Details

Autor(en) / Beteiligte

• Polman, Chris H
• O'Connor, Paul W
• Havrdova, Eva
• Hutchinson, Michael
• Kappos, Ludwig
• Miller, David H
• Phillips, J. Theodore
• Lublin, Fred D
• Giovannoni, Gavin
• Wajgt, Andrzej
• Toal, Martin
• Lynn, Frances
• Panzara, Michael A
• Sandrock, Alfred W

Titel

A Randomized, Placebo-Controlled Trial of Natalizumab for Relapsing Multiple Sclerosis

Ist Teil von

• The New England journal of medicine, 2006-03, Vol.354 (9), p.899-910

Ort / Verlag

Boston, MA: Massachusetts Medical Society

Erscheinungsjahr

2006

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• This placebo-controlled, randomized trial of patients with relapsing multiple sclerosis demonstrated benefits of natalizumab (an α 4 integrin antagonist) in all the primary and secondary outcome measures. After two years, the probability of sustained progression of disability was 17 percent with natalizumab and 29 percent with placebo. Fatigue and allergic reaction were more common among patients receiving natalizumab. This trial of patients with relapsing multiple sclerosis demonstrated benefits of natalizumab in all the primary and secondary outcome measures. In this trial, natalizumab in combination with interferon was more effective than interferon alone. Progressive multifocal leukoencephalopathy developed in two patients. In this systematic evaluation for PML in patients who received natalizumab in clinical trials, no additional cases were identified. Relapsing multiple sclerosis is characterized by the intermittent development of inflammatory lesions in the brain and spinal cord, resulting in plaques of demyelination and axonal loss. Lymphocyte migration across the blood–brain barrier is thought to be an important early step in the formation of lesions. 1 The interaction of α 4 β 1 integrin, a protein on the surface of lymphocytes, with vascular-cell adhesion molecule 1 (VCAM-1), which is expressed on the surface of vascular endothelial cells in brain and spinal cord blood vessels, mediates the adhesion and migration of lymphocytes in areas of inflammation. 2 – 6 Furthermore, the interaction of α . . .