Abstract

Background The abnormal response to activated protein C could be the mechanism to explain the prothrombotic role of elevated coagulation factor levels. Objective We evaluated the effect of factor VIII, II, or X (FVIII, FII, or FX) levels on activated protein C resistance technique and its association with the resistant phenotype. Materials and methods The correlation between APCR and FVIII was assessed in 36 samples, after Desmopressin infusion and the correlation between FII or FX and APCR in 15 patients with plasma levels between 100–125 U/dl. Also, the effect of the addition of purified human factors (FII, FX) to a normal plasma pool (final concentration: 100, 120, 140, 180, 220 U/dl) was estimated on the APCR technique. Results APCR values correlated with FVIII increase ( r Spearman = 0.839; p < 0.001); APCR was abnormal (< 2.4) in 9 / 36 samples, showing higher FVIII values in the abnormal group (VIII abnormalAPCR = 176.7 ± 14.2; VIII normalAPCR = 103.5 ± 8.0). APCR did not correlate with endogenous FII ( r Spearman = 0.423) or FX ( r Spearman = − 0.169). However, the addition of human FII or FX to the normal plasma pool caused a decrease in APCR ( r SpearmanFII = − 0.843; r SpearmanFX = − 0.958) without reaching abnormal (< 2.4) results. FVIII levels may be associated with a resistant phenotype at values > 153.0 U/dl, according to the linear regression analysis. Exogenous FII or FX levels greater than 120 U/dl would affect the APCR, without obtaining abnormal results. Conclusions The data do not allow the direct association of the FII or FX increase with a defect in the protein C system in the current conditions.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.