title: Lack of association of PTPN22, STAT4 and TRAF1/C5 gene polymorphisms with cardiovascular risk in rheumatoid arthritis.
abstract: OBJECTIVE
  To determine whether the PTPN22, STAT4 and TRAF1/C5 gene polymorphisms may be implicated in the development of cardiovascular (CV) events and subclinical atherosclerosis manifested by the presence of endothelial dysfunction or increased carotid intima-media thickness (IMT) in a series of Spanish patients with rheumatoid arthritis (RA).
  
  
  METHODS
  Six hundred and twelve patients fulfilling the 1987 American College of Rheumatology classification criteria for RA, seen at the rheumatology outpatient clinics of Hospital Xeral-Calde, Lugo, and Hospital San Carlos, Madrid, were studied. Patients were genotyped using predesigned TaqMan single nucleotide polymorphism genotyping assays. Moreover, between March and December 2007, a subgroup of unselected RA patients with no history of CV events was studied for the presence of subclinical atherosclerosis by the assessment of the endothelial function (n=126) and the carotid artery IMT (n=110) by ultrasonography studies.
  
  
  RESULTS
  No significant differences in the allele or genotype frequencies for the PTPN22, STAT4 and TRAF1/C5 gene polymorphisms between RA patients with or without CV events were found. It was also the case when we analysed the potential influence of the genotypes in the presence of endothelial dysfunction or increased carotid artery IMT of patients with RA.
  
  
  CONCLUSIONS
  Our results do not show that the PTPN22, STAT4 and TRAF1/C5 gene polymorphisms may confer a direct risk of CV disease in patients with RA.
authors.affiliation: Instituto de Parasitologia y Biomedicina Lopez Neyra, Consejo Superior de Investigaciones Cientificas (CSIC), Granada, Spain. rpm@ipb.csic.es
authors.forename: R
authors.initials: R
authors.lastname: Palomino-Morales
authors.forename: C
authors.initials: C
authors.lastname: Gonzalez-Juanatey
authors.forename: T R
authors.initials: TR
authors.lastname: Vazquez-Rodriguez
authors.forename: L
authors.initials: L
authors.lastname: Rodriguez
authors.forename: J A
authors.initials: JA
authors.lastname: Miranda-Filloy
authors.forename: D
authors.initials: D
authors.lastname: Pascual-Salcedo
authors.forename: A
authors.initials: A
authors.lastname: Balsa
authors.forename: B
authors.initials: B
authors.lastname: Fernandez-Gutierrez
authors.forename: J
authors.initials: J
authors.lastname: Llorca
authors.forename: J
authors.initials: J
authors.lastname: Martin
authors.forename: M A
authors.initials: MA
authors.lastname: Gonzalez-Gay
mesh_terms: D001172:Arthritis, Rheumatoid / Q000453:epidemiology / Q000235:genetics*; D050197:Atherosclerosis / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000235:genetics*; D015897:Comorbidity; D003182:Complement C5 / Q000235:genetics* / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22 / Q000235:genetics* / Q000378:metabolism; D012307:Risk Factors; D050797:STAT4 Transcription Factor / Q000235:genetics* / Q000378:metabolism; D047990:TNF Receptor-Associated Factor 1 / Q000235:genetics* / Q000378:metabolism
chemical_list: D003182:Complement C5; D050797:STAT4 Transcription Factor; C494090:STAT4 protein, human; D047990:TNF Receptor-Associated Factor 1; C516765:PTPN22 protein, human; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22