Our review should provide some guidance to clinicians and patients. On the basis of high quality evidence, natalizumab and IFNß-1a (Rebif) are superior to all other treatments for preventing clinical relapses in RRMS in the short-term (24 months) compared to placebo. Moderate quality evidence supports a protective effect of natalizumab and IFNß-1a (Rebif) against disability progression in RRMS in the short-term compared to placebo. These treatments are associated with long-term serious adverse events and their benefit-risk balance might be unfavourable. IFNß-1b (Betaseron) and mitoxantrone probably decreased the odds of the participants with RRMS having relapses, compared with placebo (moderate quality of evidence). The benefit-risk balance with azathioprine is uncertain, however this agent might be effective in decreasing the odds of the participants with RRMS having relapses and disability progression over 24 to 36 months, compared with placebo. The lack of convincing efficacy data shows that IFNß-1a (Avonex), intravenous immunoglobulins, cyclophosphamide and long-term steroids have an unfavourable benefit-risk balance in RRMS. None of the included treatments are effective in decreasing disability progression in patients with progressive MS. It is important to consider that the clinical effects of all these treatments beyond two years are uncertain, a relevant point for a disease of 30 to 40 years duration. Direct head-to-head comparison(s) between natalizumab and IFNß-1a (Rebif) or between azathioprine and IFNß-1a (Rebif) should be top priority on the research agenda and follow-up of the trial cohorts should be mandatory.
No difference in efficacy of two different doses of intravenous immunoglobulins in MS: clinical and MRI assessment.
We performed a double-blind, placebo-controlled study to evaluate the efficacy of low and high dose of intravenous immunoglobulins (IVIG) in relapsing/remitting (RR) multiple sclerosis (MS). Patients (n = 49) with clinical definite RR MS were randomly allocated to three groups and treated with 0.2 g/kg (n = 17) or 0.4 g/kg (n = 15) once a month of IVIG and placebo (n = 17) for 12 months. Clinical data were assessed monthly and magnetic resonance imaging (MRI) was performed every 3 months during the study period. Annual relapse rate (ARR) and change of the mean Expanded Disability Status Scale (EDSS) and Neurological Rating Scale Score (NRSS) from baseline to study conclusion were used as the clinical end-points. For MRI activity total lesion volume on T2-weighted image (T2WI), new lesions and gadolinium (Gd)-enhanced lesions on T1WI were analysed. ARR in both IVIG groups (0.88 for 0.2 g/kg and 0.86 for 0.4 g/kg) was reduced compared with placebo (1.24) during treatment period. Neurological disability measured with EDSS decreased slightly in both the IVIG groups (0.029 and 0.066, respectively) and increased by 0.29 in placebo (P = 0.0117). The neurologic impairment measured by NRSS showed similar trend. The total lesion volume on T2WI increased by 13.56% in placebo whereas in the 0.4 g/kg IVIG group decreased by -3.95% and in the 0.2 g/kg IVIG group increased by 3.6%. The cumulative numbers of Gd-enhancing lesions and new T2WI lesions in the IVIG groups were reduced in comparison with the placebo group. Our findings suggest that the dose 0.2 g/kg of IVIG is equally effective as 0.4 g/kg in reducing MS activity.