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sE-Selectin Expression and A561C Polymorphism in Relation to Rheumatoid Arthritis Clinical Activity
ROSA ELENA NAVARRO-HERNÁNDEZ, EDITH OREGÓN-ROMERO, HÉCTOR RANGEL-VILLALOBOS, MÓNICA VÁZQUEZ-DEL MERCADO, SANDRA LUZ RUIZ-QUEZADA, MONSERRAT MALDONADO-GONZÁLEZ, REFUGIO TORRES-VITELA, and JOSÉ FRANCISCO MUÑOZ-VALLE ABSTRACT. Objective. To investigate the relationship of A561C polymorphism and sE-selectin levels with rheumatoid arthritis (RA) clinical activity. Methods. In a case-control study, we compared 60 patients with RA and 60 healthy subjects. Patients fulfilled the 1987 American College of Rheumatology criteria. Soluble E-selectin levels were measured from serum samples using the ELISA kit. We investigated E-selectin A561C polymorphism by the restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) technique. The disease activity was recorded with Spanish Health Assessment Questionnaire Disability Index (HAQ-DI), Spanish Arthritis Impact Measurement Scales (AIMS), and Disease Activity Score (DAS28) scores. A p value < 0.05 was considered significant. Results. Patients with RA showed higher sE-selectin levels than controls (mean 91.7 vs 39 ng/ml; p = 0.002). A positive correlation between sE-selectin and rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), Spanish HAQ-DI, and DAS28 scores was found. The E-selectin polymorphism analysis showed diminished frequency in RA of heterozygous A/C genotype and increased frequency of homozygous wild-type A/A genotype (p = 0.043, OR 1.45; 95% CI 1.125-16.167) versus A/C and A/A genotype in healthy subjects. No significant association between A561C polymorphism and clinical activity was present. Conclusion. The sE-selectin, RF, and ESR, in addition to clinical indices, were associated with clinical activity in RA. We highlighted the presence of A/A genotype A561C polymorphism in our patients with RA. (J Rheumatol 2006;33:1968-72) Key Indexing Terms:
sE-SELECTIN From Doctorado en Ciencias Biomédicas, Orientación en Inmunología –– Laboratorio de Inmunología; Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Centro Universitario de Ciencias de la Salud; Laboratorio de Genética Molecular, Centro Universitario de la Ciénega; and Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico. Supported by grant No. 45703-M to JFMV of the National Council of Science and Technology (CONACyT, México-Universidad de Guadalajara). R.E. Navarro-Hernández, MSc, PhD Student, Doctorado en Ciencias Biomédicas, Orientación en Inmunología –– Laboratorio de Inmunología, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Departamento de Farmacobiología; E. Oregón-Romero, MSc, PhD Student; M. Vázquez-Del Mercado, MD, PhD, Titular Professor; S.L. Ruiz-Quezada, PhD; J.F. Muñoz-Valle, PhD, Titular Professor, Doctorado en Ciencias Biomédicas, Orientación en Inmunología –– Laboratorio de Inmunología, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético; H. Rangel-Villalobos, PhD, Titular Professor, Laboratorio de Genética Molecular; M. Maldonado-González, PhD, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético; R. Torres-Vitela, PhD, Titular Professor, Departamento de Farmacobiología, Universidad de Guadalajara. Address reprint requests to Dr. J.F. Muñoz Valle, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Centro Universitario de Ciencias de la Salud, Sierra Mojada Street No. 950, P.O. Box 2-207, Guadalajara, Jalisco, México, C.P. 44281. E-mail: biologiamolecular@hotmail.com Accepted for publication May 24, 2006.
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