Limits...
Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus

Longitudinal follow-up of MOG-seropositive patients of up to 6 years reveals fluctuating anti-MOG antibody levels. Longitudinal serum samples were available for two of the four anti-MOG antibody-positive patients. Serum samples were taken 30 or 29 years after disease onset over a time course of about 2 or 6 years (22 or 74 months). Anti-MOG reactivity is expressed as the geometric mean channel fluorescence (GMCF) ratio. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). The arrow indicates a clinical relapse. Antibodies against MOG fluctuated over the disease course: An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of disease activity in the other patient (STB02).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4359547&req=5

Fig3: Longitudinal follow-up of MOG-seropositive patients of up to 6 years reveals fluctuating anti-MOG antibody levels. Longitudinal serum samples were available for two of the four anti-MOG antibody-positive patients. Serum samples were taken 30 or 29 years after disease onset over a time course of about 2 or 6 years (22 or 74 months). Anti-MOG reactivity is expressed as the geometric mean channel fluorescence (GMCF) ratio. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). The arrow indicates a clinical relapse. Antibodies against MOG fluctuated over the disease course: An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of disease activity in the other patient (STB02).

Mentions: Longitudinal follow-up samples, which were available in two patients with anti-MOG antibodies, showed fluctuating antibody levels over the follow-up period of 22 and 74 months (Figure 3). An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of any disease activity in another patient (STB02) (Figure 3).Figure 3


Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Longitudinal follow-up of MOG-seropositive patients of up to 6 years reveals fluctuating anti-MOG antibody levels. Longitudinal serum samples were available for two of the four anti-MOG antibody-positive patients. Serum samples were taken 30 or 29 years after disease onset over a time course of about 2 or 6 years (22 or 74 months). Anti-MOG reactivity is expressed as the geometric mean channel fluorescence (GMCF) ratio. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). The arrow indicates a clinical relapse. Antibodies against MOG fluctuated over the disease course: An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of disease activity in the other patient (STB02).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359547&req=5

Fig3: Longitudinal follow-up of MOG-seropositive patients of up to 6 years reveals fluctuating anti-MOG antibody levels. Longitudinal serum samples were available for two of the four anti-MOG antibody-positive patients. Serum samples were taken 30 or 29 years after disease onset over a time course of about 2 or 6 years (22 or 74 months). Anti-MOG reactivity is expressed as the geometric mean channel fluorescence (GMCF) ratio. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). The arrow indicates a clinical relapse. Antibodies against MOG fluctuated over the disease course: An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of disease activity in the other patient (STB02).
Mentions: Longitudinal follow-up samples, which were available in two patients with anti-MOG antibodies, showed fluctuating antibody levels over the follow-up period of 22 and 74 months (Figure 3). An increase of anti-MOG antibodies was associated in one patient (STB01) with an increased relapse frequency, but was independent of any disease activity in another patient (STB02) (Figure 3).Figure 3

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus