Lack of association of PTPN22, STAT4 and TRAF1/C5 gene polymorphisms with cardiovascular risk in rheumatoid arthritis. 2010

R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
Instituto de Parasitologia y Biomedicina Lopez Neyra, Consejo Superior de Investigaciones Cientificas (CSIC), Granada, Spain. rpm@ipb.csic.es

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.

UI MeSH Term Description Entries
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D002318 Cardiovascular Diseases Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM. Adverse Cardiac Event,Cardiac Events,Major Adverse Cardiac Events,Adverse Cardiac Events,Cardiac Event,Cardiac Event, Adverse,Cardiac Events, Adverse,Cardiovascular Disease,Disease, Cardiovascular,Event, Cardiac
D003182 Complement C5 C5 plays a central role in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C5 is cleaved by C5 CONVERTASE into COMPLEMENT C5A and COMPLEMENT C5B. The smaller fragment C5a is an ANAPHYLATOXIN and mediator of inflammatory process. The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX. C5 Complement,Complement 5,Complement C5, Precursor,Complement Component 5,Precursor C5,Pro-C5,Pro-complement 5,C5, Complement,C5, Precursor,C5, Precursor Complement,Complement, C5,Component 5, Complement,Precursor Complement C5,Pro C5,Pro complement 5
D005260 Female Females
D005838 Genotype The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS. Genogroup,Genogroups,Genotypes
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D001172 Arthritis, Rheumatoid A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated. Rheumatoid Arthritis
D012307 Risk Factors An aspect of personal behavior or lifestyle, environmental exposure, inborn or inherited characteristic, which, based on epidemiological evidence, is known to be associated with a health-related condition considered important to prevent. Health Correlates,Risk Factor Scores,Risk Scores,Social Risk Factors,Population at Risk,Populations at Risk,Correlates, Health,Factor, Risk,Factor, Social Risk,Factors, Social Risk,Risk Factor,Risk Factor Score,Risk Factor, Social,Risk Factors, Social,Risk Score,Score, Risk,Score, Risk Factor,Social Risk Factor
D015897 Comorbidity The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival.

Related Publications

R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
January 2010, Arthritis research & therapy,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
January 2014, Immunological investigations,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
January 2012, Cellular immunology,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
January 2014, Molecular biology reports,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
August 2015, Immunobiology,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
December 2011, Human immunology,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
January 2015, Acta reumatologica portuguesa,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
March 2024, Archives of rheumatology,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
April 2023, International journal of molecular sciences,
R Palomino-Morales, and C Gonzalez-Juanatey, and T R Vazquez-Rodriguez, and L Rodriguez, and J A Miranda-Filloy, and D Pascual-Salcedo, and A Balsa, and B Fernandez-Gutierrez, and J Llorca, and J Martin, and M A Gonzalez-Gay
February 2010, Annals of the rheumatic diseases,
Copied contents to your clipboard!