ECTRIMS eLearning

Case series of three patients with multiple sclerosis showing severe activation of disease during immunotherapy with alemtuzumab
Author(s): ,
T Wehrum
Affiliations:
Department of Neurology and Neuroscience
,
L.A Beume
Affiliations:
Department of Neurology and Neuroscience
,
I Mader
Affiliations:
Department of Neuroradiology, Medical Center - University of Freiburg, Freiburg im Breisgau
,
M Mäurer
Affiliations:
Department of Neurology, Caritas-Hospital Bad Mergentheim, Bad Mergentheim, Germany
,
A Czaplinski
Affiliations:
Neurozentrum Bellevue, Zurich, Switzerland
,
C Weiller
Affiliations:
Department of Neurology and Neuroscience
,
O Stich
Affiliations:
Department of Neurology and Neuroscience
S Rauer
Affiliations:
Department of Neurology and Neuroscience
ECTRIMS Learn. Wehrum T. 09/16/16; 146060; P1632
Thomas Wehrum
Thomas Wehrum
Contributions
Abstract

Abstract: P1632

Type: LB Poster

Abstract Category: Late Breaking News

Background: Alemtuzumab is a humanized monoclonal antibody which causes rapid and prolonged lymphocyte depletion and is a highly effective immunotherapy in relapsing-remitting multiple sclerosis. We describe three cases with severe activation of disease during immunotherapy with alemtuzumab.

Design/method: Retrospective case series

Results:

Case 1: 21 year old female, with severe cognitive impairment, sight deterioration, severe gait ataxia, urinary retention, massive progression of cerebral lesion load including new T2w-hyperintense lesions with gadolinium ring enhancement and dominance of CD19/20-positive B-lymphocytes six months after induction of alemtuzumab.

Case 2: 28 year old male with left-sided hemihypesthesia and ~60 new cerebral and spinal lesions including lesions with gadolinium ring enhancement six months after induction of alemtuzumab.

Case 3: 37 year old female with ataxia and numbness of the left thigh, 16 new gadolinium positive supratentorial lesions, partly ring-enhancing and dominance of CD19/20-positive B-lymphocytes six months after induction of alemtuzumab.

Conclusion: This is the first case series reporting severe activation of disease during immunotherapy with alemtuzumab. All patients showed onset of symptoms six months after induction of alemtuzumab, strikingly similar MRI lesion morphology, and unexpected high total B-cell count which may suggest a B-cell mediated activation of disease. Whether this is due to different rates of B- and T-cell repopulation has to be subject of further research.

Disclosure: None of the authors has financial disclosures related to the performance or content of this study and to the submission of this abstract.

Abstract: P1632

Type: LB Poster

Abstract Category: Late Breaking News

Background: Alemtuzumab is a humanized monoclonal antibody which causes rapid and prolonged lymphocyte depletion and is a highly effective immunotherapy in relapsing-remitting multiple sclerosis. We describe three cases with severe activation of disease during immunotherapy with alemtuzumab.

Design/method: Retrospective case series

Results:

Case 1: 21 year old female, with severe cognitive impairment, sight deterioration, severe gait ataxia, urinary retention, massive progression of cerebral lesion load including new T2w-hyperintense lesions with gadolinium ring enhancement and dominance of CD19/20-positive B-lymphocytes six months after induction of alemtuzumab.

Case 2: 28 year old male with left-sided hemihypesthesia and ~60 new cerebral and spinal lesions including lesions with gadolinium ring enhancement six months after induction of alemtuzumab.

Case 3: 37 year old female with ataxia and numbness of the left thigh, 16 new gadolinium positive supratentorial lesions, partly ring-enhancing and dominance of CD19/20-positive B-lymphocytes six months after induction of alemtuzumab.

Conclusion: This is the first case series reporting severe activation of disease during immunotherapy with alemtuzumab. All patients showed onset of symptoms six months after induction of alemtuzumab, strikingly similar MRI lesion morphology, and unexpected high total B-cell count which may suggest a B-cell mediated activation of disease. Whether this is due to different rates of B- and T-cell repopulation has to be subject of further research.

Disclosure: None of the authors has financial disclosures related to the performance or content of this study and to the submission of this abstract.

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