Glatiramer acetate or interferon-P for multiple sclerosis? A guide to drugchoice

The 1990s, the decade of the brain, have seen major advances in the managem ent of multiple sclerosis (MS). For the first time; effective agents are av ailable for the treatment of relapsing-remitting MS. These include glatiram er acetate ('Copaxone') and 3 varieties of recombinant. human interferon-be ta (IFN beta): IFN beta- 1b ('Betaseron'/'Betaferon') and 2 types of IFN be ta-1a ('Avonex' and 'Rebif'). The modes of action of all these agents are n ot fully understood; however, recent advances in our understanding of the i mmunopathogenesis of MS suggest that the immunomodulatory properties of the se drugs are involved in their effects in the disease. Based on evidence accumulated in major clinical trials and post-marketing e xperience, all 4 medications reduce relapse rates by about one-third and ma y slow disease progression. The interferons have a beneficial effect on dis ease activity as reflected on magnetic resonance imaging (MRI) scans, where as only limited MRI data are available for glatiramer acetate. The principal adverse effects of the interferons are transient flu-like sym ptoms and injection site reactions, but other adverse effects that necessit ate clinical and laboratory monitoring may occur. Glatiramer acetate has th e most favourable adverse effect profile, with mild injection site reaction s and a rare self-limited systemic post-injection reaction. All 4 agents ar e indicated for ambulatory patients with relapsing-remitting MS, although i ndications may expand in the future as new clinical data emerge on their ef fects on other stages of the disease. The 4 agents were tested in different clinical trials that used different d esigns, patient populations, end-points and methods of statistical analysis , making simple comparisons between them inappropriate. Furthermore, the mi nor differences in reported efficacy, combined with their overall modest ef fect on the disease, do not grant superiority to any particular one. Decisi ons about initiation of therapy and choice of agent should be individualise d, based on the severity and activity of the disease process, MRI activity and lesion volume, patient preferences and life style, concomitant illnesse s and potential for inducing adverse effects. The current availability of s everal agents allows for switching from one to another in case of treatment failure. However, if the patient is doing well, treatment with the initial ly prescribed agent should be maintained. It is hoped that future advances in basic and clinical research will result in the emergence of newer and more effective therapies for MS.