Ab0070 role of Vaspin in Atherosclerotic Disease and Cardiovascular Risk in Axial Spondyloarthritis

Abstract

Background:Vaspin is a novel anti-inflammatory adipokine associated with cardiovascular (CV) disease and inflammation in chronic inflammatory conditions different from axial spondyloarthritis (axSpA).1 Given the high incidence of CV disease (mainly due to accelerated atherosclerosis) exhibited by axSpA patients,2 we wondered if vaspin could also be a key molecule in this process. However, data on the role of vaspin regarding atherosclerotic disease in the context of axSpA is scarce.3Objectives:To evaluate the implication of vaspin, at the genetic and serological level, in subclinical atherosclerosis and CV risk in axSpA.Methods:510 patients who fulfilled the ASAS criteria for axSpA4 were included in this study. Carotid ultrasound (US) was performed to evaluate the presence of subclinical atherosclerosis. Three vaspin gene variants (rs2236242 T/A, rs7159023 G/A and rs35262691 T/C) were genotyped by TaqMan probes. Serum vaspin levels were assessed by Enzyme-Linked ImmunoSorbent Assay. Analysis was performed using a statistical software.Results:Serum vaspin levels were significantly higher in female patients than in males and also in obese patients when compared to those with normal weight (p<0.05). At the genetic level, we disclosed that the minor allele of rs2236242 (A) was associated with lower serum vaspin levels in axSpA, while the rs7159023 minor allele (A) was linked to higher serum levels (p<0.05). When the three polymorphisms assessed were combined conforming haplotypes, we disclosed that the TGC haplotype related to high serum levels of vaspin (p=0.01). However, no statistically significant association was observed between vaspin and markers of subclinical atherosclerosis, both at the genetic and serological level.Conclusion:Our results revealed that vaspin is linked to CV risk factors that may influence on the atherosclerotic process in axSpA. Additionally, we disclosed that serum vaspin concentration is genetically modulated in a large cohort of patients with axSpA.References:[1]Adv Exp Med Biol. 2019;1111:159-88.[2]Front Med (Lausanne). 2018;5:62.[3]Braz J Med Biol Res. 2016;49(7):e5231.[4]Ann Rheum Dis. 2009;68(2):ii1-44.Acknowledgements:Personal funds: RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF); SR-M: RD16/0012/0009 (ISCIII-ERDF); VP-C: PREVAL18/01 (IDIVAL); LL-G: INNVAL20/06 (IDIVAL).Disclosure of Interests:Javier Rueda-Gotor: None declared, Raquel López-Mejías: None declared, Sara Remuzgo-Martínez: None declared, Verónica Pulito Cueto: None declared, Alfonso Corrales: None declared, Leticia Lera-Gómez: None declared, Virginia Portilla: None declared, Iñigo González-Mazón: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Rosa Expósito: None declared, Cristina Mata: None declared, Javier Llorca: None declared, Vanessa Hernández-Hernández: None declared, Carlos Rodríguez-Lozano: None declared, Nuria Barbarroja Puerto: None declared, Rafaela Ortega Castro: None declared, Noelia García Castañeda: None declared, Cristina Fernández-Carballido: None declared, Maria Paz Martínez-Vidal: None declared, David Castro-Corredor: None declared, Joaquín Anino-Fernández: None declared, Diana Peiteado: None declared, Chamaida Plasencia: None declared, E Galindez: None declared, María L. García Vivar: None declared, Oreste Gualillo: None declared, Juan Carlos Quevedo-Abeledo: None declared, Santos Castañeda: None declared, Iván Ferraz-Amaro: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Fernanda Genre: None declared