S Castañeda

Publications (3)7.65 Total impact

• Article: Association of the methionine sulfoxide reductase A rs10903323 gene polymorphism with cardiovascular disease in patients with rheumatoid arthritis.

  M García-Bermúdez, R López-Mejías, C González-Juanatey, S Castañeda, Ja Miranda-Filloy, R Blanco, B Fernández-Gutiérrez, A Balsa, I González-Álvaro, C Gómez-Vaquero, J Llorca, J Martín, Ma González-Gay
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  ABSTRACT: Objective: The methionine sulfoxide reductase A (MSRA) gene is related to oxidative stress that has been involved in the susceptibility to rheumatoid arthritis (RA) in genome-wide pathway analysis and replication studies. The aim of the present study was to determine whether the MSRA gene is implicated in susceptibility to cardiovascular (CV) disease in RA patients. Methods: A total of 1302 patients fulfilling the 1987 American College of Rheumatism classification criteria for RA were genotyped for the MSRA rs10903323 (G/A) polymorphism. Two hundred and thirty-three (17.9%) patients experienced CV events. Human leucocyte antigen (HLA)-DRB1 genotyping was performed using molecular-based methods. Multiple logistic regression models were constructed with adjustments for gender, age at RA diagnosis, follow-up, rheumatoid shared epitope, and traditional CV risk as potential confounders. Results: There were no statistically significant differences in the allele or genotype frequencies for the MSRA rs10903323 polymorphism between RA patients who experienced CV events and those who did not. However, an adjusted logistic regression model disclosed that the minor allele G yielded a marginally significant increased risk of CV events in this series of patients with RA [p = 0.05, odds ratio (OR) 1.68, 95% confidence interval (CI) 1.00-2.85]. When the logistic regression model was adjusted for anti-cyclic citrullinated peptide (anti-CCP) antibody status instead of for shared epitope, an increased risk of having ischaemic heart disease was found in patients carrying the minor allele G (p = 0.04, OR 2.00, 95% CI 1.03-3.88). Conclusion: The MSRA rs10903323 gene polymorphism may be implicated in the increased risk to develop CV events, in particular ischaemic heart disease, observed in RA patients.
  Scandinavian journal of rheumatology 06/2012; 41(5):350-3. · 2.51 Impact Factor
• Article: Lack of association of IL6R rs2228145 and IL6ST/gp130 rs2228044 gene polymorphisms with cardiovascular disease in patients with rheumatoid arthritis.

  R López-Mejías, M García-Bermúdez, C González-Juanatey, S Castañeda, J A Miranda-Filloy, C Gómez-Vaquero, B Fernández-Gutiérrez, A Balsa, D Pascual-Salcedo, R Blanco, I González-Álvaro, J Llorca, J Martín, M A González-Gay
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  ABSTRACT: Interleukin-6 (IL-6) is a key mediator of inflammation in rheumatoid arthritis (RA) and its actions may be controlled by the IL-6 receptor (IL-6R). IL-6 transducer (IL-6ST/ gp130) is the signal transducing subunit of the IL-6R. We assessed the influence of the IL6R and the IL6ST/gp130 genes in the risk of cardiovascular (CV) disease in RA. For this purpose, 1250 Spanish patients with RA were genotyped for the IL6R rs2228145 and IL6ST/gp130 rs2228044 functional gene polymorphisms. Patients were stratified according to the presence or absence of CV events. Also, a subgroup of patients without CV events was assessed for the presence of subclinical atherosclerosis using two surrogate markers of atherosclerosis (flow-mediated endothelium-dependent vasodilatation and carotid intima-media thickness). No significant differences in the genotype and allele frequencies for both gene polymorphisms between patients with and without CV events were observed. It was also the case when values of surrogate markers of atherosclerosis were compared according to IL6R and IL6ST genotype frequencies. In conclusion, our results do not confirm an association of IL6R rs2228145 and IL6ST/gp130 rs2228044 polymorphisms with CV disease in RA.
  Tissue Antigens 12/2011; 78(6):438-41. · 2.59 Impact Factor
• Article: Role of the CCR5/Δ32CCR5 polymorphism in biopsy-proven giant cell arteritis.

  F David Carmona, Luis Rodríguez-Rodríguez, Santos Castañeda, José A Miranda-Filloy, Inmaculada C Morado, Javier Narváez, Beatriz Marí-Alfonso, Ainhoa Unzurrunzaga, Raquel Ríos-Fernández, Ricardo Blanco, Eugenio de Miguel, Javier Martín, Miguel A González-Gay
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  ABSTRACT: To further explore the potential role of chemokines in giant cell arteritis (GCA), we have studied whether the CCR5/Δ32CCR5 polymorphism is implicated in the susceptibility to the disease and its specific features. A total of 352 Spanish patients with biopsy-proven GCA and 479 matched controls were assessed. DNA was obtained from peripheral blood. Samples were genotyped by PCR with specific primers spanning the 32-bp deletion region. No statistically significant difference in the Δ32CCR5 allele frequency between GCA patients (6.1%) and controls (6.8%) was observed (p = 0.58). This was also the case when the CCR5 /Δ32CCR5 genotype distribution was assessed (p = 0.49). The Δ32CCR5 allele frequency did not differ between patients with or without specific manifestations of the disease, such as polymyalgia rheumatica, visual ischemic manifestations, or irreversible occlusive disease. Hence, our results do not support a potential influence of Δ32CCR5 in the susceptibility to or clinical spectrum of GCA.
  Human immunology 02/2011; 72(5):458-61. · 2.55 Impact Factor