Test Name
Lipoprotein (a) (LPA)
CPT Codes
83695
Clinical Information
Evaluation of coronary artery disease risk associated with elevations of the atherogenic lipoprotein (a).
Methodology
Nephelometry (NEPH)
Turnaround Time
1 – 2 days
Specimen Requirements
Type:
Serum
Volume:
1 mL
Minimum Volume:
0.5 mL
Specimen Container:
Gold BD Hemogard™ Serum Separation Tubes (SST)™
Transport Temperature:
Refrigerated
Allow specimen to clot completely at room temperature. Separate serum from cells within 2 hours of collection.
Stability
Ambient:
8 hours after separation from cells
Refrigerated:
14 days after separation from cells
Frozen:
30 months after separation from cells
Patient Preparation
Patients should fast for at least 12 hours before blood is drawn.
Reference Range
0-40 mg/dL
Additional Information
Background Information
Lipoprotein (a) [Lp(a)] is a spherical lipid particle that is genetically determined and remains at relatively constant levels over an individual’s lifetime. It contains two crosslinked proteins as part of its structure: apolipoprotein(a) covalently bound to apolipoprotein B-100. Lp(a) is important as a serum marker for coronary artery disease independent of diet and lipid levels. Elevated Lp(a) levels are associated with increased risk and severity of atherosclerosis, coronary heart disease, and stroke.
Similar to LDL-cholesterol, Lp(a) is synthesized in the liver. Although Lp(a) shows some homology to LDL-cholesterol in structure, Lp(a) differs from LDL in molecular weight, electrophoretic mobility, and protein/lipid ratio. Physiologic circulating levels of Lp(a) do not appear to be regulated by the same mechanisms of LDL-cholesterol. Likewise, cholesterol feeding does not appear to increase levels of Lp(a) in plasma, although it does increase levels of LDL cholesterol. Most pharmacologic agents that have an effect on lowering LDL-cholesterol levels have little effect on levels of Lp(a), thus also indicating regulation under different metabolic control.
The causes of high Lp(a) are kidney disease and certain family (genetic) lipid disorders.
Clinical Indications
Patients with a family history of elevated Lp(a) and/or a family history of premature cardiovascular disease that is not explained by high LDL or low HDL.
Also used for heart disease patients with a normal lipid profile and mildly elevated cholesterol and/or low-density lipoprotein cholesterol (LDL-C), as it is believed that an elevated Lp(a) may worsen other heart and vascular disease processes.
An elevated Lp(a) may suggest the need for more aggressive treatment of LDL and other, more treatable risk factors down to acceptable levels.
Limitations
For the most accurate results, wait at least two months after a heart attack, surgery, stroke, infection, injury, or pregnancy to check blood level.
In general, lipids should not be measured right after excessive alcohol intake, with severely uncontrolled diabetes, or during rapid weight loss.
Methodology
Lipoprotein (a) in serum is quantitatively measured on the IMMAGE 800 Immunochemistry system by rate nephelometry. Antibody to human Lp(a) is brought into contact with Lp(a) in a sample.
The IMMAGE 800 Test measures the rate of increase in light scattered from particles suspended in solution as a result of complexes formed during an antigen-antibody reaction.
The increase in light scatter resulting from the antigen-antibody reaction is converted to a peak rate signal, which is a function of the sample Lp(a) concentration. Following calibration, the peak rate signal for a particular assay is automatically converted to concentration units by the analyzer.
References
1. IMMAGE 800 Immunochemistry System Operations Manual, Instructions #A11403, March 2004, Beckman Coulter Instruments, Inc., Fullerton, CA 92834-3100.
2. Beckman Coulter IMMAGE 800 Immunochemistry System, Chemistry Information Manual, Beckman Coulter Instructions #962248, March 2000, Beckman Coulter Instruments, Inc., Fullerton, CA 92834-3100.
3. Tietz, NW. Specimen Collection and Processing: Sources of Biological Variation. Textbook of Clinical Chemistry. WB Saunders, Philadelphia, PA. 1986;478-518.
4. National Committee for Clinical Laboratory Standards. Procedures for the Handling and Processing of Blood Specimens, Approved Guideline. NCCLS publication H18-A, Villanova, PA.1990.
5. Schreiner, JP, Heiss G, Tyroler HA, Morrisett JD, Davis CD, Smith R. Race and Gender Differences in the Association of Lp(a) with Carotid Artery Wall Thickness: The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb Vasc Biol. 1996;16:471-478.
6. National Committee for Clinical Laboratory Standards, How to Define, Determine, and Utilize Reference Intervals in the Clinical Laboratory: Proposed Guideline. NCCLS publication C28-P, Villanova, PA. 1990.
7. Tietz, NW. Clinical Guide to Laboratory Tests. 2nd ed, WB Saunders, Philadelphia, PA. 1990.
8. Henry JB, ed. Clinical Diagnosis and Management by Laboratory Methods. 17th edition. 1984.
9. Statland, Bernard E. Clinical Decision Levels for Lab Tests. Medical Economic Book, Oradel, New Jersey.1983.
10. Tietz, NW, ed. Fundamentals of Clinical Chemistry. 3rd Edition, WB Saunders, Philadelphia, PA.1987.
11. National Committee for Clinical Laboratory Standards. Method Comparison and Bias Estimation Using Patient Samples: Tentative Guideline. NCCLS publication EP9-T, Villanova, PA. 1993.
12. National Committee for Clinical Laboratory Standards. Precision Performance of Clinical Chemistry Devices: Tentative Guideline, 2nd Edition. NCCLS publication EP5-T2, Villanova, PA. 1992.
13. Wild SH, Fortmann SP, Marcovina Sm. A Prospective Case-Control Study of Lipoprotein(a) Levels and Apo(a) Size and Risk of Coronary Heart Disease in Stanford Five-City Project Participants. Arterioscler Thromb Vasc Biol. 1997;17:239-245.