ArticleCurrent treatment options in neurology2010
Pathogenesis and Treatment of Anti-MAG Neuropathy.
Article in Current treatment options in neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Guideline for the diagnosis, treatment and response criteria for Bing-Neel syndrome.Haematologica · 2017Guideline
- Monoclonal Gammopathy of Neurological Significance: Toward an Integrated Hematologic-Neurologic Perspective-A Single-Center Retrospective Study.International journal of molecular sciences · 2026Article
- Glycopolymer binds pathogenic IgM autoantibodies and pulls them into the mononuclear phagocyte system for degradation.Scientific reports · 2025Article
- Rituximab retreatment guided by CD27+ B-cell count vs. clinical relapse in anti-MAG polyneuropathy: a cost-effective approach with lower cumulative doses.Frontiers in neurology · 2025Article
- Malignancy in neuromuscular patients on chronic IVIG.Frontiers in neurology · 2025Article
- Article
- Bing-Neel syndrome, a rare manifestation of WM; a case report and review of literature.Clinical case reports · 2024Article
- Autocrine TNF-α Increases Penetration of Myelin-Associated Glycoprotein Antibodies Across the Blood-Nerve Barrier in Anti-MAG Neuropathy.Neurology(R) neuroimmunology & neuroinflammation · 2023Article
- Monoclonal gammopathies of clinical significance (MGCS): In pursuit of optimal treatment.Frontiers in immunology · 2022Review
- Mechanisms of Nerve Damage in Neuropathies Associated with Hematological Diseases: Lesson from Nerve Biopsies.Brain sciences · 2021Review
- Treatment Approaches for Atypical CIDP.Frontiers in neurology · 2021Review
- Selective inhibition of anti-MAG IgM autoantibody binding to myelin by an antigen-specific glycopolymer.Journal of neurochemistry · 2020Article
- Review
- Immune-Mediated Neuropathies.Current treatment options in neurology · 2019Review
- Peripheral Demyelinating Diseases: From Biology to Translational Medicine.Frontiers in neurology · 2019Review
- Article
- Advances in the diagnosis, immunopathogenesis and therapies of IgM-anti-MAG antibody-mediated neuropathies.Therapeutic advances in neurological disorders · 2018Review
- Anti-MAG associated cerebellar ataxia and response to rituximab.Journal of neurology · 2018Article
- Autoantibodies in chronic inflammatory neuropathies: diagnostic and therapeutic implications.Nature reviews. Neurology · 2017Review
- Selective in vivo removal of pathogenic anti-MAG autoantibodies, an antigen-specific treatment option for anti-MAG neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
opinion statementPolyneuropathies associated with IgM monoclonal gammopathies comprise a distinct entity. In spite of the apparent pathogenicity of the IgM antibodies and the specific immunoreactivity to myelin antigens, the disease has been difficult to treat. This review describes the clinical phenotype, addresses recent data on immunoreactivity of IgM to various nerve antigens, and discusses the latest progress on treatment.Most of these patients present with paresthesias and sensory ataxia followed by a varying degree of sensorimotor deficits. In more than 75% of the patients, the monoclonal IgM recognizes myelin-associated glycoprotein (MAG) and sulfoglucuronyl glycosphingolipid (SGPG), best detected by ELISA, or other peripheral nerve glycolipids. Recent experiments have demonstrated that animals immunized with SGPG develop sensory ataxia, suggesting a pathogenic role for this antigen. Although cladribine, cyclophosphamide with prednisone, and intravenous immunoglobulin have offered transient benefits to some patients, most have remained treatment-resistant. Open label studies and a recent randomized controlled trial indicate that rituximab is emerging as the best agent available, providing long-term benefits to almost half of these patients. Rituximab appears to work by suppressing the IgM as well as the anti-MAG antibodies and by inducing immunoregulatory T cells. Patients with more sensory deficits and higher anti-MAG antibodies are more likely to respond but may require re-treatment after several months.These encouraging results need confirmation with a larger trial. Data on long-term efficacy and immune markers associated with response to therapy or need for re-treatment are still needed.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.