Anticoagulants and Hypercoagulability

Abstract

Anticoagulants are chemical substances that prevent coagulation or prolong the clotting time by suppressing the functions or synthesis of coagulation factors in the blood. Anticoagulation mechanisms are essential in controlling the formation of a blood clot at the site of injury. The abnormalities in the coagulation and fibrinolytic mechanisms could lead to a hypercoagulability state. Inherited hypercoagulable state due, including Factor V Leiden (FVL), prothrombin gene mutation, defective natural proteins that inhibit coagulation, including antithrombin III (ATIII), protein C and S, high levels of FVII, FIX and FXI, are well-documented. Abnormalities of the fibrinolytic system, including tissue-type plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA), and elevated levels of plasminogen activator inhibitor-1 (PAI-1) have been linked to hypercoagulation. Acquired conditions, including certain cancers and their medications, trauma or surgery, pregnancy, obesity and hyperlipidaemia, have been implicated with hypercoagulable events. The clinical symptoms of hypercoagulability can be devastating and may even have lethal outcomes. This activity reviews the principles of anticoagulation, haemostasis, deficiencies associated with hypercoagulability (both coagulation and fibrinolytic disorders), mechanisms of action of some natural-based products with anticoagulant potentials and highlights new clinical and traditional therapeutic strategies to be taken in improving healthcare for patients demanding anticoagulation.