Evidence map›Paper›PMID 32266541›Full record

ReviewJournal of neurology2021

Distinguish CIDP with autoantibody from that without autoantibody: pathogenesis, histopathology, and clinical features.

Lisha Tang, Qianyi Huang, Zhen Qin, Xiangqi Tang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. 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
    Article
  7. Article
  8. Anti-pan-neurofascin nodopathy: cause of fulminant neuropathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  9. The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Review
  10. CIDP/autoimmune nodopathies with nephropathy: a case series study.Annals of clinical and translational neurology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Observational
  17. CIDP mimics: a case series.BMC neurology · 2021
    Article
  18. Article
  19. Article
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 2 institutions in 1 country.

Lisha TangDepartment of Neurology, The Second Xiangya Hospital, Central South University, Renmin Road 139#, Changsha, 410011, Hunan, China.
Qianyi HuangDepartment of Neurology, The Second Xiangya Hospital, Central South University, Renmin Road 139#, Changsha, 410011, Hunan, China.
Zhen QinDepartment of Neurology, The Second Xiangya Hospital, Central South University, Renmin Road 139#, Changsha, 410011, Hunan, China.
Xiangqi TangDepartment of Neurology, The Second Xiangya Hospital, Central South University, Renmin Road 139#, Changsha, 410011, Hunan, China. txq6633@csu.edu.cn.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is considered to be an immune-mediated heterogeneous disease involving cellular and humoral immunity. In recent years, autoantibodies against nodal/paranodal protein neurofascin155 (NF155), neurofascin186 (NF186), contactin-1 (CNTN1), and contactin-associated protein 1 (CASPR1) have been identified in a small subset of patients with CIDP, which disrupt axo-glial interactions at nodes/paranodes. Although CIDP electrodiagnosis was made in patients with anti-nodal/paranodal component autoantibodies, macrophage-induced demyelination, the characteristic of typical CIDP, was not observed. Apart from specific histopathology, the pathogenic mechanisms and clinical manifestations of CIDP with autoantibody are also distinct. We herein compared pathogenesis, histopathology, clinical manifestations, and therapeutic response in CIDP with autoantibody vs. CIDP without autoantibody. CIDP with autoantibodies should be considered as an independent disease entity, not a subtype of CIDP due to many differences. They possibly should be classified as CIDP-like chronic nodo-paranodopathy, which can better characterize these disorders, help diagnose and make the most effective therapeutic decisions.

Indexed as

Polyradiculoneuropathy, Chronic Inflammatory DemyelinatingAutoantibodiesAxonsContactin 1HumansNeurogliaAutoantibodiesContactin 1AutoantibodyChronic inflammatory demyelinating polyradiculoneuropathyContactin1Contactin-associated protein 1Neurofascin155

Identifiers

PMID32266541
OpenAlexW3014944961

What OpenQuestion holds

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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.