3 - 6 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
For more information, please view the literature below.
Serum, shipped refrigerated or plasma
Plain red-top tube (preferred); NMR LipoTube (black-and-yellow-top tube), lavender-top (EDTA-no gel) tube, or green-top (heparin-no gel) tube is acceptable.
Collect specimen in plain red-top tube, which is the preferred specimen. Hold tube upright at room temperature for 45 minutes and allow to clot. Centrifuge specimen after clotting according to manufacturer's specifications. Transfer to a transport tube for storage at 2°C to 8°C until shipped.
For NMR LipoTube (black-and-yellow-top tube), keep upright at room temperature for 30 minutes and allow to clot. Centrifuge at 1800 to 2200g for 10 to 15 minutes immediately after clotting. If the sample cannot be centrifuged immediately, it must be refrigerated at 2°C to 8°C and centrifuged within 24 hours of collection. The NMR tube should then be stored at 2°C to 8°C until shipped.
Separate plasma from lavender-top (EDTA-no gel) tube or green-top (heparin-no gel) tube immediately after collection and transfer to a plastic transport tube for shipment to the laboratory.
Do not open NMR LipoTube. Serum or plasma drawn in gel-barrier collection tubes other than the NMR LipoTube should not be used.
Refrigerate; stable for 14 days. Stable at room temperature for 60 hours or frozen for 24 months. Freeze/thaw cycles: x3
Patient fasting is not necessary prior to draw.
Unspun LipoTube or unseparated plain red-top or EDTA tube; serum or plasma specimen drawn in gel-barrier collection tube other than the NMR LipoTube; hemolysis (may reduce GlycA concentrations more than 10%)
As an (1) aid in the identification and stratification of individuals at risk for future cardiovascular (CV) disease, (2) independent marker of prognosis for recurrent cardiovascular events in patients with stable coronary disease or acute coronary syndrome, (3) aid in the assessment of disease activity and risk of CV disease in adult Rheumatoid Arthritis (RA) and psoriasis patients, when used in conjunction with standard clinical assessment and for monitoring of anti-inflammatory treatment.
Measurements from EDTA plasma specimens are, on average, 3% to 5% lower than from serum samples. Measurements from NMR LipoTube specimens are, on average, 5% to 6% higher than from serum samples collected in red-top tubes.
GlycA is an indicator for a wide range of disease processes and should not be interpreted without a complete clinical history. Recent medical events resulting in tissue injury, infections, or inflammation, which may cause elevated GlycA levels, should also be considered when interpreting results.
Hemolysis may reduce GlycA concentrations more than 10%.
This test was developed, and its performance characteristics determined, by LabCorp. It has not been cleared or approved by the US Food and Drug Administration (FDA).
Nuclear magnetic resonance (NMR)
GlycA Medical decision limit:
• Low <400 μmol/L
• High ≥400 μmol/L
The GlycA test quantifies an NMR signal that appears in a region of the NMR LipoProfile® test spectrum separate from that used for lipoprotein particle analysis. Data indicate that this signal is a marker of systemic inflammation, suggesting it may have clinical utility similar or complementary to high sensitivity C-reactive protein (hsCRP), fibrinogen, and other biomarkers of inflammation.1,2
The NMR signal, named "GlycA," originates from the N-acetyl methyl groups of the N-acetylglucosamine moieties on the carbohydrate portions of circulating glycoproteins.1,3 The measured amplitude of this signal reflects the extent of plasma protein glycosylation (not to be confused with nonenzymatic glycation reflecting glucose levels). Most acute phase proteins, released from the liver during an inflammatory response, are glycosylated, and some are glycosylated differentially as a function of inflammation. Acute-phase proteins, such as α1-acid glycoprotein (also known as orosomucoid), haptoglobin, α1-antitrypsin, α1-antichymotrypsin, and transferrin circulate at high enough concentrations to make major contributions to the GlycA signal.1 Therefore, GlycA is hypothesized to be a nonspecific measure of global inflammation status.
Unlike existing biomarkers of inflammation that are discrete molecular species, such as CRP or inflammatory cytokines, GlycA is a composite biomarker that integrates the protein levels and glycosylation states of several of the most abundant acute-phase proteins in serum. This allows for a more stable measure of systemic inflammation with lower intra-individual variability for GlycA than hsCRP.1 While guidelines recommend two serial measurements be taken at least two weeks apart when using hsCRP for CV disease risk assessment, only one measurement is necessary for evaluation of a patient's CV risk using the GlycA test.
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