deamino-arginine-vasopressin and Activated-Protein-C-Resistance

The abnormal response to activated protein C could be the mechanism to explain the prothrombotic role of elevated coagulation factor levels.. 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.. 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.. 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.. 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.

Topics: Activated Protein C Resistance; Deamino Arginine Vasopressin; Factor VIII; Factor X; Hemostatics; Humans; Protein C; Prothrombin

Topics: 3' Untranslated Regions; Activated Protein C Resistance; Aged; Anticoagulants; Arthroplasty, Replacement, Hip; Contraindications; Coronary Disease; Deamino Arginine Vasopressin; Factor V; Factor VIII; Female; Genetic Predisposition to Disease; Genotype; Heparin; Humans; Hypertension; Postoperative Complications; Prothrombin; Pulmonary Embolism; Thrombophilia; von Willebrand Diseases; von Willebrand Factor

Several methods are now available for the laboratory assessment of activated protein C resistance (APCR). In this study, we evaluated two activated partial thromboplastin time-based assays [Coatest activated protein C (APC) and Diagen protein C activator (PCA)], with and without predilution of test plasma in factor V-deficient plasma (FVdp) and an amidolytic assay (Immuno Ltd, Vienna, Austria). Testing plasmas from normal volunteers who had received 1-deamino-8-D-arginine vasopressin (DDAVP) also assessed the effect of elevated factor VIII on APCR. In the unmodified clotting tests, the Coatest kit gave overlapping results for normal and heterozygous FV:Q506 samples; some FV:Q506 samples on oral anticoagulant therapy (OAT) were misclassified as normal, and some normal samples with high factor VIII levels would be classified as APC resistant. The unmodified Diagen kit correctly classified these three types of sample, but had the disadvantage that prolonged PCA clotting times gave serious problems with instrument end-point detection. Both kits modified by diluting the samples in FVdp correctly classified all the samples, as well as samples from patients with lupus anticoagulant (LA) and patients receiving heparin. The Immunochrom kit correctly classified the normal and FV:Q506 samples, but would have misclassified most normal persons on OAT as well as some patients with LA or receiving heparin therapy as APC resistant.

Topics: Activated Protein C Resistance; Administration, Oral; Anticoagulants; Blood Coagulation Tests; Chromogenic Compounds; Deamino Arginine Vasopressin; Endpoint Determination; Factor V; Factor V Deficiency; Factor VIII; False Negative Reactions; Genotype; Heparin; Humans; Lupus Coagulation Inhibitor; Partial Thromboplastin Time; Protein C; Protein S; Reagent Kits, Diagnostic; Reference Values; Sensitivity and Specificity