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Free keywords:
MYELIN OLIGODENDROCYTE GLYCOPROTEIN; PEDIATRIC MULTIPLE-SCLEROSIS;
GUILLAIN-BARRE-SYNDROME; DEMYELINATING DISEASES; ANTIMYELIN ANTIBODIES;
BASIC-PROTEIN; AUTOANTIBODIES; SPECIFICITY; CHILDREN; ASSOCIATIONClinical Neurology;
Abstract:
Objective: To study the longitudinal dynamics of anti-myelin
oligodendrocyte glycoprotein (MOG) autoantibodies in childhood
demyelinating diseases.
Methods: We addressed the kinetics of anti-MOG immunoglobulins in a
prospective study comprising 77 pediatric patients. This was
supplemented by a cross-sectional study analyzing 126 pediatric
patients with acute demyelination and 62 adult patients with multiple
sclerosis (MS). MOG-transfected cells were used for detection of
antibodies by flow cytometry.
Results: Twenty-five children who were anti-MOG immunoglobulin (Ig)
positive at disease onset were followed for up to 5 years. Anti-MOG
antibodies rapidly and continuously declined in all 16 monophasic
patients with acute disseminated encephalomyelitis and in one patient
with clinically isolated syndrome. In contrast, in 6 of 8 patients
(75%) eventually diagnosed with childhood MS, the antibodies to MOG
persisted with fluctuations showing a second increase during an
observation period of up to 5 years. Antibodies to MOG were mainly IgG
1 and their binding was largely blocked by pathogenic anti-MOG
antibodies derived from a spontaneous animal model of autoimmune
encephalitis. The cross-sectional part of our study elaborated that
anti-MOG Ig was present in about 25% of children with acute
demyelination, but in none of the pediatric or adult controls. Sera
from 4/62 (6%) adult patients with MS had anti-MOG IgG at low levels.
Conclusions: The persistence or disappearance of antibodies to MOG may
have prognostic relevance for acute childhood demyelination. Neurology
(R) 2011;77:580-588
