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This assay is currently not available in New York state.
5 - 7 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.
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.
4 months (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.
Non-serum sample received; non-frozen serum received; grossly lipemic, hemolytic or icteric sample received
The BUHLMANN™ Anti-GM1 IgG ELISA is intended for the qualitative determination of human IgG autoantibodies directed against monosialotetrahexosylganglioside (GM1) in human serum.1
This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.
Enzyme Linked Immunoassay (ELISA) for IgG antibodies to the ganglioside GM1
0 - 30%
The ganglioside GM1 is expressed in the peripheral nervous system in the nodes of Ranvier, outer myelin, and the end plates of motor neurons.2 IgG antibodies against GM1 (Anti-GMI IgG) are strongly associated with motor axonal variants of Guillain-Barre syndrome.3,4
GBS is a rapid-onset, immune-mediated demyelinating polyneuropathy associated with acute flaccid paralysis.5,7 The initial symptoms of GBS typically involve symmetrical limb weakness and loss of tendon reflexes. Two major symptoms of GBS are defined by electrophysiological and pathological criteria.4,6-8 The classical, demyelinating form of GBS associated with impairment of the motor or sensory nerve fibers is referred to as Acute Inflammatory Demyelinating Polyneuropathy (AIDP). A second subtype of GBS associated with the myelin or the axonal impairment is referred to as Acute Motor Axonal Neuropathy (AMAN).6,9 AMAN is characterized by acute paralysis and loss of reflexes without sensory loss. AMAN is the most common GBS variant, accounting for as many as 5-10% of cases with much higher incidence in Asia.10
Multiple studies have found an association between AMAN and Anti-GM1 IgG seropositivity.8,9,11-18 Certain electrophysiologic features, such as reversible conduction failure, have been associated with the presence of Anti-GM1 IgG.13,18-21 It is thought that antibodies to GM1 bind to at the nodes of Ranvier activating complement and disrupting sodium-channel clusters and axoglial junctions, leading to nerve conduction failure and muscle weakness.8
The recognition that diarrheal illness can precede GBS has led some to hypothesize that an infectious agent may cause the development of Anti-GM1 IgG, possibly due to molecular mimicry resulting from antecedent infection.15 Campylobacter jejuni infection has been associated with the development of AMAN.8,22 Several other antecedent infectious agents have been recognized including the most recently identified, Zika virus.23
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|140385||GM1 IgG Autoantibodies||43240-1||140386||GM1 IgG Autoantibodies||%||43240-1|
|Reflex Table for GM1 IgG Autoantibodies|
|Order Code||Order Name||Result Code||Result Name||UofM||Result LOINC|
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