Venous thrombosis has a ‘multiple hit’ pathogenesis in which several adverse influences affecting the composition of the blood, the structure and function of the vessel wall, and blood flow together result in an acute thrombotic event.1 This is exemplified by the long recognised clinical factors which predispose to thrombosis in the deep veins of the limbs. For example, the coagulation activation associated with surgical trauma combines with stasis of venous flow due to postoperative immobility to result in a high risk of venous thromboembolism (VTE) after major surgical procedures.

Other clinical risk factors for VTE include obesity, pregnancy, and use of the combined oral contraceptive or hormone replacement preparations. A range of diseases also predispose to VTE, especially malignancy, including myeloproliferative disorders, and less common conditions such as paroxysmal nocturnal haemoglobinuria and Behçet’s disease. Among the biochemical and haemostatic variables which have been associated with VTE there has been considerable recent interest in hyperhomocysteinaemia, especially as this is partly determined by diet and it also predisposes to arterial occlusive events. Other notable associations with VTE are a raised plasma concentration of coagulation factor VIII and the antiphospholipid syndromes, where laboratory evidence of …