Hyperhomocysteinemia and thrombosis.
Homocysteine remains an enigmatic marker for vascular disease. Studies have shown hyperhomocysteinemia is a risk factor for VTE, cerebrovascular disease, and coronary artery disease. This relationship, however, has not been consistently corroborated by studies of patients with genetic polymorphisms that alter homocysteine metabolism. Studies at the molecular level reveal interactions between homocysteine, the endothelium, and the clotting system. Further investigation at the basic science level is needed to determine whether homocysteine is a marker of vascular injury and thrombotic potential or whether it plays a pathogenic role. Preliminary trials with vitamins clearly show that safe, inexpensive treatment can lower homocysteine levels. The clinical impact on decreasing vascular disease, however, has yet to be shown. Until there is evidence that treatment improves outcomes, testing for homocysteine and treating hyperhomocysteinemia will be a debatable issue. A series of vitamin intervention trials begun in 1997 will enroll tens of thousands of patients (Table 1) and will, it is hoped, provide the necessary information for developing evidence-based guidelines.
Lee
Ray
R
Department of Internal Medicine, Division of General Internal Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, TX 75235-8889, USA. ray.lee@utsouthwestern.edu
Frenkel
Eugene P
EP
D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D020138:Hyperhomocysteinemia / Q000378:metabolism / Q000503:physiopathology*; D013927:Thrombosis / Q000378:metabolism / Q000503:physiopathology*
D006710:Homocysteine