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Published on: April 15, 2014
Failure of alemtuzumab therapy in three patients with MOG antibody associated disease
Sinali O Seneviratne1,2, Mark Marriott2, Sudarshini Ramanathan3,4,5
1Curtin University, Kent Street, Bentley, Perth, WA, 6102, Australia.
Background:
Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) is most classically associated in both children and adults with phenotypes including bilateral and recurrent optic neuritis (ON) and transverse myelitis (TM), with the absence of brain lesions characteristic of multiple sclerosis (MS). ADEM phenotype is the most common presentation of MOGAD in children. However, the presence of clinical phenotypes including unilateral ON and short TM in some patients with MOGAD may lead to their misdiagnosis as MS. Thus, clinically and radiologically, MOGAD can mimic MS and clinical vigilance is required for accurate diagnostic workup.
Case Presentation:
We present three cases initially diagnosed as MS and then treated with alemtuzumab. Unexpectedly, all three patients did quite poorly on this medication, with a decline in their clinical status with worsening of expanded disability status scale (EDSS) and an increasing lesion load on magnetic resonance imaging of the brain. Subsequently, all three cases were found to have anti-MOG antibody in their serum.
Conclusions:
These cases highlight that if a patient suspected to have MS does not respond to conventional treatments such as alemtuzumab, a search for alternative diagnoses such as MOG antibody disease may be warranted.
Insights
Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) can mimic multiple sclerosis (MS). If MS patients do not respond to treatments like alemtuzumab, consider MOGAD for accurate diagnosis and care.
Area of Science:
- Neuroimmunology
- Neurology
Background:
- Myelin Oligodendrocyte Glycoprotein antibody-associated disease (MOGAD) presents with optic neuritis and transverse myelitis, often without brain lesions typical of multiple sclerosis (MS).
- Pediatric MOGAD commonly manifests as ADEM, but unilateral optic neuritis and short transverse myelitis can lead to misdiagnosis as MS.
Observation:
- Three patients initially diagnosed with MS and treated with alemtuzumab experienced clinical decline and increased brain lesion load.
- These patients showed poor response to alemtuzumab, a conventional MS treatment.
Findings:
- All three patients were subsequently found to have anti-MOG antibodies in their serum.
- This indicates a misdiagnosis of MS when the underlying condition was MOGAD.
Implications:
- Failure to respond to MS therapies like alemtuzumab warrants investigation for alternative diagnoses, including MOGAD.
- Accurate differentiation between MOGAD and MS is crucial for appropriate patient management and treatment selection.
