Blood parameters in pediatric myelin oligodendrocyte glycoprotein antibody-associated disorders.

(2) MOG antibodies (3) children (4) autoimmune (5) MS 1) cell count

Journal

European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society
ISSN: 1532-2130
Titre abrégé: Eur J Paediatr Neurol
Pays: England
ID NLM: 9715169

Informations de publication

Date de publication:
24 Apr 2024
Historique:
received: 25 08 2023
revised: 16 04 2024
accepted: 23 04 2024
medline: 6 5 2024
pubmed: 6 5 2024
entrez: 5 5 2024
Statut: aheadofprint

Résumé

Patients with myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD) clinically present e.g. with acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), transverse myelitis (TM) or aquaporin-4-IgG (AQP4-IgG) negative neuromyelitis optica spectrum disorders (NMOSD)-like phenotypes. We aimed to analyze and compare blood parameters in children with MOGAD, AQP4-IgG-positive NMOSD (hence NMOSD), multiple sclerosis (MS) and healthy controls (HC). We evaluated differences in complete blood counts (CBC), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR) and C-reactive protein (CRP) between these four groups and within the groups between clinical attack, acute treatment and remission. Our cohort consisted of 174 children and adolescents with a total of 550 timepoints: 66 patients had MOGAD (202 timepoints), 11 NMOSD (76 timepoints), 58 MS (219 timepoints) and 39 were HC (53 timepoints). At clinical attack, leukocyte counts were elevated in MOGAD compared to remission (p < 0.001) and compared to all other groups (p < 0.001). NLR was high in MOGAD and NMOSD, and PLR was high in NMOSD, however, after correction for multiple testing these findings did not remain significant. While glucocorticoids caused an increase of leukocyte counts and NLR in NMOSD and MS, these values remained stable during acute treatment in MOGAD. In remission, NLR normalized in MOGAD, while it stayed high in NMOSD. PLR increased in NMOSD and was significantly higher compared to all other groups. Some blood parameters, mainly leukocyte and differential counts, might help clinicians to evaluate disease activity, differentiate relapses from pseudo-relapses and even distinguish between different disease entities.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
Patients with myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD) clinically present e.g. with acute disseminated encephalomyelitis (ADEM), optic neuritis (ON), transverse myelitis (TM) or aquaporin-4-IgG (AQP4-IgG) negative neuromyelitis optica spectrum disorders (NMOSD)-like phenotypes. We aimed to analyze and compare blood parameters in children with MOGAD, AQP4-IgG-positive NMOSD (hence NMOSD), multiple sclerosis (MS) and healthy controls (HC).
METHODS METHODS
We evaluated differences in complete blood counts (CBC), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR) and C-reactive protein (CRP) between these four groups and within the groups between clinical attack, acute treatment and remission.
RESULTS RESULTS
Our cohort consisted of 174 children and adolescents with a total of 550 timepoints: 66 patients had MOGAD (202 timepoints), 11 NMOSD (76 timepoints), 58 MS (219 timepoints) and 39 were HC (53 timepoints). At clinical attack, leukocyte counts were elevated in MOGAD compared to remission (p < 0.001) and compared to all other groups (p < 0.001). NLR was high in MOGAD and NMOSD, and PLR was high in NMOSD, however, after correction for multiple testing these findings did not remain significant. While glucocorticoids caused an increase of leukocyte counts and NLR in NMOSD and MS, these values remained stable during acute treatment in MOGAD. In remission, NLR normalized in MOGAD, while it stayed high in NMOSD. PLR increased in NMOSD and was significantly higher compared to all other groups.
DISCUSSION CONCLUSIONS
Some blood parameters, mainly leukocyte and differential counts, might help clinicians to evaluate disease activity, differentiate relapses from pseudo-relapses and even distinguish between different disease entities.

Identifiants

pubmed: 38705015
pii: S1090-3798(24)00057-6
doi: 10.1016/j.ejpn.2024.04.011
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

86-95

Informations de copyright

© 2024 Published by Elsevier Ltd on behalf of European Paediatric Neurology Society.

Déclaration de conflit d'intérêts

Declaration of competing interest Alina Peternell, Christian Lechner, Mareike Schimmel, Joachim Zobel, Martin Preisel, Eva-Maria Wendel and Astrid Eisenkölbl have nothing to declare. Markus Breu received speaker honoraria from Sanofi Genzyme. Markus Reindl is supported by research grants from the Euroimmun, and Roche, and consulting fees and advisory board from Roche (to institution). Markus Reindl works at the Clinical Department of the Medical University of Innsbruck (Innsbruck, Austria), which offers diagnostic testing for MOG-IgG and other autoantibodies. Matthias Baumann received compensation for advisory boards and speaker honoraria from Novartis, Biogen, and Roche. Kevin Rostásy serves as consultant for Roche in Operetta II trial and received speaker’ honoraria from Merck.

Auteurs

Alina Peternell (A)

Division of Pediatric Neurology, Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria.

Christian Lechner (C)

Division of Pediatric Neurology, Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria.

Markus Breu (M)

Division of Pediatric Pulmonology, Allergology and Endocrinology, Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.

Martin Preisel (M)

Department of Pediatric Neurology, Paracelsus Medical University Salzburg, Salzburg, Austria.

Mareike Schimmel (M)

Division of Pediatric Neurology, Children's Hospital, Medical University of Augsburg, Augsburg, Germany.

Astrid Eisenkölbl (A)

Department of Pediatrics and Adolescent Medicine, Johannes Kepler University Linz, Kepler University Hospital, Linz, Austria.

Joachim Zobel (J)

Division of Pediatric Neurology, Department of Pediatrics, Medical University of Graz, Graz, Austria.

Eva-Maria Wendel (EM)

Department of Pediatric Neurology, Olgahospital Stuttgart, Stuttgart, Germany.

Markus Reindl (M)

Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Kevin Rostásy (K)

Department of Pediatric Neurology, Children's Hospital Datteln, University Witten/Herdecke, Datteln, Germany.

Matthias Baumann (M)

Division of Pediatric Neurology, Department of Pediatrics I, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: Matthias.baumann@tirol-kliniken.at.

Classifications MeSH