Atorvastatin does not alter interferon Beta-induced changes of serum matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 in patients with multiple sclerosis.

I nterferon beta, the current cornerstone of multiple sclerosis (MS) therapy, was shown to reduce the ratio of matrix metalloproteinase 9 (MMP-9)–tissue inhibitor of metalloproteinase 1 (TIMP-1) in order to attenuate overactive proteolysis and inhibit leukocyte migration. Matrix metalloproteinases, a family of extracellular matrixdegrading enzymes, are involved in the pathogenesis of MS by facilitating leukocyte migration, disruption of the bloodbrain barrier, processing of cytokines and their receptors, and demyelination. Immunomodulatory properties of 3-hydroxy-3methylglutaryl coenzyme A reductase inhibitors, including atorvastatin, may be beneficial for the treatment of MS. Among the immunomodulatory effects proposed for statins, increased attention is drawn to the modulation of MMPs. In vitro results suggest that statins may increase MMP-9 activity and disrupt the proteolytic balance restored by interferon beta. In this study, we aimed to evaluate the treatment effects of interferon beta alone and in combination with atorvastatin on parameters of proteolysis, ie, serum levels of active MMP-9 and TIMP-1 and the active MMP9–TIMP-1 ratio in patients with relapsing-remitting MS.