Myelin oligodendrocyte glycoprotein (MOG) antibodies in a patient with glioblastoma: Red flags for false positivity

2021 ◽  
pp. 577743
Author(s):  
Moein Amin ◽  
MaryAnn Mays ◽  
David Polston ◽  
Eoin P. Flanagan ◽  
Richard Prayson ◽  
...  
Neurology ◽  
2021 ◽  
Vol 96 (15) ◽  
pp. e2006-e2015
Author(s):  
Nicolas Collongues ◽  
Cecilia Alves Do Rego ◽  
Bertrand Bourre ◽  
Damien Biotti ◽  
Romain Marignier ◽  
...  

ObjectiveTo analyze the effects of pregnancy on neuromyelitis optica spectrum disorder (NMOSD) according to patients' serostatus and immunosuppressive therapy (IST).MethodsWe performed a retrospective multicenter international study on patients with NMOSD. Patients were tested for aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies (Ab). Informative pregnancies were reported when NMOSD onset occurred before or during pregnancy or up to 12 months postpartum. The mean annualized relapse rate (ARR) was calculated for the 12 months before conception, for each trimester of pregnancy, and postpartum. Events such as miscarriage, abortion, and preeclampsia were reported. IST was considered if taken in the 3 months before or during pregnancy.ResultsWe included 89 pregnancies (46 with AQP4-Ab, 30 with MOG-Ab, and 13 without either Ab) in 58 patients with NMOSD. Compared to the prepregnancy period, the ARR was lower during pregnancy in each serostatus group and higher during the postpartum period in patients with AQP4-Ab (p < 0.01). Forty-eight percent (n = 31) of pregnancies occurred during IST and these patients presented fewer relapses during pregnancy and the 12 months postpartum than untreated patients (26% vs 53%, p = 0.04). Miscarriages occurred in 10 (11%) pregnancies, and were mainly in patients with AQP4-Ab (with or without IST) and a previous history of miscarriage. Preeclampsia was reported in 2 (2%) patients who were AQP4-Ab-positive.ConclusionWe found a rebound in the ARR during the first postpartum trimester that was higher than the prepregnancy period only in AQP4-Ab-positive patients. Taking IST just before or during pregnancy reduces the risk of relapses in these conditions.


2007 ◽  
Vol 13 (1) ◽  
pp. 7-16 ◽  
Author(s):  
S J Pittock ◽  
M Reindl ◽  
S Achenbach ◽  
T Berger ◽  
W Bruck ◽  
...  

Controversy exists regarding the pathogenic or predictive role of anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with multiple sclerosis (MS). Four immunopathological patterns (IP) have been recognized in early active MS lesions, suggesting heterogeneous pathogenic mechanisms. Whether MOG antibodies contribute to this pathological heterogeneity and potentially serve as biomarkers to identify specific pathological patterns is unknown. Here we report the frequencies of antibodies to human recombinant MOG (identified by Western blot and enzymelinked immunoabsorbent assay (ELISA)) in patients with pathologically proven demyelinating disease, and investigate whether antibody status is associated with clinical course, HLA-DR2 genotype, IP or treatment response to plasmapheresis. The biopsy cohort consisted of 72 patients: 12 pattern I, 43 pattern II and 17 pattern III. No association was found between MOG antibody status and conversion to clinically definite MS, DR-2 status, IP or response to plasmapheresis. There was poor agreement between Western blot and ELISA (kappa=0.07 for MOG IgM). Fluctuations in antibody seropositivity were seen for 3/4 patients tested serially by Western blot. This study does not support a pathologic pattern-specific role for MOG-antibodies. Variable MOG-antibody status on serial measurements, coupled with the lack of Western blot and ELISA correlations, raises concern regarding the use of MOG-antibody as an MS biomarker and underscores the need for methodological consensus.


Author(s):  
JD Krett ◽  
H Hou ◽  
K Alikhani ◽  
MJ Fritzler ◽  
JM Burton

Background: Despite the availability of cell-based assays for aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies provincially, outside confirmatory testing is often performed (typically Mayo Clinic Laboratories, USA) when results deviate from expected. It is unknown how often this costly undertaking (upwards of $1,200 CAN) alters diagnosis and management. Methods: We undertook a quality improvement project evaluating the concordance/discordance rate with select chart review in all patients who had cell-based AQP4 or MOG IgG antibody testing at Mitogen Diagnostics (MitogenDx; Calgary, Alberta) and subsequent testing at Mayo Clinic Laboratories from as early as 2010 to July 2020. Results: Preliminary review of data from January 2016 to July 2020 retrieved 145 paired tests; 10 of which were discordant (concordance rate: 93.1%). Chart review confirmed 9 truly discordant cases, often associated with AQP4 or MOG weak-positive results (7/9 cases) or presumed false negative AQP4 results in prototypical neuromyelitis optica spectrum disorder (2/9 cases). Conclusions: Discordant results were rare when comparing MitogenDx local AQP4/MOG antibody test results to those referred out to Mayo Clinic Laboratories, impacting diagnosis and treatment in only 3 patients out of the total. Our results suggest costly outside confirmatory testing of AQP4/MOG antibodies could be reduced.


