Lipoprotein(a) Assay
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.
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
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)?
- 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.
Guidelines on Lp(a)
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: LDLaccumulates in intima and causes atherosclerosis |
Mechanism similar to that for LDL cholesteroland/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 (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-assayprecision |
21.0 |
1.63 |
20 |
| 51.5 |
1.53 |
20 |
| 83.05 |
2.40 |
20 |
| Inter-assayprecision |
24.19 |
3.11 |
20 |
| 32.58 |
3.52 |
20 |
| 50.48 |
2.83 |
20 |
Instrument applications available for Randox Lp(a)
- 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
- 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
