Evidence map›Paper›PMID 28708133›Full record

ReviewNature reviews. Neurology2017

Autoantibodies in chronic inflammatory neuropathies: diagnostic and therapeutic implications.

Luis Querol, Jérôme Devaux, Ricard Rojas-Garcia, Isabel Illa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
14.9field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 220 citations in OpenAlex.

  1. Pooled it
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  11. Clinical and laboratory features of juvenile-onset anti-NF155 autoimmune nodopathy.Journal of neurology, neurosurgery, and psychiatry · 2026
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  14. [Systemic lupus erythematosus complicated by autoimmune nodopathy: A case report].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article
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  16. Chronic inflammatory demyelinating polyneuropathy in end-stage renal disease patients: a case series study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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43 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 2 countries.

Luis QuerolNeuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Mas Casanovas 90, 08041 Barcelona, Spain.
Jérôme DevauxAix-Marseille Université, Centre National de la Recherche Scientifique (CNRS), CRN2M-UMR7286, Faculté de Médecine - Secteur Nord CS80011, 51 Boulevard Pierre Dramard 13344 MARSEILLE Cedex 15, France.
Ricard Rojas-GarciaNeuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Mas Casanovas 90, 08041 Barcelona, Spain.
Isabel IllaNeuromuscular Diseases Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Mas Casanovas 90, 08041 Barcelona, Spain.
Aix-Marseille Université · FRCentre for Biomedical Network Research on Rare Diseases · ESHospital de Sant Pau · ESUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chronic inflammatory neuropathies (CINs) are rare, very disabling autoimmune disorders that generally respond well to immune therapies such as intravenous immunoglobulin (IVIg). The most common forms of CIN are chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy, and polyneuropathy associated with monoclonal gammopathy of unknown significance. The field of CIN has undergone a major advance with the identification of IgG4 autoantibodies directed against paranodal proteins in patients with CIDP. Although these autoantibodies are only found in a small subset of patients with CIDP, they can be used to guide therapeutic decision-making, as these patients have a poor response to IVIg. These observations provide proof of concept that identifying the target antigens in tissue-specific antibody-mediated autoimmune diseases is important, not only to understand their underlying pathogenic mechanisms, but also to correctly diagnose and treat affected patients. This state-of-the-art Review focuses on the role of autoantibodies against nodes of Ranvier in CIDP, a clinically relevant emerging field of research. The role of autoantibodies in other immune-mediated neuropathies, including other forms of CIN, primary autoimmune neuropathies, neoplasms, and systemic diseases that resemble CIN, are also discussed.

Indexed as

AutoantibodiesCell Adhesion MoleculesContactin 1HumansNerve Growth FactorsPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingRanvier's NodesAutoantibodiesCell Adhesion MoleculesCNTN1 protein, humanContactin 1Nerve Growth FactorsNFASC protein, human

Identifiers

PMID28708133
OpenAlexW2736190034

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.