Background Anti-TNF alpha treatment may improve endothelial function and mechanical properties of large artery stiffness in patients with inflammatory rheumatic diseases, however studies remain controversial.

Objectives To study the effect of TNF alpha blockage with adalimumab for 24 weeks on brachial endothelial function and sub-clinical markers of atherosclerosis in patients with inflammatory rheumatic diseases.

Methods A total of 26 patients (14 males, 12 females; mean age, 47±11 years) with inflammatory rheumatic diseases (16, rheumatoid arthritis; 9, ankylosing spondylitis, 1, psoriasic rheumatism), resistant to disease-modifying antirheumatic drugs, were studied before the first infusion of adalimumab and again after 24 weeks of treatment. Endothelial function was assessed by measuring flow mediated dilatation using an ultrasound Doppler technique on the brachial artery. Other markers of sub clinical atherosclerosis were assessed by arterial stiffness via aortic pulse wave velocity, augmentation index and central blood pressure, and carotid intima-media thickness. Data for body mass index, disease activity using DAS-PCR and BASDAI, C-reactive protein, fasting glycaemia, and lipid profile were collected before treatment and after 24 weeks.

Results 24 weeks of adalimumab therapy resulted in a reduction of disease activity score and serum levels of C-reactive protein. No significant differences were found in body mass index, total cholesterol, triglycerides and fasting glycaemia. Brachial blood pressure and heart rate remained similar, as well as carotid intima-media thickness. After 24 weeks of treatment with adalimumab, flow mediated dilatation improved significantly; central systolic and diastolic blood pressure decreased significantly; however central pulse pressure, augmentation index and aortic pulse wave velocity remained unchanged.

Conclusions In patients with inflammatory rheumatic diseases, treatment with adalimumab for 24 weeks resulted in a significant improvement of endothelial function and central arterial pressure.

Disclosure of Interest A. L. Demoux Grant/research support from: Abbvie, K. aissi: None declared, B. chaudier: None declared, S. carijn: None declared, P.-Y. chouc: None declared, H. de baillou: None declared, P. rossi: None declared