065 Presence of anti-myelin oligodendrocyte glycoprotein antibodies in the serum of two patients following alemtuzumab therapy for suspected multiple sclerosis
| Autor: | Mastura Monif, Mark Marriott, Sinali O. Seneviratne |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
medicine.medical_specialty
Neuromyelitis optica Expanded Disability Status Scale biology business.industry Multiple sclerosis Encephalomyelitis medicine.disease Gastroenterology Myelin oligodendrocyte glycoprotein Psychiatry and Mental health Internal medicine medicine biology.protein Alemtuzumab Surgery Optic neuritis Rituximab Neurology (clinical) business medicine.drug |
| Zdroj: | Journal of Neurology, Neurosurgery & Psychiatry. 90:A21.2-A21 |
| ISSN: | 1468-330X 0022-3050 1756-2864 |
| DOI: | 10.1136/jnnp-2019-anzan.57 |
| Popis: | IntroductionMyelin oligodendrocyte glycoprotein (MOG) antibody mediated disease is an autoimmune demyelinating disorder which can resemble multiple sclerosis (MS).1 2 Thus, this condition can be misdiagnosed and treated as MS.3 We present the clinical trajectory of two cases initially diagnosed as MS, treated with Alemtuzumab followed by clinical and radiological deterioration. Both were subsequently found to have anti MOG antibody in their serum.MethodsThis is a retrospective case study based on a medical record search of neuroimmunology clinics in two teaching hospitals in Victoria. We searched for patients treated with Alemtuzumab who subsequently tested positive for MOG antibody.ResultsWe found two young women who fulfilled the eligibility criteria. One patient presented with dizziness and vertigo, the other with unilateral optic neuritis. Both had supratentorial MRI lesions and were both diagnosed as having MS. Both patients experienced multiple relapses while on treatment for MS. Hence, they were commenced on Alemtuzumab therapy. Unexpectedly, both patients experienced a decline in their clinical status with worsening of expanded disability status scale (EDSS) and an increasing lesion load on MRI brain. Their serum anti MOG antibodies were then found to be positive. Subsequently, patients were treated with rituximab and plasma exchange with a favorable response.ConclusionsThese two cases demonstrate that Alemtuzumab is ineffective and in fact can worsen cases of anti-MOG antibody associated encephalomyelitis. This highlights the importance of anti MOG antibody testing when patients diagnosed with MS do not respond to Alemtuzumab and in those patients presenting with atypical features of MS.ReferencesWeber MS, Derfuss T, Metz I, Bruck W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. Ther Adv Neurol Disord. 2018;11:1756286418762083.Narayan R, Simpson A, Fritsche K, Salama S, Pardo S, Mealy M, et al. MOG antibody disease: A review of MOG antibody seropositive neuromyelitis optica spectrum disorder. Mult Scler Relat Disord. 2018;25:66–72.Wildemann B, Jarius S, Schwarz A, Diem R, Viehover A, Hahnel S, et al. Failure of alemtuzumab therapy to control MOG encephalomyelitis. Neurology 2017;89(2):207–9. |
| Databáze: | OpenAIRE |
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