What is the role of hyperhomocysteinemia in atherosclerotic plaques?
Low serum vitamin B12, or genetic defect in uptake or utilization of B12 proteins, such as an intrinsic factor deficiency, can lead to a condition known as hyperhomocysteinemia, a condition in which there is an over-excess of homocysteine in the blood, indicating a problem in sulfur-amino acid metabolism. Hyperhomocysteinemia increases the risk of stroke as it causes an increased formation of a cyclic reactive form of homocysteine that can react with low-density lipoproteins. Such oxidation can lead to atheroma formation, (macrophagocytic lipid aggregations, secondary to increased LDL uptake by these macrophages), as well as intimal injury, oxidation of cholesterol and unsaturated lipids, platelet aggregation, thrombogenic factors, myointimal hyperplasia, deposition of sulfated GAG’s, fibrosis, and calcification of atherosclerotic plaques. The chronic effects of the buildup of these toxic thiolactone derivatives of sulfur amino acid metabolites can lead to ongoing vascular stenosis, le
