Magazine article Clinical Psychiatry News

Statins May Cut Brain Inflammation in MS

Magazine article Clinical Psychiatry News

Statins May Cut Brain Inflammation in MS

Article excerpt

Statin drugs may inhibit the inflammatory components of multiple sclerosis that lead to neurologic disability, according to the results of a multicenter, open-label study.

Studies in mouse models have suggested that statins may influence multiple sclerosis by converting T cells in the immune system into anti-inflammatory agents that counteract the brain inflammation of the neurodegenerative disease.

In a 6-month clinical study, Dr. Timothy Vollmer of the Barrow Neurological Institute in Phoenix, Ariz., and his associates tested this hypothesis by treating 30 patients with relapse-remitting multiple sclerosis with 80 mg/day of oral simvastatin.

Intially, 45 patients between 18 and 55 years of age were screened for participation in the study. All had clinically definite relapsing-remitting multiple sclerosis and no previous treatment with interferons or glatiramer in the previous 3 months or corticosteroids within 30 days of screening (Lancet 363[9421]:1607-08, 2004).

The researchers monitored the patients for 3 months, including monthly MRI scans. Patients with at least one gadolinium-enhancing lesion detected during this pretreatment phase were eligible to receive simvastatin. During the treatment phase, brain MRI scans were done at months 4, 5, and 6; two expert readers who were unaware of the study protocol manually established the location of lesions.

The main outcome measures were the mean number and volume of gadolinium-enhancing lesions observed on brain MRI scans at months 4, 5, and 6, compared with the mean number of pretreatment lesions. Secondary outcome measures were relapse rate and change in expanded disability status score. The researchers also conducted exploratory immunology studies to identify changes in the secretion of representative T helper cell, type 1 (Th1) and T helper cell, type 2 (Th2) cytokines.

Of 28 patients for whom follow-up data were available, the number of lesions declined by 44% and the volume of lesions declined by 41%, with no serious adverse events reported. Relapse rates did not differ in the pretreatment and treatment phases, nor were there relevant changes in expanded disability status scores or secretion of Th1 and Th2 cytokines. …

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