Endothelial dysfunction in ankylosing spondylitis improves after tumor necrosis factor-alpha blockade.

Chronic inflammation in ankylosing spondylitis (AS) is associated with vascular endothelial dysfunction. Infliximab improves inflammatory disease activity in AS patients, but its effect on endothelial dysfunction has still not been tested in these patients. Twelve anti-TNF naive AS patients (mean age, 32.6 +/- 3.94 years; disease duration, 5.6 +/- 0.8 years) with high disease activity [Bath ankylosing spondylitis disease activity index (BASDAI score > 4)] despite treatment with stable doses of conventional disease modifying anti-rheumatic drugs (DMARDs) were investigated. Inflammatory disease activity [BASDAI and Bath ankylosing spondylitis functional index (BASFI) scores, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) levels], serum nitrite concentration, and endothelium-dependent and endothelium-independent vasodilation of the brachial artery were measured at baseline and 12 weeks of therapy after single intravenous infusion of infliximab (5 mg/kg). Previous DMARD(s) regimen remained unchanged throughout the study period. After treatment with infliximab, flow-mediated vasodilation improved from 9.81 +/- 1.70% to 26.93 +/- 2.34% (p < 0.001), whereas there was no significant change in endothelium-independent vasodilation with nitroglycerin and baseline diameter (13.65 +/- 2.10% versus 14.59 +/- 1.93%, p = 0.08, and 4.45 +/- 0.15 versus 4.46 +/- 0.15 mm, p = 0.3, respectively). Nitrite concentration reduced from 6.50 +/- 0.21 to 2.57 +/- 0.18 micromol/l (p < 0.001), ESR from 40.90 +/- 6.00 to 11.50 +/- 1.38 mm in the first hour (p < 0.001), and CRP level from 29.08 +/- 4.11 to 2.69 +/- 0.43 mg/dl (p < 0.001). BASDAI and BASFI scores were significantly reduced from 5.40 +/- 1.14 to 1.40 +/- 0.70 (p < 0.05) and 5.05 +/- 1.76 to 0.20 +/- 0.63 (p < 0.05), respectively. The study suggests that in ankylosing spondylitis, endothelial dysfunction is a part of the disease process and infliximab improves both endothelial dysfunction and inflammatory disease activity.