Hs-crp Information and Courses from MediaLab, Inc.

The traditional CRP test has a typical reference range of < 8 mg/dL. The hs-CRP test, with its increased sensitivity has a reference or optimal range of < 3 mg/dL. As with most risk markers, the results of hs-CRP testing are generally interpreted on a relative scale; the higher the value, the higher the risk of a future cardiovascular event.The American Heart Association and Centers for Disease Control and Prevention has defined risk groups with hs-CRP as follows: Low risk: < 1.0 mg/L Average risk: 1.0 to 3.0 mg/L High risk: > 3.0 mg/L It is important to note that hs-CRP assays are measuring the same protein as traditional CRP assays. Thus, in patients with active inflammation (such as chronic, active arthritis; lupus; infection; etc.) hs-CRP values would be expected to be high and would not necessarily implicate cardiovascular risk. If values greater than 10 mg/L are seen in repeated measurements, a non-cardiovascular cause should be considered. Taking anti-inflammatory drugs (NSAIDs, aspirin, etc.) or the statin-class of cholesterol-lowering drugs may reduce CRP levels in patients. This is not an artifact, but is thought to be an effect of treating the underlying inflammatory process.

LpPLA2 refers to lipoprotein-associated phospholipase A2. This enzyme is also known as platelet-activating factor acetylhydrolase(PAF). The LpPLA2 enzyme is a lipase found predominantly on the surface of LDL particles. Note that LpPLA2 is a lipase enzyme and not an apolipoprotein. LpPLA2 is made by inflammatory cells (T cells, mast cells, macrophages) and then integrated onto the surface of lipoprotein particles. The enzymatic function of LpPLA2 is to hydrolyze oxidized phospholipids in LDL.LpPLA2 plays a corrective role in removing oxidized phospholipids. Thus, it might seem that having high levels of LpPLA2 would be good. However, although LpPLA2 has a positive role in removing oxidized lipids, it also generates inflammatory products in the process. So in fact, high levels of LpPLA2 are associated with increased cardiovascular risk. Researchers have identified high amounts of LpPLA2 in human atherosclerotic lesions. The LpPLA2 that accumulates in the vessel wall can come from LDL (which can carry LpPLA2 on its surface) or it can come from immune cells that have invaded the vessel wall. Since Lp-PLA2 is produced or localized in the plaque itself, it may be a more specific marker of cardiovascular function compared to systemic, more general inflammatory markers like hs-CRP.