Featured Reagent – sPLA₂-IIA
sPLA2-llA production of fatty acids and biologically active phospholipids plays an important role in platelet, monocyte, and endothelial activation, processes known to be critical steps in atherogenesis.1 Unlike traditional cardiac biomarkers used to predict adverse outcomes in patients with acute coronary syndrome (ACS), sPLA2-llA has been shown to act at multiple pathways involved in atherogenesis, from lipid oxidation to modulation of vascular & inflammatory cell activation and apoptosis.2
The Randox sPLA2 -IIA Assay – For Research Use Only
A niche assay from Randox meaning that Randox is one of the only manufacturers to offer an sPLA2-llA mass assay in an automated biochemistry format
Applications available detailing instrument-specific settings for the convenient use of the Randox sPLA2-IIA assay on a wide range of clinical chemistry analysers
Complementary controls and calibrators available offering a complete testing package
Automated assay which removes the inconvenience and time consumption associated with traditional ELISA based testing
Excellent correlation coefficient of r = 0.95 when compared against other commercially available methods
Liquid ready-to-use format for convenience and ease of use
Latex enhanced immunoturbidimetric method delivers high performance and confidence in results
Key observations through research has found that sPLA2-llA mediated modification of lipoproteins plays a role in the development of atherosclerosis. The surface of both low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) is surrounded by phosphatidylcholine (PC) a type of phospholipid which has been scientifically proven to serve as a good extracellular target for several isoforms of sPLA2-llA. sPLA2-llA works by hydrolysing these phospholipids resulting in the production of free fatty acids and lysophophatidylcholine (LPC) which can generate pro-inflammatory actions, accelerating atherosclerosis.1
Hydrolysis of LDL-C correlates with the production of the more atherogenic, small dense LDL cholesterol (sdLDL-C). The sPLA2-llA -processed low-density lipoprotein (LDL) contains a large amount of lysophospholipids and exhibit the property of “small-dense” or “modified” LDL, which facilitates foam cell formation from macrophages. Research has shown that high plasma levels of sdLDL-C compared to less dense, larger LDL-C create a higher risk of coronary heart disease.
Regular cardiovascular screening is important to ensure that cardiac risk factors are detected at the earliest possible stages. Cardiovascular disease (CVD) encompasses a number of diseases of the heart and blood vessels. Four of the main types of CVD include: coronary heart disease (CHD), cerebrovascular disease (CVA), peripheral arterial disease (PAD) and aortic disease. It is vital that at risk patients are diagnosed as quickly and efficiently as possible to ensure effective treatment plan implementation.4
The early diagnosis of CVD aids in reducing the risk of a secondary cardiovascular event and to ensure the patient receives appropriate treatment to prevent premature deaths. Early risk assessment is particularly important in people who are at a greater risk of CVD. This is evaluated through the identification of one or more risk factors including: hypertension, diabetes or hyperlipidaemia. 3 ,5
It is believed that by 2030, almost 23.6 million people will die from CVD, mainly CHD and CVA, and is projected to remain the single leading cause of death. This provides further confirmation that early diagnosis is vital to prevent and reduce the number of deaths attributed to CVD.3
High Performance & Unique Tests Brochure
Featured Reagent Home
Visit the Featured Reagent Home to see past featured reagents
 Secreted phospholipase A2, lipoprotein hydrolysis, and atherosclerosis: integration with lipidomics. Kei, Yamamoto, et al. 7, s.l. : Analytical and Bioanalytical Chemistry, 2011, Vol. 400.
 Circulatory secretory phospholipase A2 activity predicts recurrent events in patients with severe acute coronary syndromes. . Mallat, Ziad, Steg, Gabriel and Benessiano, Joelle. 7, s.l. : Journal of the American College of Cardiology, 2005, Vol. 46.
 World Health Organization. Cardiovascular Diseases. World Health Organization. [Online] World Health Organization, May 17, 2017. [Cited: August 21, 2018.] https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds).
 National Health Service (NHS). Cardiovascular disease. [Online] September 17, 2018. [Cited: November 30, 2018.] https://www.nhs.uk/conditions/cardiovascular-disease/.
 National Institute for Health and Care Excellence (NICE). Cardiovascular disease risk assessment and prevention. [Online] no date. [Cited: ovember 30, 2018.] https://bnf.nice.org.uk/treatment-summary/cardiovascular-disease-risk-assessment-and-prevention.html.