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Updated: Jun 15, 2026

Du-Moxibustion in a Mouse Model of Ankylosing Spondylitis
Published on: October 27, 2023
Endothelial dysfunction in ankylosing spondylitis improves after tumor necrosis factor-alpha blockade.
Ashit Syngle1, Kanchan Vohra, Anjali Sharma
1Healing Touch City Clinic, House No. 547, Sector 16-D, Chandigarh, 160015, India. ashitsyngle@yahoo.com
Infliximab treatment significantly improved endothelial dysfunction and reduced inflammation in ankylosing spondylitis (AS) patients. This suggests endothelial dysfunction is integral to AS, and infliximab offers therapeutic benefits for both aspects of the disease.
Area of Science:
- Rheumatology
- Cardiovascular Medicine
- Immunology
Background:
- Chronic inflammation in ankylosing spondylitis (AS) is linked to vascular endothelial dysfunction.
- Infliximab is known to improve AS inflammatory activity, but its impact on endothelial dysfunction in AS patients remains uninvestigated.
Purpose of the Study:
- To evaluate the effect of infliximab on endothelial dysfunction in AS patients.
- To assess changes in inflammatory markers and disease activity following infliximab treatment.
Main Methods:
- Twelve anti-tumor necrosis factor (TNF) naive AS patients with high disease activity were treated with a single intravenous infusion of infliximab (5 mg/kg).
- Measurements included disease activity scores (BASDAI, BASFI), inflammatory markers (ESR, CRP), serum nitrite concentration, and brachial artery vasodilation (endothelium-dependent and independent) at baseline and 12 weeks.
Main Results:
- Infliximab significantly improved flow-mediated vasodilation (endothelium-dependent) from 9.81% to 26.93% (p < 0.001).
- No significant changes were observed in endothelium-independent vasodilation.
- Significant reductions in nitrite concentration, ESR, CRP, BASDAI, and BASFI scores were noted post-treatment.
Conclusions:
- Endothelial dysfunction appears to be an integral component of the ankylosing spondylitis disease process.
- Infliximab effectively improves both endothelial dysfunction and inflammatory disease activity in AS patients.
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