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Oxidized LDL
Test Code92769
CPT Codes
83520
Preferred Specimen
0.5 mL serum
Minimum Volume
0.3 mL
Transport Temperature
Refrigerated (cold packs)
Specimen Stability
Room temperature: Unacceptable
Refrigerated: 5 days
Frozen -20° C: 21 days
Frozen -70° C: 28 days
Refrigerated: 5 days
Frozen -20° C: 21 days
Frozen -70° C: 28 days
Methodology
Immunoassay (IA)
Setup Schedule
Set up: Mon-Sat; Report available: 5 days
Clinical Significance
This test measures damaged lipid particles due to oxidative modification of the apolipoprotein B (apoB) subunit.
Rather than being recognized by low-density lipoprotein (LDL) receptors, oxidized LDL is recognized by scavenger receptors, allowing for increased entry into the artery wall. Within the artery wall, macrophages engulf oxidized LDL, resulting in foam cell formation, [1] vascular inflammation,[2] and initiation of atherosclerosis.[3] Unstable plaques are enriched with oxidized LDL.[2]
Individuals with high levels of oxidized LDL are 3.5x more likely to develop metabolic syndrome in the next 5 years.[4] In healthy middle-aged men, high oxidized LDL levels are associated with a 4x greater risk of developing coronary artery disease (CAD).[5] Increased oxidized LDL levels are associated with the presence of CAD [1,2,6] and increase as the severity of CAD increases.[7] Oxidized LDL levels may also be elevated in patients with kidney disease,[8] polycystic ovary syndrome,[9] and known autoimmune disorders.[10] Oxidized LDL decreases after statin administration.[2]
Individuals suitable for testing include those at risk for metabolic syndrome and those with 1 or more risk factors for the development of cardiovascular disease (CVD).
Hemolytic samples may give erroneous results. These samples should not be used for analysis.
The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.
References
1. Nishi K, et al. ATVB. 2002;22(10):1649-1654.
2. Tsimikas S, et al. N Engl J Med. 2005;353(1):46-57.
3. Berliner JA, et al. Circulation. 1995;91(9):2488-2496.
4. Holvoet P, et al. JAMA. 2008;299(19):2287.
5. Meisinger C, et al. Circulation. 2005;112(5):651-657.
6. Li D, et al. ATVB. 2000;20(4):1116-1122.
7. Ehara S, et al. Circulation. 2001;103(15):1955-1960.
8. Samouilidou EC, et al. Renal Failure. 2012;34(2):160-164.
9. Macut D, et al. Eur J Endocrinol. 2006;155(1):131-136.
10. Frostegard J, et al. Arthritis Rheumatol. 2005;52(1): 192-200.
Rather than being recognized by low-density lipoprotein (LDL) receptors, oxidized LDL is recognized by scavenger receptors, allowing for increased entry into the artery wall. Within the artery wall, macrophages engulf oxidized LDL, resulting in foam cell formation, [1] vascular inflammation,[2] and initiation of atherosclerosis.[3] Unstable plaques are enriched with oxidized LDL.[2]
Individuals with high levels of oxidized LDL are 3.5x more likely to develop metabolic syndrome in the next 5 years.[4] In healthy middle-aged men, high oxidized LDL levels are associated with a 4x greater risk of developing coronary artery disease (CAD).[5] Increased oxidized LDL levels are associated with the presence of CAD [1,2,6] and increase as the severity of CAD increases.[7] Oxidized LDL levels may also be elevated in patients with kidney disease,[8] polycystic ovary syndrome,[9] and known autoimmune disorders.[10] Oxidized LDL decreases after statin administration.[2]
Individuals suitable for testing include those at risk for metabolic syndrome and those with 1 or more risk factors for the development of cardiovascular disease (CVD).
Hemolytic samples may give erroneous results. These samples should not be used for analysis.
The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.
References
1. Nishi K, et al. ATVB. 2002;22(10):1649-1654.
2. Tsimikas S, et al. N Engl J Med. 2005;353(1):46-57.
3. Berliner JA, et al. Circulation. 1995;91(9):2488-2496.
4. Holvoet P, et al. JAMA. 2008;299(19):2287.
5. Meisinger C, et al. Circulation. 2005;112(5):651-657.
6. Li D, et al. ATVB. 2000;20(4):1116-1122.
7. Ehara S, et al. Circulation. 2001;103(15):1955-1960.
8. Samouilidou EC, et al. Renal Failure. 2012;34(2):160-164.
9. Macut D, et al. Eur J Endocrinol. 2006;155(1):131-136.
10. Frostegard J, et al. Arthritis Rheumatol. 2005;52(1): 192-200.
