Study examines inosine to increase urate levels in patients with Parkinson disease

December 23, 2013

The drug inosine appears to be a safe and effective way to raise blood and cerebrospinal fluid urate levels in patients with early Parkinson disease (PD), suggesting it may be a potential strategy to slow the disability progression of the degenerative neurological disorder, according to a report published by JAMA Neurology, a JAMA Network publication.

Urate is an end product of human metabolism. Animal experiments suggest that urate may protect against PD, and higher blood urate levels are associated with reduced risk and slower progression of PD, according to the study background. Inosine is a drug that raises urate levels and therefore may be useful for PD.

Researchers in the Parkinson Disease Study Group SURE-PD (Safety of Urate Elevation in PD) trial randomized 75 patients with early PD (average age 62 years and not yet requiring treatment for their symptoms) to placebo or doses of inosine to produce mild or moderate elevation in blood urate levels to examine the safety, tolerability and ability of inosine to elevate urate levels. Patients were administered inosine in 500-mg capsules taken orally.

Blood (serum) urate levels rose by 2.3 and 3.0 mg/dL in the two inosine groups vs. placebo, and cerebrospinal fluid (CSF) urate levels were greater in both inosine groups. Serious adverse events (17) occurred at the same or lower rates in the inosine groups compared to placebo. The treatment also was tolerated by 95 percent of patients at six months and no participants withdrew because of an adverse event.

"The results of the SURE-PD trial demonstrate that oral inosine treatment in early PD is clinically safe and tolerable and produces an increase in serum and CSF urate. ... The present findings support the development of a more definitive trial to investigate the ability of inosine treatment to slow clinical progression among persons with early PD who have lower urate," the authors conclude.
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(JAMA Neurol. Published online December 23, 2013. doi:10.1001/.jamaneurol.2013.5528. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor's Note: This project was funded by a grant from the MJFF. Additional support was provided by a National Institutes of Health grant, the Harvard NeuroDiscovery Center, the RJG Foundation and the Parkinson's Disease Foundation Advancing Parkinson's Therapies initiative. Conflict of interest disclosures were made. Please see the articles for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

The JAMA Network Journals

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