Association of plasma neurofilament light chain with disease activity in chronic inflammatory demyelinating polyradiculoneuropathy.

Biomarkers Humans Immunoglobulins, Intravenous / therapeutic use Infusions, Intravenous Intermediate Filaments Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / drug therapy
CIDP IVIg disease activity neurofilament light chain

Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
11 2022
Historique:
revised: 06 06 2022
received: 02 03 2022
accepted: 25 06 2022
pubmed: 16 7 2022
medline: 12 10 2022
entrez: 15 7 2022
Statut: ppublish

Résumé

This study was undertaken to explore associations between plasma neurofilament light chain (pNfL) concentration (pg/ml) and disease activity in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and examine the usefulness of pNfL concentrations in determining disease remission. We examined pNfL concentrations in treatment-naïve CIDP patients (n = 10) before and after intravenous immunoglobulin (IVIg) induction treatment, in pNfL concentrations in patients on maintenance IVIg treatment who had stable (n = 15) versus unstable disease (n = 9), and in clinically stable IVIg-treated patients (n = 10) in whom we suspended IVIg to determine disease activity and ongoing need for maintenance IVIg. pNfL concentrations in an age-matched healthy control group were measured for comparison. Among treatment-naïve patients, pNfL concentration was higher in patients before IVIg treatment than healthy controls and subsequently reduced to be comparable to control group values after IVIg induction. Among CIDP patients on IVIg treatment, pNfL concentration was significantly higher in unstable patients than stable patients. A pNFL concentration > 16.6 pg/ml distinguished unstable treated CIDP from stable treated CIDP (sensitivity = 86.7%, specificity = 66.7%, area under receiver operating characteristic curve = 0.73). Among the treatment withdrawal group, there was a statistically significant correlation between pNfL concentration at time of IVIg withdrawal and the likelihood of relapse (r = 0.72, p < 0.05), suggesting an association of higher pNfL concentration with active disease. pNfL concentrations may be a sensitive, clinically useful biomarker in assessing subclinical disease activity.

Sections du résumé

BACKGROUND AND PURPOSE
This study was undertaken to explore associations between plasma neurofilament light chain (pNfL) concentration (pg/ml) and disease activity in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and examine the usefulness of pNfL concentrations in determining disease remission.
METHODS
We examined pNfL concentrations in treatment-naïve CIDP patients (n = 10) before and after intravenous immunoglobulin (IVIg) induction treatment, in pNfL concentrations in patients on maintenance IVIg treatment who had stable (n = 15) versus unstable disease (n = 9), and in clinically stable IVIg-treated patients (n = 10) in whom we suspended IVIg to determine disease activity and ongoing need for maintenance IVIg. pNfL concentrations in an age-matched healthy control group were measured for comparison.
RESULTS
Among treatment-naïve patients, pNfL concentration was higher in patients before IVIg treatment than healthy controls and subsequently reduced to be comparable to control group values after IVIg induction. Among CIDP patients on IVIg treatment, pNfL concentration was significantly higher in unstable patients than stable patients. A pNFL concentration > 16.6 pg/ml distinguished unstable treated CIDP from stable treated CIDP (sensitivity = 86.7%, specificity = 66.7%, area under receiver operating characteristic curve = 0.73). Among the treatment withdrawal group, there was a statistically significant correlation between pNfL concentration at time of IVIg withdrawal and the likelihood of relapse (r = 0.72, p < 0.05), suggesting an association of higher pNfL concentration with active disease.
CONCLUSIONS
pNfL concentrations may be a sensitive, clinically useful biomarker in assessing subclinical disease activity.

Identifiants

DOI: 10.1111/ene.15496 PMID: 35837802 PMC: PMC9796374
pubmed: 35837802
doi: 10.1111/ene.15496
pmc: PMC9796374
doi:

Substances chimiques

Biomarkers 0
Immunoglobulins, Intravenous 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

3347-3357

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : U54 NS065712
Pays : United States

Informations de copyright

© 2022 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.

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Auteurs

Mahima Kapoor (M)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Department of Neurosciences, Central Clinical School, Monash University, Alfred Centre, Melbourne, Victoria, Australia.
ORCID: 0000-0001-5498-3426

Aisling Carr (A)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Centre for Neuromuscular diseases, National Hospital for Neurology and Neurosurgery, London, UK.

Martha Foiani (M)

Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, UK.
UK Dementia Research Institute at University College London, London, UK.
ORCID: 0000-0003-4157-2606

Amanda Heslegrave (A)

Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, UK.
UK Dementia Research Institute at University College London, London, UK.
ORCID: 0000-0002-7290-6405

Henrik Zetterberg (H)

Department of Neurodegenerative Disease, University College London Queen Square Institute of Neurology, London, UK.
UK Dementia Research Institute at University College London, London, UK.
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China.
ORCID: 0000-0003-3930-4354

Andrea Malaspina (A)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
University College London Queen Square Motor Neuron Disease Centre, Queen Square Institute of Neurology, London, UK.
Centre for Neuroscience and Trauma, Blizard Institute, Barts and London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
ALS Biomarkers Study, University College London, London, UK.

Laura Compton (L)

Centre for Neuromuscular diseases, National Hospital for Neurology and Neurosurgery, London, UK.

Elspeth Hutton (E)

Department of Neurosciences, Central Clinical School, Monash University, Alfred Centre, Melbourne, Victoria, Australia.
ORCID: 0000-0002-8543-7767

Alexander Rossor (A)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Centre for Neuromuscular diseases, National Hospital for Neurology and Neurosurgery, London, UK.
ORCID: 0000-0003-4648-2896

Mary M Reilly (MM)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Centre for Neuromuscular diseases, National Hospital for Neurology and Neurosurgery, London, UK.
ORCID: 0000-0003-0686-905X

Michael P Lunn (MP)

Department of Neuromuscular Diseases, University College London Queen Square Institute of Neurology, London, UK.
Centre for Neuromuscular diseases, National Hospital for Neurology and Neurosurgery, London, UK.
Neuroimmunology and CSF Laboratory, University College London Queen Square Institute of Neurology, London, UK.
ORCID: 0000-0003-3174-6027

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