In 107 asymptomatic and untreated patients with inherited syndromes associated with thrombophilia (antithrombin III, protein C and protein S deficiencies), we compared in parallel two plasma peptides which reflect activation of the common coagulation pathway: the prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA).
In 107 asymptomatic and untreated patients with inherited syndromes associated with thrombophilia (antithrombin III, protein C and protein S deficiencies), we compared in parallel two plasma peptides which reflect activation of the common coagulation pathway: the prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA).
At present, different congenital defects in several proteins--antithrombin III (AT III), protein C (PC), protein S (PS), and plasminogen (PLG)--are known to be causes of hereditary predisposition to thrombosis (thrombophilia).
At present, different congenital defects in several proteins--antithrombin III (AT III), protein C (PC), protein S (PS), and plasminogen (PLG)--are known to be causes of hereditary predisposition to thrombosis (thrombophilia).
At present, different congenital defects in several proteins--antithrombin III (AT III), protein C (PC), protein S (PS), and plasminogen (PLG)--are known to be causes of hereditary predisposition to thrombosis (thrombophilia).
The tests included in the second step of the screening are aimed at detecting the less common or less well established causes of inherited thrombophilia (low heparin cofactor II, defective release of tissue plasminogen activator, and high plasminogen activator inhibitor).
These studies suggest that protein C is important not only in the congenital deficiencies, but also in acquired deficiencies, such as during DIC or possibly the postsurgical hypercoagulable state.
The clinical history of 238 patients with inherited thrombophilia (AT III = 94, PC = 103, PS = 41) was analyzed retrospectively at diagnosis and in the follow-up period after diagnosis.
The clinical history of 238 patients with inherited thrombophilia (AT III = 94, PC = 103, PS = 41) was analyzed retrospectively at diagnosis and in the follow-up period after diagnosis.
The clinical history of 238 patients with inherited thrombophilia (AT III = 94, PC = 103, PS = 41) was analyzed retrospectively at diagnosis and in the follow-up period after diagnosis.
Resistance to activated protein C (APC) is a major cause of familial thrombophilia, and can be corrected by an anticoagulant activity expressed by purified factor V. We investigated linkage between APC resistance and the factor V gene in a large kindred with familial thrombophilia.
A poor anticoagulant response to activated protein C (APC) in an activated partial thromboplastin time (aPTT) assay (APC resistance) was recently reported to be a cause of familial thrombophilia.
After activation, mutated factor V, FV:Q506, is less efficiently degraded by APC than normal factor V, which results in increased thrombin generation and a hypercoagulable state.