OP0304 GENETIC AND FUNCTIONAL STUDY OF OMENTIN REGARDING CARDIOVASCULAR RISK IN AXIAL SPONDYLOARTHRITIS

Background Cardiovascular (CV) disease is one of the main causes of mortality in axial spondyloarthritis (axSpA). The higher incidence of CV risk factors and systemic chronic inflammation increase CV risk in axSpA.1 This is enhanced by a dysregulation of adipokines. Low levels of omentin, an anti-inflammatory adipokine, have been associated with metabolic dysfunction and CV disease in general population and conditions different from axSpA.2,3 Objectives To evaluate the implication of omentin in CV risk and subclinical atherosclerosis in axSpA at the genetic and functional (mRNA and protein) level. Methods 382 patients fulfilling the ASAS classification criteria for axSpA4 and 84 controls were included. Carotid ultrasound was performed to evaluate the presence of subclinical atherosclerosis. Serum omentin levels were assessed by ELISA. mRNA expression of ITLN1, coding omentin, was evaluated by RT-qPCR. ITLN1 rs12409609 (C/T), in complete linkage disequilibrium with a polymorphism previously associated with coronary artery disease,5 was genotyped by TaqMan probes. Results were adjusted by potential confounding factors (STATA® v.11.1). Results Serum and mRNA levels of omentin were lower in axSpA compared to controls (p Conclusion style=”font-family: ‘Times New Roman’,’serif’; font-size: 10.0pt; margin: 0cm; margin-bottom: 8.0pt; line-height: 106%; margin-left: 0cm; margin-right: 0cm; margin-top: 0cm; mso-style-name: Normal_0; text-align: justify;” fontsize=”11.0” data-pos-index=”15” class-name=”Deleted”>Omentin is linked to obesity and adverse lipid profiles in axSpA. Additionally, low serum levels of omentin are associated with the presence of IBD in axSpA. These data support a role of omentin as a CV risk biomarker in axSpA. References [1] Joint Bone Spine.2014;81:57-63. [2] Cardiovasc Hematol Disord Drug Targets.2013;13:59-72. [3] Curr Issues Pharm Med Sci.2015;28:176-80. [4] Ann Rheum Dis.2009;68:777-83. [5] Asian Cardiovasc Thorac Ann.2017;25:199-203. Acknowledgement Study supported by NVAL17/10 (IDIVAL). Personal funds: FG: Sara Borrell fellowship CD15/00095 (ISCIII-ESF); SR-M: RD16/0012/0009 (ISCIII-ERDF); VP-C: PREVAL18/01 (IDIVAL); VM and RL-M: Miguel Servet type I CP16/00033 (ISCIII-ERDF, ISCIII-ESF). Disclosure of Interests Fernanda Genre: None declared, Javier Rueda-Gotor: None declared, Sara Remuzgo-Martinez: None declared, Veronica Pulito-Cueto: None declared, Alfonso Corrales: None declared, Veronica Mijares: None declared, Leticia Lera-Gomez: None declared, Virginia Portilla: None declared, Rosa Exposito: None declared, Cristina Mata: None declared, Ivan Ferraz-Amaro: None declared, Vanessa Hernandez-Hernandez: None declared, Santos Castaneda Consultant for: Amgen, BMS, Pfizer, Lilly, MSD, Roche, Sanofi, UCB, Esther Vicente: None declared, Cristina Fernandez-Carballido: None declared, Maria Paz Martinez-Vidal: None declared, David Castro-Corredor: None declared, Joaquin Anino-Fernandez: None declared, Juan Carlos Quevedo-Abeledo: None declared, Carlos Rodriguez-Lozano: None declared, Ricardo Blanco Grant/research support from: Abbvie, MSD and Roche, Consultant for: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Oreste Gualillo: None declared, Javier Martin Ibanez: None declared, Javier Llorca: None declared, Raquel Lopez-Mejias: None declared, Miguel A Gonzalez-Gay Grant/research support from: Prof. MA Gonzalez-Gay received grants/research supports from Abbvie, MSD, Jansen and Roche., Speakers bureau: Consultation fees/participation in company sponsored speaker’s bureau from Pfizer, Lilly, Sobi, Celgene, Novartis, Roche and Sanofi.