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SAT0008 Il-17a Gene Implication in spanish Patients with Rheumatoid Arthritis
  1. F. Genre1,
  2. R. Lόpez-Mejías1,
  3. S. Remuzgo-Martínez1,
  4. M. Robustillo-Villarino2,
  5. S. Castañeda3,
  6. C. González-Juanatey4,
  7. J. Llorca5,
  8. A. Corrales1,
  9. B. Ubilla1,
  10. V. Mijares1,
  11. J.A. Miranda-Filloy6,
  12. T. Pina1,
  13. C. Gόmez-Vaquero7,
  14. L. Rodríguez-Rodríguez8,
  15. B. Fernández-Gutiérrez8,
  16. A. Balsa9,
  17. D. Pascual-Salcedo9,
  18. F.J. Lόpez-Longo10,
  19. P. Carreira11,
  20. R. Blanco1,
  21. I. González-Άlvaro3,
  22. J.J. Alegre-Sancho2,
  23. C. Magro12,
  24. E. Raya12,
  25. J. Martín13,
  26. M.Ά. González-Gay1,14,15
  1. 1Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander
  2. 2Rheumatology Department, Hospital Universitario Doctor Peset, Valencia
  3. 3Rheumatology Department, Hospital Universitario la Princesa, IIS-Princesa, Madrid
  4. 4Cardiology Division, Hospital Universitario Lucus Augusti, Lugo
  5. 5Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander
  6. 6Rheumatology Division, Hospital Universitario Lucus Augusti, Lugo
  7. 7Rheumatology Department, Hospital Universitario Bellvitge, Barcelona
  8. 8Rheumatology Department, Hospital Clínico San Carlos
  9. 9Rheumatology Department, Hospital Universitario La Paz
  10. 10Rheumatology Department, Hospital General Universitario Gregorio Marañόn
  11. 11Rheumatology Department, Hospital Universitario 12 de Octubre, Madrid
  12. 12Rheumatology Department, Hospital Clínico San Cecilio
  13. 13Institute of Parasitology and Biomedicine Lόpez-Neyra, IPBLN-CSIC, Granada, Spain
  14. 14Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
  15. 15School of Medicine, University of Cantabria, Santander, Spain

Abstract

Background Rheumatoid arthritis (RA) is an autoimmune pathology associated with increased risk of cardiovascular (CV) disease and subclinical atherosclerosis1. Consequently, both inflammatory diseases share common molecules involved in its pathogenesis. In this sense, interleukin 17A (IL-17A) is a pro-inflammatory cytokine involved in the regulation of immune responses and chronic inflammation2.

Objectives To evaluate the potential association between different IL-17A polymorphisms and CV events, as well as subclinical atherosclerosis, in a large cohort of Spanish RA patients.

Methods Five IL-17A polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were genotyped by TaqMan assays in a 7900 HT Real-Time polymerase chain reaction system in 1,974 Spanish patients diagnosed with RA (fulfilling the 2010 American College of Rheumatology classification criteria for RA3), recruited from different Spanish hospitals. 318 patients (16.1%) had experienced CV events, and 822 had undergone carotid ultrasonography studies to assess subclinical atherosclerosis (presence/absence of plaques and carotid intima media thickness [cIMT]). The relationship between IL-17A alleles, genotypes and haplotypes and CV events, presence/absence of plaques and cIMT values was assessed. Results were adjusted for sex, age at diagnosis and traditional CV risk factors.

Results No statistically significant differences were observed when allelic/genotypic frequencies of each IL-17A polymorphism were assessed regarding presence/absence of CV events, plaques or cIMT values. This was also the case when the five polymorphisms were combined to form haplotypes.

Conclusions Our results do not confirm an association between the five IL-17A polymorphisms studied and the development of CV events or subclinical atherosclerosis in our cohort of Spanish RA patients.

  1. Avina-Zubieta JA et al. Ann Rheum Dis. 2012;71:1524–9.

  2. Shabgah AG et al. Postepy Dermatol Alergol. 2014;31(4):256–61.

  3. D. Aletaha T et al. Arthritis Rheum. 2010;62:2569–81.

Acknowledgement This study was supported by European Union FEDER funds and “Fondo de Investigaciόn Sanitaria” (PI12/00060 and PI15/00525) (Spain), and partially supported by RETICS Programs RD12/0009 (RIER) from “Instituto de Salud Carlos III” (ISCIII) (Spain). FG is a recipient of a Sara Borrell postdoctoral fellowship from the ISCIII (Spain) (CD15/00095). RL-M and BU are supported by funds from the RETICS Program (RIER) (RD12/0009/0013).

Disclosure of Interest None declared

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