Title
Boosting endogenous neuroprotection in multiple sclerosis: the ASsociation of Inosine and Interferon <tex>$\beta$</tex> in relapsing- remitting Multiple Sclerosis (ASIIMS) trial
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Publication type
article
Publication
Subject
Human medicine
Source (journal)
Multiple sclerosis: clinical and laboratory research. - -
Volume/pages
16(2010) :4 , p. 455-462
ISSN
1352-4585
ISI
000276530000010
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Abstract
Anti-inflammatory drugs are effective on relapses, but neuroprotective agents to prevent disability are still unavailable. Uric acid has neuroprotective effects in experimental models including encephalomyelitis and appears to be involved in multiple sclerosis. Oral administration of inosine, a precursor of uric acid, increases serum uric acid levels and is well tolerated. Our objective was to test the possibility that a combination therapy associating an anti-inflammatory drug (interferon β) and an endogenous neuroprotective molecule (uric acid) would be more effective than interferon β alone on the accumulation of disability. Patients with relapsingremitting multiple sclerosis on interferon β for at least 6 months were randomized to interferon β + inosine or interferon β + placebo for 2 years. The dose of inosine was adjusted to maintain serum uric acid levels in the range of asymptomatic hyperuricaemia (≤10 mg/dl). The primary end points were percentage of patients with progression of disability and time to sustained progression (KaplanMeier analysis). The combination of interferon β and inosine was safe and well tolerated but did not provide any additional benefit on accumulation of disability compared with interferon β alone. We conclude that endogenous neuroprotective mechanisms recently identified in multiple sclerosis are complex and uric acid does not reflect the entire story.
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