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Myelin Associated Glycoprotein (MAG) IgM Autoantibodies
This assay is not approved for patients of New York State physicians.
Expected Turnaround Time
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.
0.1 mL (Note: This volume does not allow for repeat testing.)
Gel-barrier tube or red-top tube
Separate serum from cells. Transfer the serum into a LabCorp PP transpak frozen purple tube with screw cap (LabCorp No. 49482). Freeze immediately and maintain frozen at ≤ -20°C until tested. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
1 year (stability determined by manufacturer or literature reference)
Stable x2 (stability determined by manufacturer or literature reference)
Lipemic samples can be avoided by having the patient fast for 12 hours prior to collection.
Causes for Rejection
Non-serum sample received; non-frozen serum received; grossly lipemic, hemolytic or icteric sample received; cryoglobulin present
The BUHLMANN Anti-MAG™ ELISA is intended for the quantitative in vitro diagnostic determination of human IgM autoantibodies directed against Myelin Associated Glycoprotein (MAG).1
Results of this test are labeled for research purposes only by the assay's manufacturer. The performance characteristics of this assay have not been established by the manufacturer. The result should not be used for treatment or for diagnostic purposes without confirmation of the diagnosis by another medically established diagnostic product or procedure. The performance characteristics were determined by LabCorp.
BUHLMANN™ anti-MAG ELISA. This assay measures antibodies to purified human MAG.1,2,12-25
MAG is a transmembrane lectin that preferentially binds to alpha-2,3-linked sialic acid terminal carbohydrates on cell surface molecules. It is localized in the oligodendroglial membranes of myelin sheaths and Schwann cells. Several different forms of motor and sensory neuropathies are associated with antibodies against the sulphated glucuronic acid moieties of MAG. The clinical picture of anti-MAG neuropathy is characterized by a distal and symmetric, mostly sensory neuropathy.2-6 The clinical course of anti- MAG neuropathy is usually slowly progressive with evidence of demyelination and a variable degree of axonal loss associated with gait ataxia.7 However, the clinical presentation of these patients can be variable, suggesting autoimmunity to other components of myelin may play a role in the disease.8
Anti-MAG autoantibodies frequently occur with IgM paraproteinemia. Approximately half the patients with Monoclonal Gammopathy of Uncertain Significance (MGUS) of IgM type with peripheral neuropathies have antibodies against MAG.2,6 Anti-MAG IgM has also been identified in Waldenstrom's macroglobulinemia and IgM secreting lymphoma. These MAG autoantibodies are believed to be pathogenic.2,9 A joint task force of the European Federation of Neurological Societies (EFNS) and Peripheral Nerve Society (PNS) have constructed clinically useful guidelines for the diagnosis, investigation and treatment of patients with both, a demyelinating neuropathy and a paraprotein.10
Patients with anti-MAG antibodies may respond favorably to therapeutic intervention but to date there is no consensus on the treatment of this disease.2,11,12 Testing for the presence of these autoantibodies is useful for diagnosis as well as for monitoring of therapy.13,14 Historically, clinicians have applied a variety of approaches to treatment of anti-MAG neuropathy including:
• Reduction of circulating IgM anti-MAG antibodies by removal by [plasma exchange],
• Inhibition with Intravenous Immunoglobulin (IVIg), or
• Reduction of their synthesis by corticosteroids, immunosuppressive agents, cytotoxic agents or interferon alpha.9,15
Recent reports suggest Rituximab may be effective in some patients with anti-MAG neuropathy.4,7,16-20 However, the effectiveness of this approach has not been confirmed in all cases.12,21,22