rather than clotting assays to avoid false-high results that could mask congenital thrombophilia.
p-value: p=<0.001
Aim In this study, the effect of direct oral anticoagulants (DOACs) on protein C (PC) activity was examined using several measuring reagents. Materials and Methods In total, 90 patients (60 male and ３0 female) with nonvalvular atrial fibrillation or venous thromboembolism (VTE) who were on anticoagulation therapy with DOACs (rivaroxaban, apixaban, or edoxaban) were studied. The plasma levels of PC activity were measured by means of a clotting assay and chromogenic substrate assay, using three reagents for each type of assay. Result Prothrombin time (PT) and activated partial thromboplastin time (APTT) were significantly prolonged in a dose-dependent manner in patients who were taking rivaroxaban or edoxaban. PC activity, as measured by all three reagents using the clotting assay, was influenced only by rivaroxaban, indicating an increase in PC activity in a dose-dependent manner. Apixaban did not have any influence on the measurements made using all three reagents in the clotting assay. On the other hand, none of the three FXa inhibitors had any influence on PC activity when it was measured using the three reagents in the chromogenic substrate assay. Plasma samples were collected before, as well as two and four to eight weeks after rivaroxaban administration in seven patients with AF or VTE sequentially. In all three regents using the clotting assay, plasma levels of PC activity had increased after the administration of rivaroxaban. On the other hand, all three regents using the chromogenic assay had very little influence on PC activity after the administration of rivaroxaban. Conclusion The inhibitory effects of the different types of DOACs on clotting activity interfere with clotting test measurement systems in patients receiving DOAC therapy. When measuring PC activity while the patient is taking rivaroxaban or edoxaban, it is necessary to use the chromogenic substrate assay to avoid false highs. Moreover, collecting specimens when blood levels of drugs are low, e.g. during the trough phase, whenever possible, would be one way to minimize interference.
寺上 et al. (Mon,) conducted a observational in Nonvalvular atrial fibrillation or venous thromboembolism (n=90). Direct oral anticoagulants (rivaroxaban, apixaban, edoxaban) vs. Chromogenic substrate assay vs Clotting assay was evaluated on Protein C activity measured by clotting assay versus chromogenic substrate assay (p=<0.001). Rivaroxaban dose-dependently caused false high protein C activity in clotting assays (r=0.695, p<0.001), whereas chromogenic assays were unaffected by any tested direct oral anticoagulants.
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