ECTRIMS eLearning

Acute Tumefactive Demyelination in a patient on Rituximab; a case report
ECTRIMS Learn. Chaudhry B. 10/25/17; 199659; EP1639
Burhan Chaudhry
Burhan Chaudhry
Contributions
Abstract

Abstract: EP1639

Type: ePoster

Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression

Introduction: Recent clinical trials demonstrating the efficacy ofCD20-depleting agents like rituximab, ocrelizumab, and ofatumumab have highlighted the importance of B cells in MS pathogenesis. Although rituximab has extensive use in other autoimmune disorders, relatively limited data exist regarding rituximab real world MS use. We report a case of tumefactive inflammatory demyelination in a relapsing remitting multiple sclerosis (RRMS) patient during rituximab therapy.
Case report: A 55 year old man with RRMS, diagnosed in 2013, was started on rituximab 1000mg IV every 6 months after having continued activity despite treatment with IV methylprednisolone, glatiramer acetate, natalizumab, and cyclophosphamide. He remained stable clinically and radiographically for 2.5 years. Six weeks after his fifth cycle, he developed urinary urgency, left hemiplegia and ataxia. Brain MRI demonstrated a large right parietal lobe lesion with incomplete ring enhancement, surrounding edema, and mild mass effect. His cervical and thoracic spine MRI showed several enhancing lesions. Due to the concern for progressive multifocal leukoencephalopathy, as he was JCV antibody positive, and lymphoma, he was hospitalized. CSF demonstrated signs of active inflammation but was negative for infectious causes including JCV PCR. Flow cytometry revealed no repopulation of B cells. After failing to improve with 5 days of IV methylprednisolone, 5 plasma Exchange resulted in improvement in his clinical symptoms and improvement of his lesion on neuroimaging. Subsequent therapy currently is under consideration - alemtuzumab, adding an immunosuppressant agent to rituximab, or autologous hematopoietic stem cell transplantation.
Discussion: Extensive literature review did not yield any previous reports of tumefactive lesion in a rituximab treated patient. Rather, rituximab is sometimes listed as a potential treatment for this condition. This report calls for need for heighten surveillance of MS patient with highly active MS on B cell modulation and raises questions on the best approach going forward.
Disclosure: Burhan Chaudhry: nothing to disclose
Mary A. Willis: I have received compensation for speaking for Genzyme and Biogen
Jeffrey A. Cohen: I have received consulting fees from Adamas, Merck, Mallinckrodt, Novartis, and Receptos and compensation as Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical

Abstract: EP1639

Type: ePoster

Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression

Introduction: Recent clinical trials demonstrating the efficacy ofCD20-depleting agents like rituximab, ocrelizumab, and ofatumumab have highlighted the importance of B cells in MS pathogenesis. Although rituximab has extensive use in other autoimmune disorders, relatively limited data exist regarding rituximab real world MS use. We report a case of tumefactive inflammatory demyelination in a relapsing remitting multiple sclerosis (RRMS) patient during rituximab therapy.
Case report: A 55 year old man with RRMS, diagnosed in 2013, was started on rituximab 1000mg IV every 6 months after having continued activity despite treatment with IV methylprednisolone, glatiramer acetate, natalizumab, and cyclophosphamide. He remained stable clinically and radiographically for 2.5 years. Six weeks after his fifth cycle, he developed urinary urgency, left hemiplegia and ataxia. Brain MRI demonstrated a large right parietal lobe lesion with incomplete ring enhancement, surrounding edema, and mild mass effect. His cervical and thoracic spine MRI showed several enhancing lesions. Due to the concern for progressive multifocal leukoencephalopathy, as he was JCV antibody positive, and lymphoma, he was hospitalized. CSF demonstrated signs of active inflammation but was negative for infectious causes including JCV PCR. Flow cytometry revealed no repopulation of B cells. After failing to improve with 5 days of IV methylprednisolone, 5 plasma Exchange resulted in improvement in his clinical symptoms and improvement of his lesion on neuroimaging. Subsequent therapy currently is under consideration - alemtuzumab, adding an immunosuppressant agent to rituximab, or autologous hematopoietic stem cell transplantation.
Discussion: Extensive literature review did not yield any previous reports of tumefactive lesion in a rituximab treated patient. Rather, rituximab is sometimes listed as a potential treatment for this condition. This report calls for need for heighten surveillance of MS patient with highly active MS on B cell modulation and raises questions on the best approach going forward.
Disclosure: Burhan Chaudhry: nothing to disclose
Mary A. Willis: I have received compensation for speaking for Genzyme and Biogen
Jeffrey A. Cohen: I have received consulting fees from Adamas, Merck, Mallinckrodt, Novartis, and Receptos and compensation as Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical

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