Related Experiment Videos
Endogenous or exogenous coagulation factor level and the response to activated protein C
Laura C Gennari1, Alicia N Blanco, Maria P Domínguez
1División Hemostasia, Departamento de Hemostasia y Trombosis, Instituto de Investigaciones Hematológicas Mariano R. Castex, Academia Nacional de Medicina, Buenos Aires, Argentina. laugennari@hematologia.anm.edu.ar
Thrombosis Research
|September 7, 2005
Summary
Elevated factor VIII (FVIII) levels correlate with abnormal activated protein C resistance (APCR), suggesting a prothrombotic risk. However, increased factors II (FII) or X (FX) did not directly associate with APCR defects in this study.
Area of Science:
- Hematology
- Thrombosis and Hemostasis
- Clinical Coagulation
Background:
- Abnormal activated protein C resistance (APCR) may explain the prothrombotic role of elevated coagulation factors.
- Investigating the link between specific coagulation factor levels and APCR is crucial for understanding thrombotic risk.
Purpose of the Study:
- To assess the impact of factor VIII (FVIII), factor II (FII), and factor X (FX) levels on APCR.
- To determine the association between these factor levels and the development of an APCR-resistant phenotype.
Main Methods:
- Assessed correlation between APCR and FVIII in 36 samples post-Desmopressin infusion.
- Evaluated correlation between FII/FX and APCR in 15 patients with plasma levels of 100-125 U/dl.
- Measured the effect of adding purified FII and FX to normal plasma on APCR.
Main Results:
- APCR values significantly correlated with FVIII increase (r=0.839, p<0.001).
- Abnormal APCR (<2.4) was observed in 9/36 samples with higher FVIII levels (176.7 U/dl vs 103.5 U/dl).
- APCR did not correlate with endogenous FII or FX, but exogenous FII/FX addition decreased APCR without causing abnormal results.
Conclusions:
- Elevated FVIII levels (>153.0 U/dl) may be associated with an APCR-resistant phenotype.
- Exogenous FII or FX levels above 120 U/dl can influence APCR, but do not necessarily lead to abnormal results.
- Current data do not directly link increased FII or FX to a defect in the protein C system under the studied conditions.