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SAA (Serum Amyloid A)

Analyte: Serum Amyloid A

Specimen Type: Serum, EDTA Plasma, Inquire for addiitional option(s)

Optimum Volume: 0.5 mL

Stability:

2-8°C -20°C -70°C
8 days 1 year 4.5 years

Reporting units: mg/L

Method: ELISA

Biological or Clinical Significance:

Serum Amyloid A (SAA) is an acute-phase protein. During acute events, the rise in SAA levels is one of the most rapid and intense increases of all acute phase proteins. When elevated above normal levels SAA is almost exclusively bound to High Density Lipoproteins (HDL). SAA circulates at trace levels (1-5 µg/mL) during normal conditions; however 4-6 hours after inflammatory stimulus, SAA levels can increase by as much as 1000 fold thus making SAA a sensitive marker of inflammatory response.

High levels of SAA can be seen in patients with acute and chronic inflammation. Secondary amyloidosis may develop as a result prolonged or repeated inflammatory conditions in which SAA levels remain elevated.

Measuring SAA levels may be a useful indicator of degree of inflammation and response to therapy. Inflammatory disorders such as rheumatoid arthritis, juvenile arthritis, ankylosing spondylitis, familial Mediterranean fever, progressive sclerosis as well as chronic infections such as tuberculosis and osteomyelitis are predisposed to developing amyloidosis.

Principle of Test Method:

Serum Amyloid A assay is a solid-phase ELISA designed to measure human SAA in serum or plasma. It employs quantitative sandwich enzyme immunoassay principle.

References:

1. Roberts WL. CDC/AHA workshop on markers of inflammation and cardiovascular disease. Application to clinical and public health practice. Laboratory tests available to assess inflammation-performance and standardization. A background paper. Circulation. 2004; 10:e572-e576.
2. Klein R, Klein BEK, Knudtson MD, Wong TY, Tsai MY. Are inflammatory factors related to retinal vessel caliber? Arch Opthalmol. 2006: 124:87-94.
3. MacGregor AJ, Gallimore JR, Spector TD, Pepys MB. Genetic effects on baseline values of C-reactive protein and serum amyloid A protein; A comparison of monozygotic and dizygotic twins. Clin Chem. 2004; 50: 130-134.
4. Narins CR, Zareba W, Moss AJ, Marder VJ, Ridker PM, Krone RJ, Lichstein E. Relationship between intermittent claudication, inflammation, thrombosis, and recurrent cardiac events among survivors of myocardial infarction. Arch Intern Med. 2004; 164:440-446.
5. Moss, AJ, Goldstein RE, Marder VJ, Sparks CE, Oakes D, Greenberg H, Weiss HJ, et al. Thrombogenic factors and recurrent coronary events. Circulation 1999; 99:2517-2522.

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