OP0304 GENETIC AND FUNCTIONAL STUDY OF OMENTIN REGARDING CARDIOVASCULAR RISK IN AXIAL SPONDYLOARTHRITIS
Authors: Fernanda Genre, Javier Rueda-Gotor, Sara Remuzgo-Martínez, Verónica Pulito-Cueto, Alfonso Corrales, Verónica Mijares, Leticia Lera-Gómez, Virginia Portilla, Rosa Expósito, Cristina Mata, Iván Ferraz-Amaro, Vanessa Hernández-Hernández, Santos Castañeda, Esther Vicente, Cristina Fernández-Carballido, Maria Paz Martínez-Vidal, David Castro-Corredor, Joaquín Anino-Fernández, Juan Carlos Quevedo-Abeledo, Carlos Rodríguez-Lozano, Ricardo Blanco, Oreste Gualillo, Javier Martin Ibanez, Javier Llorca, Raquel López-Mejías, Miguel A González-Gay
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> 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.<sup>1</sup> 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.<sup>2,3</sup> <h3>Objectives</h3> To evaluate the implication of omentin in CV risk and subclinical atherosclerosis in axSpA at the genetic and functional (mRNA and protein) level. <h3>Methods</h3> 382 patients fulfilling the ASAS classification criteria for axSpA<sup>4</sup> 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 <i>ITLN1</i>, coding omentin, was evaluated by RT-qPCR. <i>ITLN1</i> rs12409609 (C/T), in complete linkage disequilibrium with a polymorphism previously associated with coronary artery disease,<sup>5</sup> was genotyped by TaqMan probes. Results were adjusted by potential confounding factors (STATA® v.11.1). <h3>Results</h3> Serum and mRNA levels of omentin were lower in axSpA compared to controls (p&lt;0.001). Low omentin serum levels were observed in obese patients, patients with inflammatory bowel disease (IBD) and in those with an atherogenic index indicative of dyslipidemia (p=0.002, 0.006 and 0.004, respectively). Interestingly, the C allele of rs12409609 (both when alleles and genotypes were assessed) was associated with low mRNA levels of omentin in axSpA (p&lt;0.001). No association was observed between omentin and markers of subclinical atherosclerosis at the DNA, mRNA and protein level. <h3>Conclusion</h3> 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"&gt;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. <h3>References</h3> [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. <h3>Acknowledgement</h3> 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). <h3>Disclosure of Interests</h3> Fernanda Genre: None declared, Javier Rueda-Gotor: None declared, Sara Remuzgo-Martínez: None declared, Verónica Pulito-Cueto: None declared, Alfonso Corrales: None declared, Verónica Mijares: None declared, Leticia Lera-Gómez: None declared, Virginia Portilla: None declared, Rosa Expósito: None declared, Cristina Mata: None declared, Iván Ferraz-Amaro: None declared, Vanessa Hernández-Hernández: None declared, Santos Castañeda Consultant for: Amgen, BMS, Pfizer, Lilly, MSD, Roche, Sanofi, UCB, Esther Vicente: None declared, Cristina Fernández-Carballido: None declared, Maria Paz Martínez-Vidal: None declared, David Castro-Corredor: None declared, Joaquín Anino-Fernández: None declared, Juan Carlos Quevedo-Abeledo: None declared, Carlos Rodríguez-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 López-Mejías: None declared, Miguel A González-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.