Mechanisms of thrombogenesis and accelerated atherogenesis in homocysteinaemia.

摘要: Thrombogenesis and accelerated atherogenesis occur in the homocystinurias, both those due to recessively inherited cystathionine β-synthase deficiency disorders of remethylation homocysteine methionine. The evidence strongly implicates high levels plasma as mediator. Homocysteine damages cultured human venous arterial endothelial cells enhances detachment from their substrate, changes not found with comparable concentrations other amino acids tested. is oxidized vitro homocystine an oxygen-dependent reaction producing hydrogen peroxide. Since effects cell cultures can be prevented by catalase, hydrogen-peroxide-induced injury may mechanism responsible. Five different laboratories have documented association between mild homocysteinaemia premature vascular disease. majority affected patients are heterozygotes for whose enhanced susceptibility homocysteine. Mild also occurs chronic renal failure which disease prominent. Mechanisms linking possible yet understood, but could involve prostaglandins low-density lipoprotein, possibly free radicals.