Long-Term Stability of Neuroaxonal Structure in Alemtuzumab-Treated Relapsing-Remitting Multiple Sclerosis Patients.


Journal

Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society
ISSN: 1536-5166
Titre abrégé: J Neuroophthalmol
Pays: United States
ID NLM: 9431308

Informations de publication

Date de publication:
03 2020
Historique:
entrez: 12 2 2020
pubmed: 12 2 2020
medline: 29 5 2021
Statut: ppublish

Résumé

Patients with multiple sclerosis (MS) experience progressive thinning in optical coherence tomography (OCT) measures of neuroaxonal structure regardless of optic neuritis history. Few prospective studies have investigated the effects of disease-modifying therapies on neuroaxonal degeneration in the retina. Alemtuzumab is a monoclonal antibody shown to be superior to interferon β-1a in treating relapsing-remitting MS (RRMS). The purpose of this study was to assess the effects of alemtuzumab and first-line injectable treatments on OCT measures of neuroaxonal structure including peripapillary retinal nerve fiber layer (RNFL) thickness and combined ganglion cell-inner plexiform (GCIP) layer volume in RRMS patients followed up over 5 years. In this retrospective pilot study with prospectively collected double cohort data, spectral domain OCT measures of RNFL thickness and GCIP volume were compared between alemtuzumab-treated RRMS patients (N = 24) and RRMS patients treated with either interferon-β or glatiramer acetate (N = 21). Over a median of 60 months (range 42-60 months), the alemtuzumab cohort demonstrated a change in the mean RNFL thickness (thinning from baseline) of -0.88 μm (95% confidence interval [CI] -2.63 to 0.86; P = 0.32) and mean GCIP volume of +0.013 mm (95% CI -0.006 to 0.032; P = 0.18). Over the same time period, the first-line therapy-treated cohort demonstrated greater degrees of RNFL thinning (mean change in RNFL thickness was -3.65 μm [95% CI -5.40 to -1.89; P = 0.0001]). There was also more prominent GCIP volume loss relative to baseline in the first-line therapy group (-0.052 mm [95% CI -0.070 to -0.034; P < 0.0001]). Alemtuzumab-treated patients with RRMS demonstrated relative stability of OCT-measured neuroaxonal structure compared with RRMS patients treated with either interferon-β or glatiramer acetate over a 5-year period. These findings, along with previous demonstration of improved brain atrophy rates, suggest that alemtuzumab may offer long-term preservation of neuroaxonal structure in patients with RRMS.

Sections du résumé

BACKGROUND
Patients with multiple sclerosis (MS) experience progressive thinning in optical coherence tomography (OCT) measures of neuroaxonal structure regardless of optic neuritis history. Few prospective studies have investigated the effects of disease-modifying therapies on neuroaxonal degeneration in the retina. Alemtuzumab is a monoclonal antibody shown to be superior to interferon β-1a in treating relapsing-remitting MS (RRMS). The purpose of this study was to assess the effects of alemtuzumab and first-line injectable treatments on OCT measures of neuroaxonal structure including peripapillary retinal nerve fiber layer (RNFL) thickness and combined ganglion cell-inner plexiform (GCIP) layer volume in RRMS patients followed up over 5 years.
METHODS
In this retrospective pilot study with prospectively collected double cohort data, spectral domain OCT measures of RNFL thickness and GCIP volume were compared between alemtuzumab-treated RRMS patients (N = 24) and RRMS patients treated with either interferon-β or glatiramer acetate (N = 21).
RESULTS
Over a median of 60 months (range 42-60 months), the alemtuzumab cohort demonstrated a change in the mean RNFL thickness (thinning from baseline) of -0.88 μm (95% confidence interval [CI] -2.63 to 0.86; P = 0.32) and mean GCIP volume of +0.013 mm (95% CI -0.006 to 0.032; P = 0.18). Over the same time period, the first-line therapy-treated cohort demonstrated greater degrees of RNFL thinning (mean change in RNFL thickness was -3.65 μm [95% CI -5.40 to -1.89; P = 0.0001]). There was also more prominent GCIP volume loss relative to baseline in the first-line therapy group (-0.052 mm [95% CI -0.070 to -0.034; P < 0.0001]).
CONCLUSIONS
Alemtuzumab-treated patients with RRMS demonstrated relative stability of OCT-measured neuroaxonal structure compared with RRMS patients treated with either interferon-β or glatiramer acetate over a 5-year period. These findings, along with previous demonstration of improved brain atrophy rates, suggest that alemtuzumab may offer long-term preservation of neuroaxonal structure in patients with RRMS.

Identifiants

pubmed: 32045393
doi: 10.1097/WNO.0000000000000802
pii: 00041327-202003000-00007
doi:

Substances chimiques

Immunosuppressive Agents 0
Alemtuzumab 3A189DH42V

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

37-43

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Auteurs

Jillian K Chan (JK)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Elena Hernandez Martínez de Lapiscina (E)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Carolyn Taylor (C)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Ai-Lan Nguyen (AL)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Salut Alba-Arbalat (S)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Virginia Devonshire (V)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Ana-Luiza Sayao (AL)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Robert Carruthers (R)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Fiona Costello (F)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

Anthony Traboulsee (A)

Department of Medicine (Neurology) (JKC, VD, A-LS, RC, AT), University of British Columbia, Vancouver, Canada; Department of Neurology (EHMdL, SA-A), Center of Neuroimmunology, Hospital Clinic of Barcelona, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; Department of Statistics (CT), University of British Columbia, Vancouver, Canada; Department of Neruology (A-LN), University of Melbourne, Melbourne, Australia; Royal Melbourne Hospital (A-LN), Melbourne, Australia; and Departments of Clinical Neurosciences and Surgery (Ophthalmology) (FC), University of Calgary, Clinician Scientist with the Hotchkiss Brain Institute (HBI), Calgary, Canada.
Department of Neurology and Neurotherapeutics (SCB), University of Texas Southwestern Medical Center, Dallas, Texas.

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