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Cited by 27Peripheral Neuropathies and DisordersAutoimmune Neurological Disorders and TreatmentsMultiple Sclerosis Research Studies

The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.

Antibody testing in neuropathy associated with anti-Myelin-Associated Glycoprotein antibodies: where we are after 40 years

Open access
Latov, Norman·2021·Current Opinion in Neurology
DOI 10.1097/wco.0000000000000975
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Abstract

PURPOSE OF REVIEW: The diagnosis of Myelin-Associated Glycoprotein (MAG) neuropathy is based on the presence of elevated titers of IgM anti-MAG antibodies, which are typically associated with IgM monoclonal gammopathy, and a slowly progressive, distal demyelinating phenotype. The condition, however, can be under or over diagnosed in patients with mildly elevated antibody titers, absent monoclonal gammopathy, or an atypical presentation. The purpose of this paper is to examine recent advances in our understanding of the currently available anti-MAG antibody assays, their reliability, and their use in deciding treatment or monitoring the response to therapy. RECENT FINDINGS: Higher titers of anti-MAG antibodies are more likely to be associated with the typical MAG phenotype or response to therapy. Mildly elevated antibody levels can occur in patients with chronic inflammatory demyelinating polyneuropathy. Testing for cross-reactivity with HNK1 can add to the specificity of the antibody assays. Patients with MAG neuropathy can present with an atypical phenotype and in the absence of a detectable monoclonal gammopathy. SUMMARY: Assays for anti-MAG antibodies by Enzyme-Linked Immunosorbent Assay can be improved by testing for antibody binding at multiple serum dilutions, the inclusion of antigen-negative microwells as internal controls for each sample, testing for cross-reactivity with HNK1, and formal validation. The diagnosis needs to be considered in patients with demyelinating neuropathy, even in the absence of a monoclonal gammopathy or typical phenotype. The change in antibody levels needs to be considered in evaluating the response to therapy with B-cell depleting agents.

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Crossref · 10.1097/wco.0000000000000975

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Citations

Cites

Research works printed but not linked: 2

  1. Tagawa, 2000, Anti-SGPG antibody in CIDP: nosological position of IgM anti-MAG/SGPG antibody-associated neuropathy, Muscle Nerve, 23, 895, 10.1002/(SICI)1097-4598(200006)23:6<895::AID-MUS8>3.0.CO;2-G · DOI
  2. Van den Berg, 1996, Anti-MAG and anti-SGPG antibodies in neuropathy, Muscle Nerve, 19, 637, 10.1002/(SICI)1097-4598(199605)19:5<637::AID-MUS12>3.0.CO;2-K · DOI

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Metadata

Authors
Latov, N.
Affiliations
Weill Cornell Medicine (US)
Corresponding author
Latov, Norman
ORCID
Latov, Norman
Venue
Current Opinion in Neurology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2021-08-12
Volume
34
Issue
5
Pages
625-630
ISSN
  • 1350-7540 (ISSN-L)
  • 1473-6551
DOI
10.1097/wco.0000000000000975
OpenAlex
W3179499453
Cited by
27
References
55
Citations by year
2026: 4 · 2025: 5 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 1
FWCI
2.15
Type
journal article
Language
en
Open access
Licence
Locations
  • Current Opinion in Neurology (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Peripheral Neuropathies and Disorders
  • Health Sciences › Medicine › Clinical Neurology › Autoimmune Neurological Disorders and Treatments
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Keywords
anti-MAG antibodies, IgM monoclonal gammopathy, demyelinating neuropathy, chronic inflammatory demyelinating polyneuropathy, antibody titers, B-cell depletion therapy, treatment response monitoring, atypical presentation
MeSH terms
Autoantibodies, Humans, Immunoglobulin M, Paraproteinemias, Reproducibility of Results, Myelin-Associated Glycoprotein, Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

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Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.