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Lipoprotein-associated phospholipase A2 clinical application

Lipoprotein-associated phospholipase A2 clinical application

Physiological and biochemical characteristics
Lipoprotein-associated phospholipase A2 (Lp-PLA2), a platelet-activating factor acetylhydrolase, is a type of phospholipase that is closely related to arteriosclerosis and ischemic cardiovascular and cerebrovascular diseases in recent years. A2 superfamily, a new inflammatory marker and an independent risk factor. Which has the role of proinflammatory, so the production and release of Lp-PLA2 from inflammatory cells can also be interpreted as an excellent pre-inflammatory response indicators.
Lp-PLA2 is encoded by PLA2G7 and contains 441 amino acids with a molecular weight of 45 kDa. In blood, Lp-PLA2 is mainly transported along with LDL, and less than 20% of Lp-PLA2 is associated with HDL. Lp-PLA2 mainly inflammatory cells, such as macrophage secretion, can be hydrolyzed LDL oxidized phospholipids.
Lp-PLA2 produces oxidative molecules in the vessel wall, which are more prone to cause atherosclerosis and produce unstable plaques. Elevated levels of Lp-PLA2 are a significant risk of plaque formation and rupture, and are independent of other lipids and CRP levels. By detecting the level of Lp-PLA2 in the circulatory system, it is possible to independently predict the pathogenesis of cardiovascular and cerebrovascular diseases. Human plasma Lp-PLA2 relative molecular mass of 50000, mainly by mature macrophages and lymphocytes synthesis and secretion, and by the regulation of inflammatory mediators, human circulation of Lp-PLA in lipoprotein particles with the form of binding, in which 2/3 and LDL binding, 1/3 and HDL, VLDL binding u. There was a positive correlation between plasma Ip-PLA2 activity and Lp-PLA2 concentration. Lp-PLA can hydrolyze platelet activating factor (PAF) to make it inactive, it is also known as platelet-activating factor acetylhydrolase (PAF-AH). But the enzyme substrate specificity is not strong, in addition to hydrolysis of PAF, but also hydrolysis of LDL on the oxidation of lecithin to produce lysolecithin and oxidized free fatty acids, the latter two are pro-inflammatory mediators, by stimulating adhesion factors and cytokines Generation, and promote monocytes from the lumen to the inner membrane aggregation, derived from macrophages, macrophages engulfed oxidized LDL into foam cells, foam cells gathered into atherosclerotic plaques, plaques in the cytokines and proteases The role of ulcers or rupture, thrombosis and cardiovascular events. Therefore, theoretically Lp-PLA. With the promotion of atherosclerosis and the occurrence of cardiovascular events.

Clinical application
1, Lp-PLA2 and coronary heart disease
Lp-PLA2 was found to be strongly expressed in the necrotic core and surrounding macrophages of vulnerable plaques and ruptured plaques, and was relatively difficult to detect in stable plaques, suggesting that Lp-PLA2 potentially promotes plaques Instability. The direct consequence of plaque instability is an increased risk of cardiovascular disease. Plasma Lp-PLA2 activity in patients with coronary heart disease was significantly higher than non-coronary heart disease patients, but in patients with stable angina and acute coronary syndrome no significant difference. This shows that plasma Lp-PLA2 activity can reflect the severity of coronary atherosclerotic lesions, and coronary artery disease stability has nothing to do.
With the change of coronary blood flow and the response of coronary artery diameter to intracoronary acetylcholic acid as the evaluation criteria of endothelial function, it was found that with the concentration of plasma Lp-PLA2, the coronary blood flow was significantly decreased and epicardial coronary artery Acetylcholic acid reactive contraction significantly enhanced. Therefore, Lp-PLA2 is also an independent predictor of coronary artery endothelial dysfunction.
2, Lp-PLA2 and atherosclerosis
Recent studies have shown that atherosclerosis (As) is an inflammatory disease that is involved in the development of atherosclerotic plaque formation, as well as loss of stability and atherosclerotic plaques Rupture shedding plays an important role. Inflammatory response is one of the important mechanisms of As formation. At the early stage of atherosclerosis, Lp-PLA2 is produced in the coronary circulation, and the subsequent lyso-lecithin is associated with coronary endothelial dysfunction. Therefore, plasma Lp-PLA2 can be used as a marker of atherosclerotic risk. In addition, Lp-PLA2 levels in different regions and populations are consistent with cardiovascular and cerebrovascular risk, which makes the potential role of Lp-PLA2 in the clinical cardiovascular and cerebrovascular events as eye-catching as possible therapeutic targets.
3, Lp-PLA2 and ischemic stroke
Recently, several large epidemiological and clinical prospective studies have found that plasma Lp-PLA2 concentration or activity of ischemic stroke is an independent risk factor. Elevated plasma Lp-PLA2 patients, coronary heart disease events and the risk of ischemic stroke increased significantly. In addition, Lp-PLA2 can be a good predictor of stroke recurrence risk.

Principles of clinical application
Normal reference value: 8-150 ng / ml
> 150 ng / ml suggest increased atherosclerotic plaque instability, increased risk of cardiovascular and cerebrovascular diseases.

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