title: Spironolactone improves endothelial dysfunction in ankylosing spondylitis.
abstract: Chronic inflammation in ankylosing spondylitis (AS) is associated with vascular endothelial dysfunction which leads to accelerated atherosclerosis. Accelerated atherosclerosis contributes to premature cardiovascular disease and increased cardiovascular mortality in AS. Spironolactone inhibits the production of proinflammatory cytokines and improves endothelial dysfunction in rheumatoid arthritis. This study aimed to determine the effect of spironolactone in antitumor necrosis factor (TNF)-naive AS patients. Twenty anti-TNF-naive AS patients (M/F = 15/5) with high disease activity (Bath ankylosing spondylitis disease activity index, BASDAI >4) despite treatment with stable doses of conventional disease-modifying antirheumatic drugs 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 -independent vasodilatation of the brachial artery were measured at baseline and after 12 weeks of therapy with oral spironolactone 2 mg/kg/day. Ten healthy subjects matched for age and sex acted as the control. Flow-mediated dilation (FMD) in AS patients at baseline was significantly impaired compared with healthy control group (p < 0.001). After treatment, FMD improved from 11.3 ± 1.70 to 24.69 ± 2.34% (p < 0.001); nitrite concentration reduced from 7.9 ± 0.28 to 4.79 ± 0.19 μmol/L (p < 0.001); ESR from 33.8 ± 4.38 to 15.13 ± 1.30 mm in the first hour, (p < 0.001); and CRP level from 22.39 ± 3.80 to 6.3 ± 1.29 mg/dL, (p < 0.001). BASDAI and BASFI also reduced significantly (p < 0.001). The study suggests that in AS endothelial dysfunction is a part of the disease process. This is the first study to show that treatment with spironolactone improves both endothelial dysfunction and inflammatory disease activity in AS.
authors.affiliation: Healing Touch City Clinic, Chandigarh, India.
authors.forename: Ashit
authors.initials: A
authors.lastname: Syngle
authors.forename: Kanchan
authors.initials: K
authors.lastname: Vohra
authors.forename: Dinesh
authors.initials: D
authors.lastname: Khichi
authors.forename: Nidhi
authors.initials: N
authors.lastname: Garg
authors.forename: Inderjeet
authors.initials: I
authors.lastname: Verma
authors.forename: Ladbans
authors.initials: L
authors.lastname: Kaur
mesh_terms: D000293:Adolescent; D000328:Adult; D050197:Atherosclerosis / Q000188:drug therapy / Q000473:pathology; D001799:Blood Sedimentation; D001916:Brachial Artery / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism; D004232:Diuretics / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology*; D005260:Female; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D009573:Nitrites / Q000097:blood; D010865:Pilot Projects; D011446:Prospective Studies; D012720:Severity of Illness Index; D013148:Spironolactone / Q000627:therapeutic use*; D013167:Spondylitis, Ankylosing / Q000188:drug therapy*; D055815:Young Adult
chemical_list: D004232:Diuretics; D009573:Nitrites; D013148:Spironolactone; D002097:C-Reactive Protein