Abstract
Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis (axSpA). CV risk is enhanced by dysregulation of adipokines. Low omentin levels were associated with metabolic dysfunction and CV disease in conditions different from axSpA. Accordingly, we evaluated the genetic and functional implication of omentin in CV risk and subclinical atherosclerosis in a cohort of 385 axSpA patients. Subclinical atherosclerosis was evaluated by carotid ultrasound. Omentin rs12409609, in linkage disequilibrium with a polymorphism associated with CV risk, was genotyped in 385 patients and 84 controls. Serum omentin levels were also determined. omentin mRNA expression was assessed in a subgroup of individuals. Serum and mRNA omentin levels were lower in axSpA compared to controls. Low serum omentin levels were related to male sex, obesity, inflammatory bowel disease (IBD) and high atherogenic index. rs12409609 minor allele was associated with low omentin mRNA expression in axSpA. No association was observed with subclinical atherosclerosis at the genetic or functional level. In conclusion, in our study low omentin serum levels were associated with CV risk factors in axSpA. Furthermore, rs12409609 minor allele may be downregulating the expression of omentin. These data support a role of omentin as a CV risk biomarker in axSpA.
Highlights
Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis
It is of main clinical relevance to find non-invasive blood biomarkers that, along with clinical features and imaging techniques, could help us to identify axSpA patients at risk of CV events
In this study we aimed to assess the implication of omentin, a novel adipokine, in the CV risk and subclinical atherosclerosis of axSpA patients
Summary
Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis (axSpA). In most of the cases, the first step in CV disease is the development of atherosclerosis This process begins with damage to the vascular endothelium, triggered by the CV risk factors above mentioned, which can lead to structural changes in the vascular wall and that can be detected at the subclinical phase by non-invasive technologies such as carotid ultrasound[2,5,6]. In this regard, it has been shown that SpA patients develop thickening of the arterial wall and formation of carotid plaques more commonly than matched controls[5,7]. This is why it is so important to find biomarkers that may help to predict CV risk in these patients
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
