Details

Autor(en) / Beteiligte

• Coles, Alasdair J
• Compston, D Alastair S
• Selmaj, Krzysztof W
• Lake, Stephen L
• Moran, Susan
• Margolin, David H
• Norris, Kim
• Tandon, P K

Titel

Alemtuzumab vs. Interferon Beta-1a in Early Multiple Sclerosis

Ist Teil von

• The New England journal of medicine, 2008-10, Vol.359 (17), p.1786-1801

Ort / Verlag

Boston, MA: Massachusetts Medical Society

Erscheinungsjahr

2008

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• In this randomized, phase 2 trial involving previously untreated patients with early, relapsing–remitting multiple sclerosis, alemtuzumab, a monoclonal antibody targeting CD52 on lymphocytes and monocytes, was more effective than interferon beta-1a in reducing the progression of disability and relapse. Alemtuzumab caused autoimmune complications, including immune thrombocytopenic purpura (resulting in one death) and thyroid disorders. In this trial involving previously untreated patients with early, relapsing–remitting multiple sclerosis, alemtuzumab, a monoclonal antibody targeting CD52 on lymphocytes and monocytes, was more effective than interferon beta-1a in reducing the progression of disability and relapse. Multiple sclerosis typically follows a relapsing–remitting course, but most patients eventually convert to a secondary progressive phase characterized by deficits that increase in the absence of further relapses. This clinical evolution reflects the complex interplay of focal inflammation, demyelination, and axonal degeneration in the central nervous system. Current disease-modifying treatments decrease the frequency of relapse and modestly reduce the accumulation of disability but have not been shown to prevent secondary progression. 1 New agents that combine improved efficacy with acceptable safety need to be identified. The humanized monoclonal antibody alemtuzumab (Campath-1H; Campath, or MabCampath; Genzyme) targets CD52 on lymphocytes and monocytes. . . .