Significant sE-Selectin levels reduction after 6 months of anti-TNF-α therapy in non-diabetic patients with moderate-to-severe psoriasis

Abstract

Purpose: Psoriasis patients have high risk of atherosclerosis, characterized by endothelial dysfunction. We aimed to study the association of the endothelial activation biomarkers monocyte chemoattractant protein 1 (MCP-1), soluble (s) E-selectin and P-selectin with disease activity and severity in psoriasis patients treated with anti-TNF-α therapy. Also, to evaluate the relationship of metabolic syndrome features with these biomarkers and the effect of anti-TNF-α therapy on these molecules.

Methods: Twenty-nine consecutive non-diabetic patients with moderate-to-severe psoriasis who underwent 6 months of anti-TNF-α-adalimumab therapy were studied. Metabolic and clinical evaluation was performed prior to anti-TNF-α treatment (time 0) and 6 months later. MCP-1, sE-selectin and sP-selectin serum levels were determined by ELISA.

Results: Dyslipidemic and obese patients showed higher MCP-1 levels at month 6 from the onset of anti-TNF-α therapy (p = .05 and .01, respectively). sE-selectin positively correlated with pro-inflammatory molecules such as asymmetric dimethylarginine, sP-selectin and resistin at baseline and month 6 (p < .05). sE-selectin levels significantly reduced after 6 months of therapy (p = .0006).

Conclusions: Metabolic syndrome features are associated with endothelial activation in patients with moderate-to-severe psoriasis. Adalimumab therapy led to a reduction in sE-selectin levels, supporting the beneficial effect of anti-TNF-α therapy on mechanisms associated with the development of atherosclerosis in psoriasis.

Keywords:

• Endothelial cell activation
• atherosclerosis
• psoriasis
• biologic therapy
• biomarkers

Acknowledgements

We wish to thank all the patients that participated to make this study possible. We want to specially thank Rodrigo Ochoa and Patricia Fuentevilla for their technical assistance.

Disclosure statement

The authors had sole responsibility for data analysis and manuscript preparation. The opinions expressed in this paper are those of the authors and do not necessarily represent those of Abbvie Inc. All the authors declare that they have no conflict of interest.

Additional information

Funding

The study was supported by a research grant from Abbvie Inc (to MAG-G) [grant ACA-SPAI-10-21]. FG is a recipient of a Sara Borrell postdoctoral fellowship from the Instituto de Salud Carlos III (ISCIII), Spain [grant CD15/00095]. RL-M is supported by funds of the Miguel Servet type I program from the ISCIII, Spain [grant CP16/00033]. BU and SR-M are supported by funds from the RETICS Program (RIER) from the ISCIII, Spain [grants RD12/0009/0013 and RD16/0012/0009, respectively].