Evidence map›Paper›PMID 42057292›Full record

ReviewBrain and behavior2026

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): A Comprehensive Review of Types, Pathophysiology, and Treatment Approaches.

Ayesha Khan, Arsal Khan, Kuldeep Dalpat Rai, Anzel Saeed, Harsh Kumar, Aneesh Kumar Sangtiani, Tehreem Fatima, Muhammad Tanveer Alam, Faiza Rajput, Sakshi Chawla and 2 more

Abstract readReview
In one paragraph

Review in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Ayesha KhanDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0005-0444-5095
Arsal KhanDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0006-9445-4215
Kuldeep Dalpat RaiDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0000-2135-0673
Anzel SaeedDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0006-9602-4569
Harsh KumarDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0009-0339-7270
Aneesh Kumar SangtianiDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0005-9965-020X
Tehreem FatimaDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0009-8366-3179
Muhammad Tanveer AlamDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.
Faiza RajputDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0001-9112-2892
Sakshi ChawlaDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.
Hussain Haider ShahDepartment of Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0000-0002-8032-7462
Humaira KalamShaheed Tajuddin Ahmad Medical College, Gazipur, Bangladesh.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThis review aims to provide a comprehensive analysis of chronic inflammatory demyelinating polyneuropathy (CIDP), focusing on its clinical manifestations, pathophysiology, and treatment advancements, with particular emphasis on efgartigimod as a novel therapeutic agent. RECENT

findingsCIDP is a chronic autoimmune disorder caused by demyelination and axonal degeneration, leading to progressive weakness and impaired sensory function. While conventional treatments, including corticosteroids, IVIg, and plasma exchange, provide symptomatic relief, their limitations include significant side effects and resistance in some cases. Efgartigimod, an FcRn blocker targeting the IgG catabolic pathway, has emerged as a promising therapy. The ADHERE study demonstrated a 61% reduction in CIDP relapses with efgartigimod, alongside improved disability scores and a favorable safety profile. SUMMARY: CIDP presents significant diagnostic and therapeutic challenges, requiring tailored approaches to management. Efgartigimod introduces a targeted mechanism of action, offering hope for patients unresponsive to traditional therapies. Further research is needed to establish its long-term efficacy and optimal role in CIDP treatment strategies.

Indexed as

Polyradiculoneuropathy, Chronic Inflammatory DemyelinatingAntibodies, Monoclonal, HumanizedHumansAntibodies, Monoclonal, Humanizedefgartigimod alfaautoimmune disorderschronic inflammatory demyelinating polyneuropathydemyelinationefgartigimodemerging therapiesFcRn blockersintravenous immunoglobulinneuropathy treatmentpathophysiologyplasma exchange

Identifiers

PMID42057292
PMCPMC13128971

What OpenQuestion holds

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Registered trials

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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.