2021 ◽  
Vol 12 ◽  
Author(s):  
Keita Takahashi ◽  
Hideyuki Takeuchi ◽  
Ryoko Fukai ◽  
Haruko Nakamura ◽  
Keisuke Morihara ◽  
...  

Here we report three cases of anti-myelin oligodendrocyte glycoprotein (MOG) antibody–associated disease (MOGAD) mimicking multiple sclerosis in which seropositivity for anti-MOG antibodies occurred during disease-modifying drug dimethyl fumarate (DMF) treatment. These patients developed relapses with anti-MOG antibody seroconversion after switching from fingolimod or steroid pulse therapy to DMF, which was associated with peripheral lymphocyte recovery. MOGAD is considered a humoral immune disease, and DMF reportedly enhances Th2-skewed humoral immune activity. Therefore, we suggest that DMF, but not fingolimod, may exacerbate humoral immune imbalance and enhance autoantibody production, leading to aggravation of MOGAD.


2018 ◽  
Vol 387 ◽  
pp. 170-173 ◽  
Author(s):  
Josef Maxwell Gutman ◽  
Mark Kupersmith ◽  
Steven Galetta ◽  
Ilya Kister

2010 ◽  
Vol 17 (3) ◽  
pp. 297-302 ◽  
Author(s):  
PH Lalive ◽  
MG Häusler ◽  
H Maurey ◽  
Y Mikaeloff ◽  
M Tardieu ◽  
...  

Background: Myelin oligodendrocyte glycoprotein (MOG) may be implicated in the immunopathogenesis of multiple sclerosis (MS) inducing demyelination in the animal model of MS. In adults reported anti-MOG antibody frequencies have been variable across a number of studies and can also be detected in controls. Objective: To measure antibodies against MOG in paediatric patients with demyelinating disorders of the central nervous system and in controls. Methods: Serum antibodies against MOG and myelin basic protein were measured by ELISA, flow cytometry (FACS) and in the liquid phase in 11 children with acute disseminated encephalomyelitis (ADEM), 22 children with MS, seven children with acute viral encephalitis and 13 healthy controls. The serostatus of Epstein–Barr virus (EBV) infections were assessed. Results: Anti-MOG antibodies, measured either by ELISA or FACS were exclusively detected in children with demyelination. In ADEM these antibodies were highly reactive. Anti-MBP reactivity was detectable equally in all groups. The presence of either autoantibodies did not associate with EBV serostatus, age, gender or disease course. Conclusions: This study independently corroborates recently published results of seroprevalence and specificity of the assay. Due to their low sensitivity anti-MOG antibodies will not serve as disease-specific biomarkers, but could help to support the diagnosis of ADEM in difficult cases.


2020 ◽  
Vol 26 (11) ◽  
pp. 1441-1443
Author(s):  
Romain Deschamps ◽  
Guillaume Poillon ◽  
Alexandre Marill ◽  
Romain Marignier ◽  
Olivier Gout ◽  
...  

An 87-year-old man presented with a 2-day history of painful bilateral visual loss. On examination, exophthalmos, lid edema, chemosis, and optic disc edema, on the left side only, were found. Visual acuity was 4/10 OD and no light perception OS. Magnetic resonance imaging (MRI) revealed bilateral optic neuritis and a diffuse and severe infiltration of the intra- and extraconal fat on the left. Laboratory testing was negative except for serum myelin oligodendrocyte glycoprotein (MOG) antibodies. This presentation adds a new variant to the MOG-associated disease spectrum. Testing for MOG antibodies should be considered in patients presenting with diffuse orbital inflammation and optic neuritis.


2019 ◽  
Vol 50 (05) ◽  
pp. 273-279 ◽  
Author(s):  
Jonathan D. Santoro ◽  
Tanuja Chitnis

AbstractAcute disseminated encephalomyelitis (ADEM) is a common yet clinically heterogenous syndrome characterized by encephalopathy, focal neurologic findings, and abnormal neuroimaging. Differentiating ADEM from other demyelinating disorders of childhood can be difficult and appropriate interpretation of the historical, clinical, and neurodiagnostic components of a patient's presentation is critical. Myelin oligodendrocyte glycoprotein (MOG) antibody-associated diseases are a recently recognized set of disorders, which include ADEM presentations, among other phenotypes. This review article discusses the clinical diagnosis, differential diagnosis, interpretation of data, and treatment/prognosis of this unique syndrome with distinctive review of the spectrum of MOG antibodies.


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