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The aim of treatment is to reduce the frequency, and limit the lasting effects, of relapses, relieve symptoms, prevent disability arising from disease progression, and promote tissue repair.
Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial
Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial
Alemtuzumab vs. interferon beta-1a in early multiple sclerosis.
In patients with early, relapsing-remitting multiple sclerosis, alemtuzumab was more effective than interferon beta-1a but was associated with autoimmunity, most seriously manifesting as immune thrombocytopenic purpura.
The window of therapeutic opportunity in multiple sclerosis
It is speculated that the beneficial effects of early rescue of neurons and axons from a toxic inflammatory environment, and that prevention of demyelination will prevent long–term axonal degeneration, are currently being tested in a controlled trial comparing Campath–1H and IFN–beta in the treatment of drug–naïve patients with early, active RR MS.
Disease-relevant autoantibodies in first episode schizophrenia
These cases were hypothesized that these antibodies would be present in a proportion of patients with early schizophrenia, in the absence of overt seizures, movement disorders, or other neurological signs, and the autoantibody positive cases fulfilled criteria for DSM-IV schizophrenia.
Alemtuzumab treatment of multiple sclerosis: long-term safety and efficacy
Alemtuzumab is associated with disease stabilisation in the majority of patients with highly active RRMS over an average seven-year follow-up, with trends for longer disease duration and older age at first treatment.
Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis
Evidence is provided supporting the emerging view that treatment in multiple sclerosis must be given early in the course, before the consequences of inflammation are irretrievably established, and the formulation that inflammation and demyelination are responsible for relapses of multiple sclerosis is supported.
B-Cell Reconstitution and BAFF After Alemtuzumab (Campath-1H) Treatment of Multiple Sclerosis
- S. Thompson, Joanne L. Jones, A. Cox, D. Compston, A. Coles
- Biology, MedicineJournal of Clinical Immunology
B-cell recovery is rapid, returning to baseline by 3 months and rising to 165% of baseline by 12 months after treatment, which coincides with a surge in serum B-cell activating factor (BAFF), which remains elevated by 33% for at least 12 Months after alemtuzumab.