Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/45017
Title: The - 383A>C TNFRI polymorphism is associated with soluble levels and clinical activity in rheumatoid arthritis
Author: Zavaleta-Muniz, S.A.
Martin-Marquez, B.T.
Gonzalez-Lopez, L.
Gonzalez-Montoya, N.G.
Diaz-Toscano, M.L.
Ponce-Guarneros, J.M.
Ruiz-Padilla, A.J.
Mercado, M.V.-D.
Maldonado-Gonzalez, M.
Fafutis-Morris, M.
Flores-Martinez, S.E.
Martinez-García, E.A.
Gamez-Nava, J.I.
Issue Date: 2013
Abstract: Objective. There is a lack of information about the genotype frequencies of IL-6 -174G/C and -572G/C polymorphisms in Mexicans with rheumatoid arthritis (RA). Therefore, the aim of this study was to evaluate the association of the IL-6 -174G/C and -572G/C polymorphisms in Mexican mestizo with RA. Methods. We included 137 patients with RA and 102 healthy controls. Patients were assessed for clinical characteristics. IL-6 -174G/C and -572G/C polymorphisms were genotyped using PCR-RFLP analysis. Allele and genotype frequencies and the Hardy-Weinberg equilibrium were computed. Odds ratios (ORs) were computed to identify the risk for RA associated with the presence of GG genotype in comparison with the GC or CC genotypes. Results. The genotype -174GG occurred at a higher frequency in cases and controls (77.4% versus 78.4%, P = 0.845). We found similar results for the genotype -572GG (54% in patients versus 60.8% in controls, P = 0.295). Conclusions. This is the first study to evaluate the association of -174G/C and -572G/C polymorphisms of the IL-6 gene with RA in Mexican mestizo patients. These two polymorphisms were not associated with RA in the studied sample. Additional studies are required to evaluate if these IL-6 polymorphisms have relevance to the development of more severe disease. " 2013 S. A. Zavaleta-Muñiz et al.",,,,,,"10.1155/2013/959084",,,"http://hdl.handle.net/20.500.12104/45017","http://www.scopus.com/inward/record.url?eid=2-s2.0-84885664849&partnerID=40&md5=6e2f1ce16cc94e772069530750a57f7a
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=medl&AN=24223608",,,,,,,,"Clinical and Developmental Immunology",,,,"2013",,"Scopus
MEDLINE",,,,"Index Medicus;Adult;Alleles;Arthritis, Rheumatoid/bl [Blood];Arthritis, Rheumatoid/di [Diagnosis];Arthritis, Rheumatoid/ge [Genetics];Case-Control Studies;Female;Gene Frequency;Genotype;Humans;Interleukin-6/bl [Blood];Interleukin-6/ge [Genetics];Male;Mexico;Middle Aged;Polymorphism, Single Nucleotide;Promoter Regions, Genetic",,,,,,,,"The -174G/C and -572G/C interleukin 6 promoter gene polymorphisms in Mexican patients with rheumatoid arthritis: A case-control study",,"Article" "46788","123456789/35008",,"Valle, Y., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, Posdoctorado en Ciencias Biomédicas (Inmunología), Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Padilla-Gutiérrez, J.R., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, Posdoctorado en Ciencias Biomédicas (Inmunología), Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Torres-Carrillo, N.M., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Ledezma-Lozano, I.Y., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Corona-Sánchez, E.G., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, Hospital De Especialidades Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social (IMSS), Unidad de Investigación Clínica y Epidemiológica, Guadalajara, Jalisco, Mexico; Vázquez-Del Mercado, M., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, División de Medicina Interna, Departamento de Reumatología, Hospital Civil Dr. Juan I Menchaca, Guadalajara, Jalisco, Mexico; Rangel-Villalobos, H., Centro Universitario de la Cienega, Instituto de Investigación en Genética Molecular, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico; Gómez-Nava, J.I., Hospital De Especialidades Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social (IMSS), Unidad de Investigación Clínica y Epidemiológica, Guadalajara, Jalisco, Mexico; González-López, L., Hospital De Especialidades Centro Médico Nacional de Occidente, Instituto Mexicano del Seguro Social (IMSS), Unidad de Investigación Clínica y Epidemiológica, Guadalajara, Jalisco, Mexico; Muñoz-Valle, J.F., Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico, Departamento de Biología Molecular y Genómica, Instituto de Investigacion en Reumatologia y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Colonia Lomas de Atemajac, Insurgentes 244-1, 45178 Zapopan, Jalisco, Mexico",,"Valle, Y.
Padilla-Gutierrez, J.R.
Torres-Carrillo, N.M.
Ledezma-Lozano, I.Y.
Corona-Sanchez, E.G.
Vazquez-Del Mercado, M.
Rangel-Villalobos, H.
Gamez-Nava, J.I.
Gonzalez-Lopez, L.
Munoz-Valle, J.F.",,"2010",,"Tumor necrosis factor-? (TNF-?) plays a central role in inflammation, and it has been directly implicated in the pathogenesis of rheumatoid arthritis (RA). TNF-? activity is mediated through TNFRI and TNFRII cell surface receptors, which act as physiological attenuators of TNF-? activity. We recruited 190 RA patients and 190 healthy subjects (HS) in order to associate the - 383A>C TNFRI polymorphism with sTNFRI levels and DAS28 score in RA. In results, sTNFRI levels were higher in RA patients than HS (P = 0.04). The - 383A>C TNFRI polymorphism did not show significant differences in both studied groups. However, in the RA group the sTNFRI levels were significantly elevated (P = 0.004) in A/A genotype carriers. In addition, the A/A genotype carriers had the higher DAS28 score than A/C genotype (P = 0.02). These data suggest that - 383A>C TNFRI polymorphism is not a susceptibility marker in RA, whereas the increased levels of sTNFRI could reflect the clinical activity in RA patients. " Springer-Verlag 2009.
URI: http://hdl.handle.net/20.500.12104/45009
http://www.scopus.com/inward/record.url?eid=2-s2.0-77951023590&partnerID=40&md5=595743a90d0cbd2bb684a2ea600731d9
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