Contributions
Abstract: EP1803
Type: ePoster
Abstract Category: Therapy - disease modifying - 32 Others
Background and goal: To report early MRI findings in a clinically unstable patient with active MS following natalizumab cessation and during alemtuzumab initiation.
Methods: Patient case report.
Results: The patient (female, aged 39) had a 21-year history of MS, including periventricular T2 lesions, multiple T1 lesions, and signs of brain tissue loss. Prior MS treatments included SC and IM IFNB-1a, SC IFNB-1b, glatiramer acetate, fingolimod, and 2 separate periods of natalizumab (total: 75 cycles; discontinued due to disease activity and John Cunningham virus [JCV] antibody positivity). Three months after natalizumab cessation, the patient was hospitalised with severe relapse (dysarthria, diplopia, right hemiparesis); MRI showed a new, non-Gd-enhancing left midbrain lesion. Methylprednisolone and IVIG were administered. Two weeks later, the patient was confused, unable to walk, and LP showed red blood cells (RBC) 2/µL, white blood cells (WBC) 13/µL, protein 39 mg/dL, glucose 52 mg/dL, oligoclonal band-positive, and JCV PCR-negative (ARUP Laboratories). One week before alemtuzumab initiation, right hemiparesis had worsened; patient was lethargic and nonambulatory. Alemtuzumab Course 1
(12 mg; 5 consecutive days) was started 4.5 months after natalizumab cessation. On alemtuzumab
Day 3, decreased mentation, lethargy, poorly reactive left pupil, severe dysarthria, and right hemiparesis were noted. MRI after alemtuzumab Day 5 showed prominent diffuse T2 signals in juxtacortical regions of left temporal, parietal and occipital lobes, and right cerebellum. These lesions were not Gd-enhancing and were evident on diffusion-weighted imaging. Progressive multifocal leukoencephalopathy (PML) was considered; repeat CSF 10 days later demonstrated: RBC 14/µL, WBC 0/µL, protein 47 mg/dL, glucose 68 mg/dL, JCV PCR-negative (Quest Diagnostics). MRI 3 months post-alemtuzumab showed substantial resolution of previous diffuse T2 changes. At last follow-up 5.5 months post-alemtuzumab, clinical signs were improved with minimal dysarthria, mild right hemiparesis, and unassisted walking.
Conclusion: The basis of this patient's distinct MRI after discontinuing natalizumab is uncertain. Subsequent clinical and radiological improvement after alemtuzumab initiation indicates an explanation other than PML. This isolated case may suggest a beneficial role for alemtuzumab in a clinically unstable patient after natalizumab cessation, where a return of MS activity is occasionally observed.
Study support: None.
Disclosure:
JLG: Promotional speaker (Biogen, Mallinckrodt, Novartis, Sanofi Genzyme, and Teva); advisory board participant (Biogen, Genentech, Mallinckrodt, Novartis, Sanofi Genzyme, Serono, and Teva); clinical investigator (Biogen, Genentech, Novartis, and Sanofi Genzyme).
DMZ: Clinical investigator (Biogen, Genentech, Novartis, and Sanofi Genzyme).
NAB: Advisory board participant and consultant (Novocure, Inc).
AKJ, CER: Employees of Sanofi.
DP: Advisory board participant (EMD Serono, Novartis, Roche, Sanofi Genzyme, TG Therapeutics, and Vertex); grant/research support (Biogen).
Editorial support was provided by Richard Hogan, PhD, and Linda Wychowski, PhD, Envision Scientific Solutions, and was funded by Sanofi
Abstract: EP1803
Type: ePoster
Abstract Category: Therapy - disease modifying - 32 Others
Background and goal: To report early MRI findings in a clinically unstable patient with active MS following natalizumab cessation and during alemtuzumab initiation.
Methods: Patient case report.
Results: The patient (female, aged 39) had a 21-year history of MS, including periventricular T2 lesions, multiple T1 lesions, and signs of brain tissue loss. Prior MS treatments included SC and IM IFNB-1a, SC IFNB-1b, glatiramer acetate, fingolimod, and 2 separate periods of natalizumab (total: 75 cycles; discontinued due to disease activity and John Cunningham virus [JCV] antibody positivity). Three months after natalizumab cessation, the patient was hospitalised with severe relapse (dysarthria, diplopia, right hemiparesis); MRI showed a new, non-Gd-enhancing left midbrain lesion. Methylprednisolone and IVIG were administered. Two weeks later, the patient was confused, unable to walk, and LP showed red blood cells (RBC) 2/µL, white blood cells (WBC) 13/µL, protein 39 mg/dL, glucose 52 mg/dL, oligoclonal band-positive, and JCV PCR-negative (ARUP Laboratories). One week before alemtuzumab initiation, right hemiparesis had worsened; patient was lethargic and nonambulatory. Alemtuzumab Course 1
(12 mg; 5 consecutive days) was started 4.5 months after natalizumab cessation. On alemtuzumab
Day 3, decreased mentation, lethargy, poorly reactive left pupil, severe dysarthria, and right hemiparesis were noted. MRI after alemtuzumab Day 5 showed prominent diffuse T2 signals in juxtacortical regions of left temporal, parietal and occipital lobes, and right cerebellum. These lesions were not Gd-enhancing and were evident on diffusion-weighted imaging. Progressive multifocal leukoencephalopathy (PML) was considered; repeat CSF 10 days later demonstrated: RBC 14/µL, WBC 0/µL, protein 47 mg/dL, glucose 68 mg/dL, JCV PCR-negative (Quest Diagnostics). MRI 3 months post-alemtuzumab showed substantial resolution of previous diffuse T2 changes. At last follow-up 5.5 months post-alemtuzumab, clinical signs were improved with minimal dysarthria, mild right hemiparesis, and unassisted walking.
Conclusion: The basis of this patient's distinct MRI after discontinuing natalizumab is uncertain. Subsequent clinical and radiological improvement after alemtuzumab initiation indicates an explanation other than PML. This isolated case may suggest a beneficial role for alemtuzumab in a clinically unstable patient after natalizumab cessation, where a return of MS activity is occasionally observed.
Study support: None.
Disclosure:
JLG: Promotional speaker (Biogen, Mallinckrodt, Novartis, Sanofi Genzyme, and Teva); advisory board participant (Biogen, Genentech, Mallinckrodt, Novartis, Sanofi Genzyme, Serono, and Teva); clinical investigator (Biogen, Genentech, Novartis, and Sanofi Genzyme).
DMZ: Clinical investigator (Biogen, Genentech, Novartis, and Sanofi Genzyme).
NAB: Advisory board participant and consultant (Novocure, Inc).
AKJ, CER: Employees of Sanofi.
DP: Advisory board participant (EMD Serono, Novartis, Roche, Sanofi Genzyme, TG Therapeutics, and Vertex); grant/research support (Biogen).
Editorial support was provided by Richard Hogan, PhD, and Linda Wychowski, PhD, Envision Scientific Solutions, and was funded by Sanofi