Lipoprotein-Associated Phospholipase A2 Measurements: Mass, Activity, but Little Productivity

[摘要] Given its biology and epidemiology, lipoprotein-associated phospholipase A2 (Lp-PLA2)2 provides both an attractive target for assessing cardiovascular disease (CVD) risk and a target for intervention to reduce CVD. First described just over 2 decades ago, Lp-PLA2, an enzyme found in increased concentrations in unstable or vulnerable plaques, cleaves oxidized phospholipids to the proinflammatory moieties lysophosphatidylcholine and oxidized fatty acids, which in turn act as monocyte chemoattractants and activate macrophages (1). Over the last 10 years, since the development of specific assays to measure Lp-PLA2, first its mass and then its activity, numerous cross-sectional and longitudinal (prospective) epidemiologic studies have reported an association of Lp-PLA2 with CVD events (2–5). These studies, with the Lp-PLA2 measurements usually funded or performed by the commercial manufacturers of the assays, led in 2005 to US Food and Drug Administration clearance of an assay to measure Lp-PLA2 mass (PLAC®; diaDexus) for the purpose of predicting CVD risk (6). More recently, some US consensus groups, such as the National Lipid Association, have recommended measurement of Lp-PLA2 in certain clinical circumstances (7) to assist in identifying patients with risk scores that may not clearly indicate the need for drug therapy, according to current National Cholesterol Education Program Adult Treatment Program guidelines (8).Two fundamental questions remain, however: ( a) Is Lp-PLA2 truly an independent marker or risk factor for CVD; and ( b ) if Lp-PLA2 is indeed independent, does it add value in the risk assessment and alter treatment decisions? The study by Ridker et al. in this issue of Clinical Chemistry (9) provides additional insight and a timely opportunity to review the role of Lp-PLA2 measurements in clinical practice.The majority, but not all, of the published studies have shown a …

[学科分类] 过敏症与临床免疫学