Ganglioside - IgG antibody

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Autoantibodies against gangliosides.

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Ganglioside - IgG Antibody Test Information Guide

Why is it done?
- Detects IgG autoantibodies against gangliosides, which are lipid components found on the surface of nerve cells and the peripheral nervous system
- Used to diagnose autoimmune neuropathies, particularly Guillain-Barré Syndrome (GBS) and its variants, including Miller Fisher Syndrome (MFS)
- Helps identify chronic inflammatory demyelinating polyneuropathy (CIDP) and other autoimmune peripheral neuropathies
- Ordered when patients present with acute or subacute ascending paralysis, weakness, or sensory abnormalities
- Typically performed during acute phase of suspected neuropathy, though can be positive for months to years following symptom onset
- Used as a supportive diagnostic tool alongside clinical evaluation, electrophysiological studies, and lumbar puncture findings
Normal Range
- Negative or Undetectable - Typical values <1:100 titer or <0.11 units (depending on laboratory method and platform)
- Units of Measurement - Result typically reported as titer (ratio), optical density (OD) units, or quantitative units (U/mL)
- Negative Result - Indicates absence of detectable IgG antibodies against gangliosides; consistent with healthy individuals or alternative diagnoses
- Positive Result - Indicates presence of anti-ganglioside IgG antibodies; may suggest autoimmune neuropathy but requires clinical correlation
- Borderline/Equivocal Results - Some laboratories report intermediate titers (1:100-1:400) as borderline; clinical context is essential for interpretation
- Specific Types - Results often specify which ganglioside is targeted (e.g., GM1, GD1a, GD1b, GQ1b)
Interpretation
- Positive Anti-GM1 IgG - Strongly associated with acute motor axonal neuropathy (AMAN) and motor neuropathy subtypes of GBS; approximately 50% of AMAN cases are positive
- Positive Anti-GD1a IgG - Frequently found in patients with motor neuropathy; can occur alongside anti-GM1 antibodies; present in motor-predominant GBS variants
- Positive Anti-GD1b IgG - Associated with demyelinating forms of GBS and sensorimotor polyneuropathy; less common than GM1 or GD1a positivity
- Positive Anti-GQ1b IgG - Highly specific for Miller Fisher Syndrome (MFS), a variant of GBS characterized by ophthalmoplegia, ataxia, and areflexia; found in 80-90% of MFS cases
- Negative Results - Do not exclude autoimmune neuropathy; approximately 50% of GBS cases test negative for anti-ganglioside antibodies; absence of antibodies does not rule out diagnosis
- Multiple Antibodies - Presence of multiple anti-ganglioside antibodies may indicate more severe disease or different neuropathy phenotype; correlates with clinical progression
- Timing Considerations - Antibodies may appear late in acute phase or persist for months to years; seroconversion may occur after symptom onset; negative result early in disease does not exclude diagnosis
- Disease-Specific Patterns - Different neuropathy phenotypes show distinct antibody patterns: motor neuropathies correlate with anti-GM1/GD1a; MFS correlates with anti-GQ1b; CIDP may show varying patterns
- Factors Affecting Results - Laboratory method variability, timing of blood draw relative to symptom onset, immunotherapy received, disease duration, and individual immune response variations
Associated Organs
- Primary System - Peripheral nervous system (PNS), specifically nerve fiber axons and myelin; secondary involvement of cranial nerves and autonomic nervous system possible
- Guillain-Barré Syndrome (GBS) - Acute, autoimmune polyradiculoneuropathy; life-threatening condition affecting motor function, respiratory muscles, and autonomic nervous system; most common cause of acute flaccid paralysis
- Miller Fisher Syndrome (MFS) - Variant of GBS characterized by ophthalmoplegia, ataxia, and areflexia; typically associated with anti-GQ1b antibodies; affects cranial nerves and coordination
- Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - Chronic disorder with progressive weakness and demyelination of peripheral nerves; may show anti-ganglioside antibodies in subset of patients
- Acute Motor Axonal Neuropathy (AMAN) - Motor-predominant variant of GBS with axonal involvement; strongly associated with anti-GM1 antibodies; typically seen in Asian populations
- Potential Complications - Respiratory failure requiring mechanical ventilation, autonomic dysfunction, cardiac arrhythmias, severe muscle weakness, permanent neurological sequelae, need for intensive care admission
- Secondary Effects - Can affect brainstem, motor cortex, and autonomic nuclei; may cause oculomotor involvement, facial weakness, swallowing difficulties, and parasympathetic dysfunction
Follow-up Tests
- Electrophysiological Studies - Nerve conduction velocity (NCV) and electromyography (EMG) testing to identify demyelinating vs axonal patterns; helps classify GBS subtype and correlate with antibody findings
- Cerebrospinal Fluid (CSF) Analysis - Lumbar puncture to evaluate protein levels, cell count, and intrathecal immunoglobulin synthesis; characteristic albumino-cytologic dissociation supports GBS diagnosis
- Additional Serum Antibody Panels - Anti-ganglioside panel testing multiple antigens (GM1, GD1a, GD1b, GQ1b) simultaneously; testing for other autoantibodies (anti-NMDA receptor, anti-CASPR2, anti-LGI1)
- IgM Anti-Ganglioside Antibody Testing - Complement-activating IgM antibodies appear early in infection; may precede IgG antibody appearance; useful when IgG is negative but clinical suspicion remains high
- MRI of Spinal Cord and Nerve Roots - Imaging to evaluate for demyelination, nerve root enhancement, and exclude other spinal pathology; helpful in atypical presentations
- Infectious Serologies - Testing for preceding infections (Campylobacter jejuni, CMV, EBV, Zika virus, influenza) that may trigger immune response; infection patterns correlate with antibody subtypes
- Monitoring During Treatment - Serial antibody testing may be performed to monitor disease progression or response to immunotherapy; repeat testing 2-4 weeks after initial assessment recommended
- Clinical Neurological Assessment - Detailed neurological examination, GBS Disability Scale scoring, muscle strength testing; essential for correlating antibody results with clinical status
- Monitoring Frequency - Acute phase: testing within 1-2 weeks of symptom onset optimal; for chronic conditions like CIDP, testing may be done at diagnosis and annually during monitoring; testing not typically repeated in stable, well-characterized cases
Fasting Required?
- Fasting Status: No - Fasting is NOT required for ganglioside IgG antibody testing
- Sample Collection - Blood draw can be performed at any time of day without dietary restriction; serum sample preferred; most laboratories require 1-2 mL of serum in appropriate tube
- Medication Considerations - No need to stop medications before test; continue regular medications as prescribed; immunosuppressive medications do NOT typically affect antibody detection in blood
- Patient Preparation - Standard blood draw precautions; patient should be calm and relaxed; inform phlebotomist if patient has history of difficult draws; no special positioning required
- Sample Handling - Allow blood to clot at room temperature per laboratory protocol; centrifuge within 30 minutes; serum can be refrigerated at 2-8°C if testing delayed; avoid hemolysis or lipemia that may interfere with assay
- Special Instructions - Timing of draw relative to symptom onset important; earliest testing optimal within 2 weeks of symptom onset; late testing (>4 weeks) may miss some positive results; specimen label should include dates and times
- Turn-Around Time - Results typically available in 3-7 business days; some reference laboratories may require 7-14 days; stat testing may be available at major medical centers in urgent circumstances

How our test process works!