Pathological cerebrospinal fluid protein concentration and albumin quotient at relapse predicts short-term disability progression in multiple sclerosis: a retrospective single center observational study.

EDSS albumin quotient cerebrospinal fluid progression protein

Journal

Therapeutic advances in neurological disorders
ISSN: 1756-2856
Titre abrégé: Ther Adv Neurol Disord
Pays: England
ID NLM: 101480242

Informations de publication

Date de publication:
2020
Historique:
received: 23 08 2020
accepted: 27 10 2020
entrez: 15 1 2021
pubmed: 16 1 2021
medline: 16 1 2021
Statut: epublish

Résumé

Blood-brain barrier dysfunction in active multiple sclerosis (MS) lesions leads to pathological changes of cerebrospinal fluid (CSF). Theoretically, CSF analyses could help to predict relapse recovery and the course of disability. In this monocentric study, we investigated the impact of CSF findings assessed during the first relapse of MS on the short-term course of disability. We performed a retrospective observational study including MS patients with available CSF data after onset of first MS relapse. Clinical symptoms had to be accompanied by gadolinium-enhanced lesion on magnetic resonance imaging. Expanded Disability Status Scale (EDSS) assessments at timepoint of relapse and after relapse recovery were studied to analyze disability. A two-step multivariate linear regression analysis adjusted for EDSS at spinal tab, duration of symptoms, sex, time until post relapse EDSS assessment, immunotherapy post relapse, and relapse treatment with glucocorticoids/plasma exchange to predict relapse associated disability was run. In the first step of the regression model, pathological albumin quotient (QAlb) [regression coefficient 0.50, 95% confidence interval (CI) (0.07-0.92), Our study conducted in MS patients during first relapse confirmed that both increased CSF protein concentration and pathological QAlb have a negative impact on EDSS after relapse. As secondary finding, we identified time from symptom onset to lumbar puncture as predictor of disability recovery after relapse.

Sections du résumé

BACKGROUND BACKGROUND
Blood-brain barrier dysfunction in active multiple sclerosis (MS) lesions leads to pathological changes of cerebrospinal fluid (CSF). Theoretically, CSF analyses could help to predict relapse recovery and the course of disability. In this monocentric study, we investigated the impact of CSF findings assessed during the first relapse of MS on the short-term course of disability.
METHODS METHODS
We performed a retrospective observational study including MS patients with available CSF data after onset of first MS relapse. Clinical symptoms had to be accompanied by gadolinium-enhanced lesion on magnetic resonance imaging. Expanded Disability Status Scale (EDSS) assessments at timepoint of relapse and after relapse recovery were studied to analyze disability. A two-step multivariate linear regression analysis adjusted for EDSS at spinal tab, duration of symptoms, sex, time until post relapse EDSS assessment, immunotherapy post relapse, and relapse treatment with glucocorticoids/plasma exchange to predict relapse associated disability was run.
RESULTS RESULTS
In the first step of the regression model, pathological albumin quotient (QAlb) [regression coefficient 0.50, 95% confidence interval (CI) (0.07-0.92),
DISCUSSION CONCLUSIONS
Our study conducted in MS patients during first relapse confirmed that both increased CSF protein concentration and pathological QAlb have a negative impact on EDSS after relapse. As secondary finding, we identified time from symptom onset to lumbar puncture as predictor of disability recovery after relapse.

Identifiants

pubmed: 33447262
doi: 10.1177/1756286420975909
pii: 10.1177_1756286420975909
pmc: PMC7780321
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1756286420975909

Informations de copyright

© The Author(s), 2020.

Déclaration de conflit d'intérêts

Conflict of interest statement: The authors declare that there is no conflict of interest.

Références

Mult Scler. 2016 May;22(6):770-81
pubmed: 26362893
Arq Neuropsiquiatr. 2016 Jun;74(6):501-12
pubmed: 27332077
Front Immunol. 2019 Jan 10;9:3116
pubmed: 30687321
Arch Psychiatr Nervenkr (1970). 1983;232(6):521-32
pubmed: 6860119
Neurol Neuroimmunol Neuroinflamm. 2019 Jun 18;6(5):e584
pubmed: 31355320
JAMA Neurol. 2019 Jul 1;76(7):841-849
pubmed: 31034002

Auteurs

Lara Diem (L)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Freiburgstrasse, Bern, 3010, Switzerland.

Maxine Bürge (M)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

Alexander Leichtle (A)

University Institute of Clinical Chemistry, Inselspital, Bern University Hospital, University of Bern, Switzerland.

Arsany Hakim (A)

University Institute of Diagnostic and Interventional Neuroradiology, Bern University Hospital, Inselspital, University of Bern, Bern, Switzerland.

Andrew Chan (A)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

Anke Salmen (A)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

Maria-Eleptheria Evangelopoulos (ME)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

Robert Hoepner (R)

Department of Neurology, Inselspital, Bern University Hospital and University of Bern, Bern, Switzerland.

Classifications MeSH