Lipoprotein (a) Test - Lipid Reagents

Lipoprotein(a) Assay

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What is Lipoprotein(a)? Guidelines on Lp(a) Randox Lp(a) assay details Instrument applications References
Lipoprotein(a) Assay

Features of Randox Lipoprotein(a) Assay

Independent marker correlating with increased risk of atherosclerotic disorders
Only method not affected by Apo(a) size related bias
Liquid ready-to-use IT assay
Excellent stability (open vial stability 30 days on board)
No sample preparation required
Fully automated applications available for a wide range of analysers

Our highly successful Lipoprotein (a) test is the only method in the world to accurately and reliably measure Lp(a), it is not affected by Apo (a) size related bias like most other methods.

Elevated Lp(a) concentration in plasma is an independent genetic marker correlating with increased risk of atherosclerotic disorders including myocardial and cerebral infarction. Levels are also elevated in nephritic syndrome, patients undergoing renal dialysis, patients with uncontrolled diabetes mellitus and hypothyroidism.

In June 2010, the European Atherosclerosis Society (EAS) published a consensus paper on Lp(a), recommending its widespread use as a screening tool in those at intermediate or high risk of cardiovascular disease. Click here to view the paper. Click here to view the paper.

What is Lipoprotein(a) : Lp(a)? to the top

Lp(a) is a major independent genetic risk factor for cardiovascular disease².
Lp(a) particles are similar to LDL consisting of a cholesterol-rich core, with an apoB-100 protein attached³.
However, Lp(a) uniquely differs to LDL in that it also has an apo(a) protein attached via a disulfide bond.
The apo(a) is comprised of a series of kringle structures.
There are 10 types of kringle IV and only one copy of each type except for type 2. Kringle IV, type 2 (KIV₂) is particularly susceptible to being manufactured repeatedly, depending on an individual's genetics (2-40 repeats).
The number of KIV₂ repeats generates different isoforms and a major affect on the size of the apo(a) protein which affects the level of Lp(a).
Apo(a) is synthesised in liver and binds to newly synthesised apoB-100.
The size of the apo(a) protein is genetically determined and varies widely1 hence, levels of Lp(a) can vary up to 1000-fold between individuals1.
Plasma levels rise shortly after birth up to a consistent level within several months, typical plasma levels of Lp(a) are similar in men and women: one in five (20%) have levels above 50 mg/dL.

The evidence clearly supports Lp(a) as a priority for reducing cardiovascular risk, beyond that associated with LDL cholesterol. Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease - EAS Consensus Panel⁵

Guidelines on Lp(a)⁴ to the top

Recent years have seen major scientific advances in the understanding of Lp(a) and its causal role in premature CVD.

Elevated Lp(a) levels associate robustly and specifically with increased CVD risk. This association is continuous in shape and does not depend on high levels of LDL or non-HDL cholesterol, nor the presence of other CVD risk factors. Lp(a) levels, like elevated LDL, is causally related to premature development of atherosclerosis and CVD.

Table I Comparison of evidence supporting the contention that elevated LDL cholesterol and elevated Lp(a) each cause cardiovascular disease4
Assay details	Elevated LDL cholesterol	Elevated Lp(a)
Human epidemiology	Direct association in numerous studies	Direct association in numerous studies
Human genetic studies	Direct association in numerous studies, e.g. familial hypercholesterolaemia	Direct association in numerous studies, e.g. for kringle IV type 2 polymorphism
Mechanistic studies	Mechanism clearly demonstrated: LDL accumulates in intima and causes atherosclerosis	Mechanism similar to that for LDL cholesterol and/or prothrombotic/anti-fibrinolync effects
Animal models	Proatherogenic effect in numerous studies	Proatherogenic effect in numerous studies
Human intervention trials	Statin trials gave final proof of causality	Niacin trials are favourable

Randox Lp(a) assay details to the top

High Performance Reagents

Assay Range: - 2.1-90 mg/dl.
Sensitivity: - 2.1 mg/dl.
Precision: - The following coefficients of variation were obtained on a HitachiT 717 analyser.

