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Simvastatin slows brain atrophy in secondary progressive multiple sclerosis

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Encouraging results need further exploration

Cautious optimism is the catchphrase for this new study of simvastatin in multiple sclerosis, Dr. Jacqueline Palace and Dr. Neil Robertson wrote in an accompanying editorial.

The study "is a promising and novel development," for a disease that has no long-term progression-modifying therapies. "This form of multiple sclerosis has been largely neglected by a pharmaceutical industry that has so far focused on the early inflammatory processes. A substantial advantage of this study is the fairly low cost, availability, and documented safety profile of the drug."

Simvastatin’s effect on neurodegeneration rather than inflammation also suggests a novel mechanism that might be utilized in combination with anti-inflammatory treatments.

"Caution in interpretation of these preliminary data is, however, needed. ... The expected effects of simvastatin on inflammation were not shown. Furthermore, the disability outcome was a surrogate measure and not the usual outcome used in phase III trials. This finding is relevant because single disability measures show great variability in the short term, and the trial was clearly underpowered to identify an effect on arguably the least sensitive of disability measures (EDSS). The meaning of an effect on atrophy, without a reduction in lesion activity, in predicting the future effect on sustained disability outcomes is unknown."

Nonetheless, the authors wrote, the study uncovers a potential that needs exploration. (Lancet 2014 March 19 [doi: 10.1016/S0140-6736(13)62641-0]).

"Further phase III studies to measure the effect of simvastatin on sustained disability, particularly in patients with nonrelapsing secondary progressive and primary progressive multiple sclerosis, are clearly needed, but this trial represents a promising point from which to develop trials of progressive disease."

Dr. Palace leads the neuromyelitis optica service at John Radcliffe Hospital, Oxford, England. Dr. Robertston is professor of neurology in the Institute of Psychological Medicine and Clinical Neurosciences at Cardiff (Wales) University. Both reported financial relationships, including personal remuneration, from several pharmaceutical companies marketing drugs for multiple sclerosis.


 

FROM THE LANCET

A high dose of simvastatin decreased whole-brain atrophy by 43% per year over 24 months, compared with placebo, in a phase II, randomized, controlled trial in patients with secondary progressive multiple sclerosis.

The drug had no apparent effect on relapses or new lesions. But patients who took it showed significantly better scores on the Multiple Sclerosis Impact Scale–29 (MSIS-29) and the Expanded Disability Status Scale (EDSS), suggesting that slowing brain atrophy may have a beneficial effect on function, reported Jeremy Chataway, Ph.D., of the University College London (Lancet 2014 March 19 [doi:10.1016/S0140-6736(13)62242-4]).

However, those results should be interpreted cautiously because functional status wasn’t the primary endpoint of the trial, wrote Dr. Chataway and his coauthors.

The study randomized 140 patients with secondary progressive multiple sclerosis to placebo or 80 mg/day simvastatin for 24 months. Brain volume and functional and psychological status were assessed at baseline and 1, 6, 12, and 24 months. The mean age of the patients was 52 years, and average disease duration was 21 years. The mean whole-brain volume was 1,100 mL. The mean EDSS score was 5.8, and the mean MSIS-29 score was 70.

Nine patients did not complete the full trial. Treatment compliance was 90% or greater for 77%-78% of the remaining patients.

At 24 months, whole-brain volume had declined in both groups. But the annual decline was significantly less in those taking simvastatin (–0.288% vs. –0.584%). The adjusted difference in annual atrophy was 0.254% per year, resulting in 43% less volume loss per year in the simvastatin group than in the placebo group. This effect was seen in MRI scans at both 12 and 24 months, and occurred in three-fourths of the treated population.

The rate of new or enlarging lesions was not significantly different, although there was a trend toward benefit in the treated group (1.50 vs. 2.19 per person per year). The relapse rates were similar (0.20 vs. 0.16 events per person/year).

At 24 months, the mean EDSS score in the simvastatin group was significantly lower than in the placebo group (a mean difference of –0.254 after adjustment for baseline measurements). The total mean MSIS-29 also showed a significant between-group difference in favor of simvastatin (–4.78 after adjustment). The difference was most pronounced in the physical subscale of the MSIS-29 (–3.73), but the psychological subscale was not significantly different. Overall, changes in these secondary measures by 24 months reflected worsening in both groups, but more so in the placebo group.

Cholesterol also decreased significantly in the simvastatin group (from 5.5 mmol/L to 4.1 mmol/L); it did not change in the placebo group. However, there were no differences in inflammatory markers.

Drug-related adverse events occurred in 23% of patients on simvastatin, compared with 19% of those on placebo. Simvastatin was generally well tolerated, with no safety issues.

It’s not entirely clear how a statin would slow disease progression, the researchers said. "gAccumulating evidence shows that statins have cell protective properties. For example, inhibition of inducible nitric oxide synthase, thus reducing release of free radicals from activated microglia and astrocytes or exerting a neuroprotective effect by prevention of glutamate-mediated excitotoxic effects."h

Simvastatin might also improve cerebral vasomotor reactivity, which could protect against hypoxic damage, they added. The general benefit of statins on vascular health could also be a contributor.

The study was partially supported by a grant from the U.K. National Institute for Health Research, the Moulton Foundation, the Berkeley Foundation, the Multiple Sclerosis Trials Collaboration, the Rosetrees Trust, and a personal contribution.

None of the authors had any financial disclosures.

msullivan@frontlinemedcom.com

On Twitter @alz_gal

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