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July 28, 2004

New Service Announcement
 

 

LIPOPROTEIN (a)

 

   ITxM Diagnostics is pleased to offer a quantitative assay for lipoprotein(a) (Lp(a)) for the assessment of risk for coronary heart disease (CHD) in specific populations.

   BACKGROUND

   Lipoprotein (a) is a cholesterol-rich lipoprotein, similar to low-density lipoprotein (LDL) and found in human plasma. This “sticky” molecule is made up of an apo B and apo(a) that binds to fibrin, LDL receptors, and plasminogen binding sites.   Lp(a) inhibits fibrinolysis by competition with plasminogen for fibrin.  Additionally, Lp(a) can bind to the endothelium and arterial wall resulting in localized cholesterol accumulation forming atherosclerotic plaques promoting clogging of arteries.

  

   Lp(a) levels are genetically determined and the normal range of Lp(a) in humans varies by ethnic population.  The normal range is the same in Caucasian and Asian populations.  However people of African descent have demonstrated normal ranges that are twice higher than Caucasian populations while Native American and Mexican populations have normal ranges that are half of the Caucasian population.

 

   Lp(a) has been referred to as a predictor of premature atherosclerotic vascular disease.  Excess Lp(a) concentrations have been associated with an increased risk of coronary artery disease (CAD), and premature CAD in Caucasian males.  The variability of Lp(a) levels by ethnic population requires careful interpretation of results based on a knowledge of the patient and other cardiac risk factors which may be present.

   METHODS

Lp(a) testing uses an Enzyme Linked Immunosorbant Assay (ELISA) format.  The test utilizes antibodies that bind to the apo(a) moiety of Lp(a) to capture the protein from the sample.  The concentration of Lp(a) mass (mg/dL) is quantitatively determined by comparison of the absorbance of the sample with a standard curve prepared with known concentrations of  Lp(a).

 

   CLINICAL APPLICATION

The association of elevated levels of Lp(a) with risk of myocardial infarction(MI) has been  documented and has substantiated Lp(a) to be an independent risk factor for MI (1,2).  Almost all cross sectional and retrospective studies on Caucasian men have shown an increased risk of coronary disease and stroke or peripheral and cerebrovascular atherosclerotic disease associated with plasma Lp(a) values greater than the 80th percentile (>300 mg/L)(3).  An elevated Lp(a) coupled with a low HDL puts a patient at 8.3 times the relative risk for CHD (4).  Clinical studies have shown elevated levels of Lp(a) to be associated with stenosis and restenosis after percutaneous transluminal coronary angioplasty (5,6).  Familial studies of patients with premature CHD suggest that Lp(a) may be an important initiator and promoter of, as well as an early marker for, the atherosclerotic process (7,8).  Therefore it is recommended the Lp(a) assay be used in the following clinical situations:

  • Patients with premature CHD

  • Patients with peripheral and/or cerebrovascular atherosclerotic disease

  • Risk assessment of patients with abnormal lipid studies

   HOW TO ORDER

In order to assure the accuracy of our test results, plasma should be collected from one (1) blue top tube.  This sample must be spun within one hour of collection, performing centrifugation for 15 minutes at 3000 RPM, at a temperature that never exceeds 18oC.  The sample is then frozen at -20oC or less and shipped on dry ice.  It is important that the plasma be free of platelet contaminants.

The fee for the lipoprotein (a) assay is $150.00.

TEST CODE:  5653                            CPT CODE:  82172
 

For further information call:   412-209-7270  or  1-800 967-9672

 

   REFERENCES

  1. Kark JD, Sandholzer C, et al.  Atherosclerosis 98: 1993: 139-151.

  2. Hobbs HH, White AL.  Curr Opin Lipidol 10: 1999: 225-236.

  3. Kostner G, Avogaro P, et al.  Atherosclerosis (Netherlands) 38: 1981: 51-61.

  4. von Eckardstein et al.  J Am Coll Cardiol 37: 2001: 434-439.

  5. Solymoss BC, Marcil M, et al.  Can J Cardiol 9: 1993: 30-84.

  6. Tenda K, Saikawa T, et al.  Jpn Circ J 57: 1993, 789-795.

  7. Bostom AG, Cupples AL, et al.  JAMA 1996: 276/7: 544-548.

  8. Wald NJ, Law M, et al.  Lancet 1994: 343: 75-79

 

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