	Lipoprotein (a) Mean (mg/dl)	Mean % CV	n
Intra-assay precision	21.0	1.63	20
	51.5	1.53	20
	83.05	2.40	20
Inter-assay precision	24.19	3.11	20
	32.58	3.52	20
	50.48	2.83	20

Product Description	Size	Cat. No.
Lp(a) Kit	1x10 ml, 1x6 ml	LP3403	buy online
Lp(a) Kit	1x30 ml, 1x15ml	LP2757	buy online
Lp(a) Kit for Dimension®	4x40 T	LP2878	buy online
Lp(a) Calibrator	5x1 ml	LP3404	buy online
Lp(a) Control (Level 3)	3x1 ml	LP3406	buy online
Lipid Control (Level 1)	5x3 ml	LE2661	buy online
Lipid Control (Level 1)	5x1 ml	LE2668	buy online
Lipid Control (Level 2)	5x3 ml	LE2662	buy online
Lipid Control (Level 2)	5x1 ml	LE2669	buy online
Lipid Control (Level 3)	5x3 ml	LE2663	buy online
Lipid Control (Level 3)	5x1 ml	LE2670	buy online

Instrument applications available for Randox Lp(a) to the top

Abbott Aeroset/Architect
ABX Pentra 400
BS 120/200/300/400
BT 2000/BT3000/ILAB 300/Targa
CL 7200, ILab 1800, ILab 900
Express 550
Humalyzer 850, Humalyzer 900S
ILAB 600
ILAB 900/ILAB1800/Shimadzu CL 7200
Kone Progress, Kone Specific
Konelab 20i/30i/60i
Lisa 200-500/Mascott Plus/Clinline
Manual
Menarini Alcyon 300/Alcyon Falcor
Olympus AU400/AU600/AU2700
Olympus AU560
Olympus AU800/AU1000
Ortho Vitros Fusion

Prestige 24i/Saphire
RA 1000, RA Opera, RA XT
Randox RX daytona, RX imola
Roche Cobas 4000
Roche Cobas 6000 (c501)
Roche Cobas FARA
Roche Cobas Integra 400
Roche Hitachi 704
Roche Hitachi 717
Roche Hitachi 747/Modular P
Roche Hitachi 902
Roche Hitachi 904/911/912
Roche Hitachi 917/P Module
Siemens Dimension
Synchron CX 4/5/7/9/LX20
Unicel 600/800
Technicron RA1000/RAXT/Opera
Vitalab Flexor/Selectra E/Selectra II

References to the top

Kamstrup PR, Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG. Genetically elevated lipoprotein(a) and increased risk of myocardial infarction. JAMA 2009;301:2331-2339.
Erqou S, Kaptoge S, Perry PL, Di AE, Thompson A, White IR, Marcovina SM, Collins R, Thompson SG, Danesh J. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA 2009;302:412-423.
Utermann G. Lipoprotein(a). In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic and Molecular Bases of Inherited Disease. 8th ed. New York: McGraw-Hill; 2001. p. 2753-2787
Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, Ginsberg H, Amarenco P, Catapano A, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjarg-Hansen A; European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010; 31(23):2844-53.
http://www.eas-society.org/consensus-position-paper-initiative.aspx
Chapman MJ, Redfern JS, McGovern ME, and Giral P. Niacin and fibrates in atherogenic dyslipidemia: Pharmacotherapy to reduce cardiovascular risk. Pharmacol Ther 2010; 126:314-315
Marcovina SM, Albers JJ, Scanu AM, Kennedy H, Giaculli F, Berg K, Couderc R, Dati F, Rifai N, Sakurabayashi I, Tate JR, Steinmetz A. Use of a reference material proposed by the International Federation of Clinical Chemistry and Laboratory Medicine to evaluate analytical methods for the determination of plasma lipoprotein(a). Clin Chem. 2000; 46(12):1956-67.
Thompson G.R. Recommendations for the use of LDL apheresis. Atherosclerosis 2008; 198:247-255