Rheumatoid arthritis does not share most of the newly identified systemic lupus erythematosus genetic factors

2009; Wiley; Volume: 60; Issue: 9 Linguagem: Inglês

10.1002/art.24748

ISSN

1529-0131

Autores

Marian Suarez-Gestal, Manuel Calaza, Rebeca Dieguez‐Gonzalez, Eva Pérez‐Pampín, José L. Pablos, Federico Navarro, Javier Narváez, José Luis Marenco, Gabriel Herrero‐Beaumont, Benjamín Fernández‐Gutiérrez, José Ramón Lamas, Arturo Rodríguez de la Serna, Ana María Ortiz, Luis Carreño, Juan D. Cañete, Rafael Cáliz, Francisco J. Blanco, Alejandro Balsa, Juan J. Gómez‐Reino, Antonio González,

Tópico(s)

Galectins and Cancer Biology

Resumo

Abstract Objective Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) share some genetic factors such as HLA , PTPN22 , STAT4 , and 6q23 . The aim of this study was to determine whether 9 other SLE genetic factors are also implicated in RA susceptibility. Methods A characteristic single‐nucleotide polymorphism (SNP) in each of 9 genetic factors, ITGAM (rs1143679), C8orf13–BLK (rs13277113), TYK2 (rs2304256), 1q25.1 (rs10798269), PXK (rs6445975), KIAA1542 (rs4963128), MECP2 (rs17435), BANK1 (rs17266594), and LY9 (rs509749), was studied in 1,635 patients with RA and 1,906 control subjects from Spain. The rs7574865 SNP in STAT4 was also included. Analyses were conducted globally and after stratification by sex and clinical features (anti–cyclic citrullinated peptide and rheumatoid factor, shared epitope, rheumatoid nodules, radiographic changes, sicca syndrome, and pneumonitis). Results No association was observed between RA and any of the 9 newly identified SLE genetic factors. A meta‐analysis using previous data was consistent with these results. In addition, there were no significant differences between individuals with and those without each of the clinical features analyzed, except the frequency of the minor allele in the C8orf13–BLK locus that was decreased in patients with sicca syndrome (14.6% versus 22.4% in controls; P = 0.003). Conclusion None of the 9 recently identified SLE risk factors showed association with RA. Therefore, common genetic factors affecting the pathogenesis of these 2 disorders seem to be limited, revealing that the genetic component contributes to the different expression of these diseases.

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