Asprosin in Behect Patients

Behcet Disease

This study aims to investigate serum Asprosin concentrations in patients with BD and their relationship with disease activity and major clinical manifestations.

Behçet's disease (BD) is a chronic, recurrent, multisystem inflammatory vasculitis characterized by various systemic manifestations involving all vessel sizes in both the arterial and venous systems \[1,2\]. Given that BD is a prototypical systemic vasculitis in which endothelial damage and vascular inflammation are central pathogenic mechanisms, the identification of novel biomarkers reflecting vascular involvement is of major clinical importance\[3\]. Asprosin is an adipokine that beyond its metabolic effects, carries growing evidence suggesting its associated with vascular pathologies \[4\]. Experimental and clinical studies have demonstrated that Asprosin contributes to endothelial dysfunction, induces phenotypic switching in vascular smooth muscle cells, and facilitates vascular remodeling by activating pro-inflammatory signaling pathways such as TLR4-NF-κB-NLRP3 \[4,5\]. Furthermore, Asprosin has been implicated in endothelial-to-mesenchymal transition through TGF-β signaling, thereby exacerbating peripheral arterial disease and vascular stiffness\[4,5\]. Although endothelial dysfunction and surrogate markers of vascular injury (e.g., impaired flow-mediated dilation, increased intima-media thickness, oxidative stress markers) have been extensively studied in BD\[3\], the role of Asprosin in this disease remains unexplored. In this context, Asprosin may represent a link between metabolic pathways and immune mediated vascular inflammation, warranting investigation in systemic vasculitis as potential biomarkers of disease activity \[6\].

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