Evaluation of the Diagnostic Contributions of Nerve Ultrasound in Chronic Inflammatory Demyelinating Polyneuropathy Associating Systemic Diseases (CIDP Echo-nerf)

NCT ID: NCT05257733

Last Updated: 2024-04-05

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

WITHDRAWN

Study Classification

OBSERVATIONAL

Study Start Date

2022-03-15

Study Completion Date

2023-12-31

Brief Summary

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Chronic inflammatory demyelinating polyradiculoneuritis (CIDP) is an autoimmune disorder of the peripheral nervous system, most commonly affecting the myelin sheath. The pathophysiology of CIDP is not completely understood, but both humoral and cellular immunity appear to be involved in the genesis of this disease. Some diseases are particularly associated with CIDP such as diabetes, monoclonal gammopathies and hematological diseases.

CIDP can occur before, after or simultaneously with the onset of systemic diseases. The systemic diseases most often seen in association with polyneuropathies are lupus, Gougerot-Sjögren's syndrome and sarcoidosis.

Ultrasound of peripheral nerves is a useful and accessible tool. In CIDP, this examination can reveal diffuse or segmental nerve hypertrophy. In addition to the size of the nerve, this exploration analyzes the echogenicity and the aspect of the different fascicles within the nerve. S. Goedee et al have shown that nerve ultrasound has very good diagnostic parameters and low interobserver variability in the diagnosis of CIDP. F. Härtig et al suggests that nerve ultrasound can predict the therapeutic response and describes 3 main patterns: hypoechoic enlargement (active inflammation), nerve enlargement with hyperechoic add-on fascicles (axonal degeneration) and almost no enlargement ("cured" CIDP).

Detailed Description

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CIDP may be progressive or relapsing, most frequently clinically symmetric, sensorimotor with proximal and distal involvement developing over at least 8 weeks but variants as distal, multifocal, focal, motor or sensory CIDP have been also described. Cell-mediated and humoral mechanisms act together in an aberrant immune response to cause damage to peripheral nerves but, by molecular mimicry it causes other autoimmune system diseases. This paper focuses on the intersection of CIDP and other autoimmune disease with an emphasis on shared pathology and mutually characteristics.

Conditions

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Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Study Design

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Observational Model Type

COHORT

Study Time Perspective

RETROSPECTIVE

Study Groups

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CIDP associated with systemic diseases

Patients with CIDP associated with systemic diseases

None, pure observationnal study

Intervention Type OTHER

pure observationnal study

CIDP without systemic diseases

Patients with CIDP without other systemic diseases

None, pure observationnal study

Intervention Type OTHER

pure observationnal study

Interventions

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None, pure observationnal study

pure observationnal study

Intervention Type OTHER

Eligibility Criteria

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Inclusion Criteria

* Patients followed at Nîmes University Hospital between 2012 and 2021
* Age \> 18 years
* Diagnosis of definite CIDP or possible CIDP according to the new EFNS/PNS 2021 criteria
* Diagnosis of definite CIDP/CIDP possible with systemic diseases and respectively diagnosis of definite CIDP/CIDP possible for the control group confirmed by electroneuromyography, concordant with the clinical examination
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Centre Hospitalier Universitaire de Nīmes

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Anissa MEGZARI

Role: STUDY_DIRECTOR

Centre Hospitalier Universitaire de Nīmes

Locations

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CHU de Nîmes

Nîmes, , France

Site Status

Countries

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France

References

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Schmidt B, Toyka KV, Kiefer R, Full J, Hartung HP, Pollard J. Inflammatory infiltrates in sural nerve biopsies in Guillain-Barre syndrome and chronic inflammatory demyelinating neuropathy. Muscle Nerve. 1996 Apr;19(4):474-87. doi: 10.1002/(SICI)1097-4598(199604)19:43.0.CO;2-9.

Reference Type RESULT
PMID: 8622727 (View on PubMed)

Sommer C, Koch S, Lammens M, Gabreels-Festen A, Stoll G, Toyka KV. Macrophage clustering as a diagnostic marker in sural nerve biopsies of patients with CIDP. Neurology. 2005 Dec 27;65(12):1924-9. doi: 10.1212/01.wnl.0000188879.19900.b7.

