TY - JOUR
T1 - Intense immunosuppression in patients with rapidly worsening multiple sclerosis
T2 - treatment guidelines for the clinician
AU - Boster, Aaron
AU - Edan, Gilles
AU - Frohman, Elliot
AU - Javed, Adil
AU - Stuve, Olaf
AU - Tselis, Alexandros
AU - Weiner, Howard
AU - Weinstock-Guttman, Bianca
AU - Khan, Omar
N1 - Funding Information:
AB is supported by a grant from the Partners Multiple Sclerosis Fellowship Program at Brigham and Women's Hospital and the Harvard Medical School through an educational grant provided by EMD Serono. OK has received grant support and/or lecture honoraria from Biogen Idec, Teva Pharmaceuticals, EMD Serono, Bayer Pharmaceuticals, Genentech, Genzyme, and Protein Design Laboratories. AT has received lecture honoraria from Teva Pharmaceuticals and EMD Serono. HW has received grant support and/or lecture honoraria from Biogen Idec, Teva Pharmaceuticals, EMD Serono, Bayer Pharmaceuticals, Genentech, Genzyme, and Protein Design Laboratories. EF has received grant support and lecture honoraria from Biogen Idec and Teva Pharmaceuticals. BWG has received grant support from Biogen Idec, Teva Neurosciences, EMD Serono, Pfizer, Acorda Pharmaceuticals, Aspreva, Cognition, and Avanir Pharmaceuticals. She has also received consultancy fees and/or lecture honoraria and has served on advisory boards for Biogen Idec, Teva Neurosciences, EMD Serono, and Novartis. OS has received grant support and/or lecture honoraria from Biogen Idec, Teva Pharmaceuticals, and Genentech. AJ has received grant support and lecture honoraria from Teva Pharmaceuticals, EMD Serono, and Bayer Pharmaceuticals. GE has received grant support and/or lecture honoraria from Biogen Idec, Teva Pharmaceuticals, EMD Serono, and Bayer Pharmaceuticals.
PY - 2008/2
Y1 - 2008/2
N2 - Several lines of evidence link immunosuppression to inflammation in patients with multiple sclerosis (MS) and provide a rationale for the increasing use of immunosuppressive drugs in the treatment of MS. Treatment-refractory, clinically active MS can quickly lead to devastating and irreversible neurological disability and treating these patients can be a formidable challenge to the clinician. Patients with refractory MS have been treated with intense immunosuppression, such as cyclophosphamide or mitoxantrone, or with autologous haematopoeitic stem cell transplants. Evidence shows that intense immunosuppression might be effective in patients who are unresponsive to immunomodulating therapy, such as interferon beta and glatiramer acetate. Natalizumab, a new addition to the armamentarium for treating MS, might also have a role in the treatment of this MS phenotype. This Review describes the use of intense immunosuppressant drugs and natalizumab in patients with rapidly worsening MS and provides clinicians with guidelines for the use of these drugs in this patient group.
AB - Several lines of evidence link immunosuppression to inflammation in patients with multiple sclerosis (MS) and provide a rationale for the increasing use of immunosuppressive drugs in the treatment of MS. Treatment-refractory, clinically active MS can quickly lead to devastating and irreversible neurological disability and treating these patients can be a formidable challenge to the clinician. Patients with refractory MS have been treated with intense immunosuppression, such as cyclophosphamide or mitoxantrone, or with autologous haematopoeitic stem cell transplants. Evidence shows that intense immunosuppression might be effective in patients who are unresponsive to immunomodulating therapy, such as interferon beta and glatiramer acetate. Natalizumab, a new addition to the armamentarium for treating MS, might also have a role in the treatment of this MS phenotype. This Review describes the use of intense immunosuppressant drugs and natalizumab in patients with rapidly worsening MS and provides clinicians with guidelines for the use of these drugs in this patient group.
UR - http://www.scopus.com/inward/record.url?scp=38349186321&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38349186321&partnerID=8YFLogxK
U2 - 10.1016/S1474-4422(08)70020-6
DO - 10.1016/S1474-4422(08)70020-6
M3 - Review article
C2 - 18207115
AN - SCOPUS:38349186321
SN - 1474-4422
VL - 7
SP - 173
EP - 183
JO - The Lancet Neurology
JF - The Lancet Neurology
IS - 2
ER -