Blood 2000, 95(5): 1517-1532
Lane,David A.; Grant,Peter J.
Since this article does not contain an abstract, we provide you with the first paragraph.
The development of thrombotic disorders in humans is one of the most common causes of morbidity and mortality in the Western world. Thrombotic disease can be classified in broad terms as that which occurs in the venous system of low flow and pressure or in the high-flow and pressure arterial system. Certain basic distinctions can be drawn between arterial and venous thrombosis, such as the composition of the thrombi (platelet rich in arterial and fibrin rich in venous) and the presence of vascular wall damage (atheroma) in arterial thrombosis. However, the distinctions are not absolute, and there are common underlying mechanisms. Perturbation of hemostasis is central to the pathogenesis of all thrombosis, even though it differs in nature depending on location. Transient or long-lasting environmental influences may play important roles in perturbing hemostasis and influencing risk for thrombosis in both the venous and the arterial systems. The term environmental is used in its broadest sense to embrace changes induced by diverse influences such as childbirth, hormone ingestion, surgery, diet, and smoking, by intercurrent disorders such as diabetes mellitus, hypertension and dyslipidemia, and hyperhomocystinemia, and by local changes to the vascular wall. Perturbation of hemostasis may also be in part genetically determined, and, when this is the case, its influence is potentially profound because of its life-long presence. Because of the late onset of the majority of thromboses, it is unlikely that genetic changes could be their sole determinant, and this points to the importance of gene–environment interactions in disease.