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Alemtuzumab for Multiple Sclerosis

Alemtuzumab is a humanised anti-CD52 monoclonal antibody approved for use in active, relapsing multiple sclerosis (MS). Administration results in a rapid depletion of circulating lymphocytes with a subsequent beneficial immune reconstitution. Early open-label experience and recent clinical trials ha...

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Detalles Bibliográficos
Autores principales: Willis, Mark D., Robertson, Neil P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971037/
https://www.ncbi.nlm.nih.gov/pubmed/27485945
http://dx.doi.org/10.1007/s11910-016-0685-y
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author Willis, Mark D.
Robertson, Neil P.
author_facet Willis, Mark D.
Robertson, Neil P.
author_sort Willis, Mark D.
collection PubMed
description Alemtuzumab is a humanised anti-CD52 monoclonal antibody approved for use in active, relapsing multiple sclerosis (MS). Administration results in a rapid depletion of circulating lymphocytes with a subsequent beneficial immune reconstitution. Early open-label experience and recent clinical trials have demonstrated a dramatic effect on relapse rates as well as a positive effect on radiological disease outcomes and disability measures. Despite a mechanism of action that results in profound lymphopaenia, opportunistic infections are rarely seen and no excess association with malignancy has been identified. However, acquired autoimmune disease (AID) is a common adverse event following treatment, necessitating rigorous monitoring in order to facilitate prompt detection and management. Despite this issue, a unique dosing schedule and durability of effect make alemtuzumab a welcome addition to currently available treatment options for MS.
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spelling pubmed-49710372016-09-01 Alemtuzumab for Multiple Sclerosis Willis, Mark D. Robertson, Neil P. Curr Neurol Neurosci Rep Demyelinating Disorders (DN Bourdette and M Cameron, Section Editors) Alemtuzumab is a humanised anti-CD52 monoclonal antibody approved for use in active, relapsing multiple sclerosis (MS). Administration results in a rapid depletion of circulating lymphocytes with a subsequent beneficial immune reconstitution. Early open-label experience and recent clinical trials have demonstrated a dramatic effect on relapse rates as well as a positive effect on radiological disease outcomes and disability measures. Despite a mechanism of action that results in profound lymphopaenia, opportunistic infections are rarely seen and no excess association with malignancy has been identified. However, acquired autoimmune disease (AID) is a common adverse event following treatment, necessitating rigorous monitoring in order to facilitate prompt detection and management. Despite this issue, a unique dosing schedule and durability of effect make alemtuzumab a welcome addition to currently available treatment options for MS. Springer US 2016-08-02 2016 /pmc/articles/PMC4971037/ /pubmed/27485945 http://dx.doi.org/10.1007/s11910-016-0685-y Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Demyelinating Disorders (DN Bourdette and M Cameron, Section Editors)
Willis, Mark D.
Robertson, Neil P.
Alemtuzumab for Multiple Sclerosis
title Alemtuzumab for Multiple Sclerosis
title_full Alemtuzumab for Multiple Sclerosis
title_fullStr Alemtuzumab for Multiple Sclerosis
title_full_unstemmed Alemtuzumab for Multiple Sclerosis
title_short Alemtuzumab for Multiple Sclerosis
title_sort alemtuzumab for multiple sclerosis
topic Demyelinating Disorders (DN Bourdette and M Cameron, Section Editors)
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971037/
https://www.ncbi.nlm.nih.gov/pubmed/27485945
http://dx.doi.org/10.1007/s11910-016-0685-y
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