Willis, Mark ORCID: https://orcid.org/0000-0003-3024-6063 and Robertson, Neil ORCID: https://orcid.org/0000-0002-5409-4909 2015. Alemtuzumab for the treatment of multiple sclerosis. Therapeutics and Clinical Risk Management 2015 (11) , pp. 525-534. 10.2147/TCRM.S80112 |
Abstract
Alemtuzumab is an anti-CD52 monoclonal antibody, recently approved for the treatment of active, relapsing multiple sclerosis (MS). Administration of alemtuzumab causes a rapid and dramatic reduction in circulating lymphocytes, with a predictable subsequent pattern of immune reconstitution. Although the precise mode of action remains unclear, treatment results in a marked reduction in annualized relapse rates, slowing of disability progression compared with an active comparator, and may even cause disability reversal. Although conferring clear clinical benefits, alemtuzumab carries a significant long-term risk of autoimmune disease (AID), which has a particular predilection for the thyroid gland, although a wide range of other disorders have also been reported. However, risks of AID can usually be anticipated and treated successfully, provided rigorous monitoring and surveillance protocols are followed by clinicians and patients alike. Despite its immunosuppressive mechanism of action serious infections are rare and malignancies commonly associated with immunodeficiency have not been observed to date. Alemtuzumab’s unique mode of administration, as well as it’s durability of effect, provides an important addition to currently available therapeutic interventions for MS, and in particular is a valuable treatment option in recent onset and highly active relapsing disease.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG) Medicine |
Subjects: | R Medicine > R Medicine (General) |
Uncontrolled Keywords: | multiple sclerosis, alemtuzumab, autoimmune disease |
Publisher: | DovePress |
ISSN: | 1178-203X |
Date of Acceptance: | 16 January 2015 |
Last Modified: | 31 Oct 2022 10:39 |
URI: | https://orca.cardiff.ac.uk/id/eprint/85589 |
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