Effect of statins on clinical and molecular responses to intramuscular interferon beta-1a  

Oleh:

Rudick, R. A. ; Pace, A. ; Rani, M.R.S.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 72 no. 23 (Jun. 2009), page 1989-1993.
Topik: INTERFERON BETA; NATALIZUMAB

Ketersediaan

Perpustakaan FK Nomor Panggil: N11.K.2009.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Background: Findings from a small clinical study suggested that statins may counteract the therapeutic effects of interferon beta (IFNß) in patients with relapsing-remitting multiple sclerosis (RRMS). Methods: We conducted a post hoc analysis of data from the Safety and Efficacy of Natalizumab in Combination With IFNß-1a in Patients With Relapsing-Remitting Multiple Sclerosis (SENTINEL) study to determine the effects of statins on efficacy of IFNß. SENTINEL was a prospective trial of patients with RRMS treated with natalizumab (Tysabri®, Biogen Idec, Inc., Cambridge, MA) plus IM IFNß-1a (Avonex®, Biogen Idec, Inc.) 30 µg compared with placebo plus IM IFNß-1a 30 µg. Clinical and MRI outcomes in patients treated with IM IFNß-1a only (no-statins group, n = 542) were compared with those of patients taking IM IFNß-1a and statins at doses used to treat hyperlipidemia (statins group, n = 40). Results: No significant differences were observed between treatment groups in adjusted annualized relapse rate (p = 0.937), disability progression (p = 0.438), number of gadolinium-enhancing lesions (p = 0.604), or number of new or enlarging T2-hyperintense lesions (p = 0.802) at 2 years. More patients in the statins group reported fatigue, extremity pain, muscle aches, and increases in hepatic transaminases compared with patients in the no-statins group. Statin treatment had no ex vivo or in vitro effect on induction of IFN-stimulated genes. Conclusions: Statin therapy does not appear to affect clinical effects of IM interferon beta-1a in patients with relapsing-remitting multiple sclerosis or the primary molecular response to interferon beta treatment.

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