Reference Type RESULT
PMID: 16380614 (View on PubMed)

Spies JM, Westland KW, Bonner JG, Pollard JD. Intraneural activated T cells cause focal breakdown of the blood-nerve barrier. Brain. 1995 Aug;118 ( Pt 4):857-68. doi: 10.1093/brain/118.4.857.

Reference Type RESULT
PMID: 7655884 (View on PubMed)

Madia F, Frisullo G, Nociti V, Conte A, Luigetti M, Del Grande A, Patanella AK, Iorio R, Tonali PA, Batocchi AP, Sabatelli M. pSTAT1, pSTAT3, and T-bet as markers of disease activity in chronic inflammatory demyelinating polyradiculoneuropathy. J Peripher Nerv Syst. 2009 Jun;14(2):107-17. doi: 10.1111/j.1529-8027.2009.00220.x.

Reference Type RESULT
PMID: 19691533 (View on PubMed)

Press R, Pashenkov M, Jin JP, Link H. Aberrated levels of cerebrospinal fluid chemokines in Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. J Clin Immunol. 2003 Jul;23(4):259-67. doi: 10.1023/a:1024532715775.

Reference Type RESULT
PMID: 12959218 (View on PubMed)

Mei FJ, Ishizu T, Murai H, Osoegawa M, Minohara M, Zhang KN, Kira J. Th1 shift in CIDP versus Th2 shift in vasculitic neuropathy in CSF. J Neurol Sci. 2005 Jan 15;228(1):75-85. doi: 10.1016/j.jns.2004.10.001. Epub 2004 Nov 12.

Reference Type RESULT
PMID: 15607214 (View on PubMed)

Kurihara M, Kurata Y, Sugimoto I, Hatanaka Y, Sakurai Y. High PR3-ANCA positivity in a patient with chronic inflammatory demyelinating polyneuropathy. eNeurologicalSci. 2016 Oct 5;6:4-5. doi: 10.1016/j.ensci.2016.10.001. eCollection 2017 Mar.

Reference Type RESULT
PMID: 29260006 (View on PubMed)

Greenberg SA. P-ANCA vasculitic neuropathy with 12-year latency between onset of neuropathy and systemic symptoms. BMC Neurol. 2002 Oct 31;2(1):10. doi: 10.1186/1471-2377-2-10.

Reference Type RESULT
PMID: 12437775 (View on PubMed)

Abraham H, Kuzhively J, Rizvi SW. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): An Uncommon Manifestation of Systemic Lupus Erythematosus (SLE). Am J Case Rep. 2017 Sep 12;18:980-983. doi: 10.12659/ajcr.903541.

Reference Type RESULT
PMID: 28894082 (View on PubMed)

Siddiqui K, Cahalane E, Keogan M, Hardiman O. Chronic ataxic neuropathy with cold agglutinins: atypical phenotype and response to anti-CD20 antibodies. Neurology. 2003 Nov 11;61(9):1307-8. doi: 10.1212/wnl.61.9.1307. No abstract available.

Reference Type RESULT
PMID: 14610153 (View on PubMed)

Rodriguez Y, Vatti N, Ramirez-Santana C, Chang C, Mancera-Paez O, Gershwin ME, Anaya JM. Chronic inflammatory demyelinating polyneuropathy as an autoimmune disease. J Autoimmun. 2019 Aug;102:8-37. doi: 10.1016/j.jaut.2019.04.021. Epub 2019 May 6.

Reference Type RESULT
PMID: 31072742 (View on PubMed)

Wolbert J, Cheng MI, Meyer zu Horste G, Su MA. Deciphering immune mechanisms in chronic inflammatory demyelinating polyneuropathies. JCI Insight. 2020 Feb 13;5(3):e132411. doi: 10.1172/jci.insight.132411.

Reference Type RESULT
PMID: 32051341 (View on PubMed)

Seeliger T, Prenzler NK, Gingele S, Seeliger B, Korner S, Thiele T, Bonig L, Suhs KW, Witte T, Stangel M, Skripuletz T. Neuro-Sjogren: Peripheral Neuropathy With Limb Weakness in Sjogren's Syndrome. Front Immunol. 2019 Jul 11;10:1600. doi: 10.3389/fimmu.2019.01600. eCollection 2019.

Reference Type RESULT
PMID: 31354737 (View on PubMed)

Other Identifiers

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LOCAL/2022/II-01

Identifier Type: -

Identifier Source: org_study_id

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