activated protein c resistance/arginine

Activated protein C resistance (APCR) describes a hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). This results in an increased risk of venous thrombosis, including deep vein thrombosis and pulmonary embolism. Protein C is a natural anticoagulant that

Activated protein C resistance is an inherited thrombophilia caused by a point mutation in the factor V gene (G to A transition in nucleotide 1691 in the factor V gene with replacement of arginine (R) 506 by glutamine (Q) in the factor V molecule). The mutation is commonly named factor V R506Q or

Inherited resistance to activated protein C (APC) was recently discovered to be a cause of familial thrombophilia and is now known to be the most common genetic risk factor for venous thrombosis. It is caused by a single point mutation in the gene for factor V, which predicts substitution or

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

Activated protein C resistance (APCR) is a coagulation abnormality often linked to FV Leiden mutation, a single nucleotide G1691A substitution resulting in arginine 506→glutamine missense factor V mutation. FV Leiden has a frequency of 20 to 30% in groups of patients with venous thrombosis while it

The anticoagulant protein C system is an important regulator of the blood coagulation process. Its targets are the procoagulant cofactors factor Va and factor VIIIa, which are cleaved and inactivated by activated protein C, protein S and intact factor V working as cofactors. Genetic defects of

An increasing number of reports have focused on activated protein C resistance (APCR) as it has been shown not only to be the most common genetic factor predisposing patients to thromboembolic disease but the most common identifiable cause overall. More than 90 percent of the cases of APCR are

Activated protein C resistance is the most prevalent cause of thrombophilia: it is found in 20% to 30% of patients with a history of deep venous thrombosis history. Activated protein C resistance is due to an arginine 506 to glutamine mutation in factor V. This mutation prevents normal inactivation

The presence of the R506Q mutation of the factor V gene is associated with an increased risk of thromboembolism, particularly during pregnancy. Recently, its involvement in the development of obstetrical complications, such as preeclampsia and fetal losses, has been evoked. The resulting factor

To determine the prevalence of activated protein C resistance and the factor V Leiden mutation (position 1691, arginine 506 to glutamine substitution) in children with thrombosis, plasma samples from children with thrombosis were tested for activated protein C resistance. DNA was analyzed for the

The mechanism of thrombophilia in patients with antiphospholipid antibodies (aPL) is not clearly understood. A number of contributing factors have been described, but more than one may be operative. It was recently found that aPL may cause the acquired activated protein C resistance phenotype,

Venous thromboembolism is often familial, suggesting that genetic risk factors are involved. Until recently, genetic defects known to predispose for thrombosis (deficiencies of antithrombin III, protein C, and protein S) had not been shown to account for more than 5-10% of the cases. Inherited

In 1993, inherited resistance to activated protein C (APC) was described as a novel risk factor for venous thrombosis. APC-resistance is present in 20-60% of venous thrombosis cases. It is caused by a single point mutation in the factor V gene which substitutes arginine (R) at position 506 with a

Although lower extremity deep venous thrombosis (LEDVT) has been associated with a hypercoagulable state, there are scant data available for patients presenting with upper extremity deep venous thrombosis (UEDVT). Therefore, we conducted a prospective study to determine whether such an association

Our laboratory recently found a novel mechanism for thrombophilia, which is characterized by an inherited resistance to activated protein C (APC). The APC-resistance test, which measures the anticoagulant response to APC in an activated partial thromboplasin time (APTT) reaction, was devised and