Exposure to TNF inhibitors is rare at MOGAD presentation

Redenbaugh, Vyanka; Flanagan, Eoin P.; Floris, V; Zara, Pietro; Bhatti, M. Tariq; Sánchez, Francisco; Koster, Matthew J.; Mariotto, Sara; Pittock, Sean J.; Chen, John J.; Cauli, Alberto; Solla, Paolo; Sechi, Elia

doi:10.1016/j.jns.2021.120044

Cited by 8 publications

(5 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Treatment with TNF-inhibitors has been associated with an increased risk of CNS demyelination (154). Although this association seems particularly true for MS and antibodynegative CNS demyelinating disorders, onset of MOGAD in patients exposed to TNF-inhibitors seems rare (155).…”

Section: Special Settings Potentially At Higher Risk Of Neurological ...mentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

et al. 2022

Self Cite

View full text Add to dashboard Cite

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is the most recently defined inflammatory demyelinating disease of the central nervous system (CNS). Over the last decade, several studies have helped delineate the characteristic clinical-MRI phenotypes of the disease, allowing distinction from aquaporin-4 (AQP4)-IgG-positive neuromyelitis optica spectrum disorder (AQP4-IgG+NMOSD) and multiple sclerosis (MS). The clinical manifestations of MOGAD are heterogeneous, ranging from isolated optic neuritis or myelitis to multifocal CNS demyelination often in the form of acute disseminated encephalomyelitis (ADEM), or cortical encephalitis. A relapsing course is observed in approximately 50% of patients. Characteristic MRI features have been described that increase the diagnostic suspicion (e.g., perineural optic nerve enhancement, spinal cord H-sign, T2-lesion resolution over time) and help discriminate from MS and AQP4+NMOSD, despite some overlap. The detection of MOG-IgG in the serum (and sometimes CSF) confirms the diagnosis in patients with compatible clinical-MRI phenotypes, but false positive results are occasionally encountered, especially with indiscriminate testing of large unselected populations. The type of cell-based assay used to evaluate for MOG-IgG (fixed vs. live) and antibody end-titer (low vs. high) can influence the likelihood of MOGAD diagnosis. International consensus diagnostic criteria for MOGAD are currently being compiled and will assist in clinical diagnosis and be useful for enrolment in clinical trials. Although randomized controlled trials are lacking, MOGAD acute attacks appear to be very responsive to high dose steroids and plasma exchange may be considered in refractory cases. Attack-prevention treatments also lack class-I data and empiric maintenance treatment is generally reserved for relapsing cases or patients with severe residual disability after the presenting attack. A variety of empiric steroid-sparing immunosuppressants can be considered and may be efficacious based on retrospective or prospective observational studies but prospective randomized placebo-controlled trials are needed to better guide treatment. In summary, this article will review our rapidly evolving understanding of MOGAD diagnosis and management.

show abstract

Section: Special Settings Potentially At Higher Risk Of Neurological ...mentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

“…Contrary to promising preclinical results of TNF blockade, however, the success of TNF suppression in MS patients did not yield uniformly positive results ( 274 ). For MOGAD in relation to TNF treatment, little is known and data from a small retrospective study ( n = 5) is inconclusive regarding negative effects, however also no clear positive outcome is documented ( 275 ). Primary progressive-EAE (PP-EAE) was further established in A.SW mice sensitized with MOG 92−106 and SJL/J mice sensitized with MOG 92−106 and curdlan ( 276 ).…”

Section: Are Mog and Mog-igg-induced Animal Models Good Models For Mo...mentioning

confidence: 99%

Delimiting MOGAD as a disease entity using translational imaging

Oertel,

Hastermann,

Paul

2023

Front. Neurol.

View full text Add to dashboard Cite

The first formal consensus diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) were recently proposed. Yet, the distinction of MOGAD-defining characteristics from characteristics of its important differential diagnoses such as multiple sclerosis (MS) and aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorder (NMOSD) is still obstructed. In preclinical research, MOG antibody-based animal models were used for decades to derive knowledge about MS. In clinical research, people with MOGAD have been combined into cohorts with other diagnoses. Thus, it remains unclear to which extent the generated knowledge is specifically applicable to MOGAD. Translational research can contribute to identifying MOGAD characteristic features by establishing imaging methods and outcome parameters on proven pathophysiological grounds. This article reviews suitable animal models for translational MOGAD research and the current state and prospect of translational imaging in MOGAD.

show abstract

“…For instance, the association between TNF inhibition and CNS demyelination has been well-documented in the literature. However, the association of TNFI and ICI with disorders such as MOGAD or NMOSD is less clear, and these antibodies have been infrequently reported ( 112 ). In particular, TNF alpha levels have been shown to be elevated in CSF in patients with AQP4 and MOG IgG autoimmunity, but not in patients with MS, and therefore the effect of TNF inhibition is likely different in these CNS inflammatory disorders ( 113 ).…”

Section: Discussionmentioning

confidence: 99%

Drug-related immune-mediated myelopathies

Gritsch

Valencia‐Sánchez²

2022

Front. Neurol.

View full text Add to dashboard Cite

Iatrogenic immune-mediated inflammatory disorders of the spinal cord are an uncommon but potentially severe complication of drug therapy for several human diseases. Particularly the introduction of novel biological agents in the treatment of systemic inflammatory disorders and cancer immunotherapy have led to a significant increase in immune-related adverse events of the central nervous system (CNS). The use of Tumor necrosis factor alpha (TNF-alpha) inhibitors in rheumatic and inflammatory bowel diseases has been associated with demyelinating and other inflammatory CNS conditions, including myelitis. The introduction of immune checkpoint inhibitors in the treatment of several human malignancies has led to an increase in drug-induced immune-related adverse events including in the CNS. Other drugs that have been associated with immune-mediated myelitis include tyrosine-kinase inhibitors and chimeric antigen receptor (CAR) T Cell therapy. A high degree of suspicion is necessary when diagnosing these conditions, as early diagnosis and treatment is crucial in preventing further neurological damage and disability. The treatment of drug-induced inflammatory myelitis typically involves administration of high-dose intravenous corticosteroids, however additional immunosuppressive agents may be required in severe or refractory cases. While most cases are monophasic and remit following discontinuation of the offending agent, chronic immunosuppressive therapy may be indicated in cases with a progressive or relapsing disease course or when a diagnosis of a specific underlying neuro-inflammatory disorder is made. Outcomes are generally favorable, however depend on the specific therapeutic agent used, the clinical presentation and patient factors. In this review we aim to describe the clinical characteristics, imaging findings and management for the most common forms of iatrogenic immune-mediated myelopathies.

show abstract

Exposure to TNF inhibitors is rare at MOGAD presentation

Cited by 8 publications

References 12 publications

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management

Delimiting MOGAD as a disease entity using translational imaging

Drug-related immune-mediated myelopathies

Contact Info

Product

Resources

About