Enhanced cardiovascular risk in ankylosing spondylitis provides a strong rationale for early therapeutical intervention. In view of the proven benefit of statins in atherosclerotic vascular disease, a study has investigated the effect of Rosuvastatin ( Crestor ) on endothelial dysfunction and inflammatory disease activity in ankylosing spondylitis.
In a single-blind, placebo-controlled, parallel study, 32 patients with ankylosing spondylitis were randomized to receive 24 weeks of treatment with Rosuvastatin ( 10 mg/day, n = 17 ) and placebo ( n = 15 ) as an adjunct to existing stable antirheumatic drugs.
Flow-mediated dilatation ( FMD ) was assessed by AngioDefender. Inflammatory measures ( BASDAI, BASFI, CRP and ESR ) and pro-inflammatory cytokines ( tumour necrosis factor-alpha [ TNF-alpha ], interleukin-6 [ IL-6 ] and interleukin-1 [ IL-1 ] ) were measured at baseline and after treatment.
Lipids and adhesion molecules ( intracellular adhesion molecule [ ICAM-1 ] and vascular cell adhesion molecule [ VCAM-1 ] ) were estimated at baseline and after treatment.
At baseline, inflammatory measures, pro-inflammatory cytokines and adhesion molecules were elevated among both groups.
After treatment with rosuvastatin, flow-mediated dilatation improved significantly ( p less than 0.01 ). Levels of inflammatory measures, TNF-alpha, IL-6 and ICAM-1 decreased significantly ( p less than 0.01 ) after treatment with Rosuvastatin.
Rosuvastatin exerted positive effect on lipid spectrum. No significant change in the placebo group.
Significant negative correlation was observed between flow-mediated dilatation and IL-6, ICAM-1, CRP after treatment with Rosuvastatin.
This is the first study to show that Rosuvastatin improves inflammatory disease activity and endothelial dysfunction in ankylosing spondylitis.
Rosuvastatin lowers the proinflammatory cytokines, especially IL-6 and TNF-alpha, which downregulates adhesion molecules and CRP production which in turns improves endothelial dysfunction.
Improvement in endothelial dysfunction in ankylosing spondylitis occurs through both cholesterol-independent and cholesterol-dependent pathways.
Rosuvastatin can mediate modest but clinically apparent anti-inflammatory effects with modification of vascular risk factors in the context of high-grade autoimmune inflammation of ankylosing spondylitis. ( Xagena )
Garg N et al, Clin Rheumatol 2015; Epub ahead of print