title: Rationale for early treatment with interferon beta-1a in relapsing-remitting multiple sclerosis.
abstract: Disease-modifying therapies are now available for the treatment of relapsing-remitting multiple sclerosis (RR-MS). These drugs have transformed the management of RR-MS from simply treating symptomatic disease to providing effective but incomplete prophylaxis against further disease activity. Our ability to modify disease activity is limited to reducing exacerbations and delaying progression of disability. No intervention has yet been shown to reverse disability once it is established. To prevent disability, therapy should be initiated early in the course of the illness. The rationale for early treatment is as follows: (1) a high percentage of patients with clinically definite RR-MS progress from isolated attacks to neurologic impairment and then to disability within a short time; (2) survival in MS is directly related to disability, so delaying the onset of disability could be expected to influence survival; (3) interferon (IFN) beta-1a has been shown to slow the progression of disability when given to RR-MS patients with impairment or mild disability; and (4) magnetic resonance imaging studies indicate that MS patients frequently have evidence of central nervous system inflammation without overt clinical symptoms, and it has been postulated that treatment of subclinical disease as identified by magnetic resonance imaging may improve long-term outcome. IFN-beta reduces the number of new T2-weighted lesions, as well as the number and volume of gadolinium-enhanced lesions. Aggressive early treatment with IFN beta-1a is recommended, particularly for patients with risk factors suggesting an unfavorable prognosis.
authors.affiliation: William C. Baird Multiple Sclerosis Research Center, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, USA.
authors.forename: F E
authors.initials: FE
authors.lastname: Munschauer
authors.forename: W H
authors.initials: WH
authors.lastname: Stuart
mesh_terms: D001921:Brain / Q000473:pathology; D006801:Humans; D000068556:Interferon beta-1a; D016899:Interferon-beta / Q000627:therapeutic use*; D008279:Magnetic Resonance Imaging; D009103:Multiple Sclerosis / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*
chemical_list: D016899:Interferon-beta; D000068556:Interferon beta-1a