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AB0013 Lack of Association between IL6 Gene and Henoch-SchÖNlein Purpura
  1. R. Lopez1,
  2. B. Sevilla Perez2,
  3. F. Genre1,
  4. S. Castañeda3,
  5. N. Ortego-Centeno2,
  6. J. Llorca4,
  7. B. Ubilla1,
  8. V. Calvo-Rio1,
  9. T. Pina1,
  10. M.C. González-Vela5,
  11. A. Marquez6,
  12. L. Sala-Icardo3,
  13. J.A. Miranda-Filloy7,
  14. J. Rueda-Gotor1,
  15. J. Martin6,
  16. R. Blanco1,
  17. M.A. Gonzalez-Gay1
  1. 1Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander
  2. 2Medicine Department, Hospital Universitario San Cecilio, Granada
  3. 3Rheumatology Department, Hospital Universitario la Princesa, IIS-Princesa, Madrid
  4. 4Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IFIMAV
  5. 5Patology Division, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander
  6. 6Instituto de Parasitología y Biomedicina Lόpez-Neyra, C.S.I.C., Granada
  7. 7Division of Rheumatology, Hospital Universitario Lucus Augusti, Lugo, Spain

Abstract

Background Henoch-Schönlein purpura (HSP) is the most common type of primary small-sized blood vessel vasculitis in children and a rare entity in adults [1]. Although the etiology of HSP remains unknown, environmental factors and a susceptible genetic background have been associated with this pathology [2]. Interleukin-6 (IL-6) is a proinflammatory cytokine with a pivotal role in the immune system [3] and polymorphisms in the IL6 gene have been associated with several autoimmune diseases

Objectives In the present study, we assessed the potential association of three genetic variants located in the IL6 gene that cover the major variability of this gene with HSP susceptibility and severity.

Methods Our study population was composed of 285 Spanish patients diagnosed with HSP and 877 sex and ethnically matched Spanish controls. In addition to genotyping the traditional promoter single nucleotide polymorphism (SNP) -174G>C (rs1800795), we assessed another two SNPs (rs2069827 and rs2069840) located in the IL6 gene that were selected by SNP-tagging.

Results No significant differences in the genotypic and allelic frequencies between HSP patients and controls were observed when the rs2069827, rs1800795 and rs2069840 polymorphisms were analyzed independently or combined conforming haplotypes. Moreover, there were no differences in the allele or genotype frequency when HSP were stratified according to the age at disease onset, presence of nephritis or gastrointestinal manifestations.

Conclusions Our results do not support association between the IL6 rs2069827, rs1800795 and rs2069840 gene polymorphisms and HSP susceptibility or specific clinical features of the disease.

References

  1. Gonzalez-Gay MA, Garcia-Porrua C. Rheum Dis Clin North Am 2001; 27: 729-749.

  2. Wyatt RJ, Julian BA. N Engl J Med 2013; 368: 2402-14.

  3. Nishimoto N, Kishimoto T. Nat Clin Pract Rheumatol 2006; 2: 619-626.

Acknowledgements This study was supported by a grant from “Fondo de Investigaciones Sanitarias” PI12/00193 (Spain). RLM is a recipient of a Sara Borrell postdoctoral fellowship from the Instituto de Salud Carlos III at the Spanish Ministry of Health (Spain). FG and BU are supported by funds from the RETICS Program (RIER) (RD12/0009/0013).

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.1766

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