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  • Investigation of a PON1 gene polymorphism (rs662 polymorphism) as predictor of subclinical atherosclerosis in patients with rheumatoid arthritis

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Investigation of a PON1 gene polymorphism (rs662 polymorphism) as predictor of subclinical atherosclerosis in patients with rheumatoid arthritis
  1. Raquel López-Mejías1,
  2. Fernanda Genre1,
  3. Alfonso Corrales1,
  4. Carlos González-Juanatey2,
  5. Begoña Ubilla1,
  6. Javier Llorca3,
  7. José A Miranda-Filloy4,
  8. Trinitario Pina1,
  9. Ricardo Blanco1,
  10. Santos Castañeda5,
  11. Javier Martín6,
  12. Miguel A González-Gay1
  1. 1 Department of Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IDIVAL, Santander, Spain
  2. 2 Cardiology Division, Hospital Lucus Augusti, Lugo, Spain
  3. 3 Department of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain
  4. 4 Division of Rheumatology, Hospital Lucus Augusti, Lugo, Spain
  5. 5 Rheumatology Department, Hospital Universitario la Princesa, IIS-Princesa, Madrid, Spain
  6. 6 Instituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Granada, Spain
  1. Correspondence to Dr Miguel A González-Gay, Rheumatology Division, Hospital Universitario Marqués de Valdecilla, IDIVAL, Avenida de Valdecilla, s/n, Santander 39008, Spain; miguelaggay{at}hotmail.com

https://doi.org/10.1136/annrheumdis-2014-205543

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    Several pieces of evidence indicate that rheumatoid arthritis (RA) is a proatherogenic disease associated with increased cardiovascular (CV) death rate.1 The mechanisms leading to that are complex, including traditional CV risk factors and also the presence of a chronic inflammatory state.1 Dyslipidemia with reduction in total cholesterol and its fractions and qualitative impairment in the high density lipoprotein (HDL)-cholesterol has been observed in RA patients with active disease.2 Chronic inflammation promotes oxidative changes that alter HDL structure and reduce apolipoprotein-A-I in patients with active RA. Decreased levels of the antioxidant HDL-associated enzyme paraoxonase (PON1) have been observed in these patients.3 Improvement of inflammation, as shown in patients undergoing biologic therapy, is associated with increases of PON1 activities.4

    RA is a polygenic disease. Previous studies have emphasised the implication of a genetic component in the risk of CV disease in RA.5 ,6 A functional, genetic T/C amino acid variant found within the PON1 gene (rs662) confers an amino acid change (Q192R) influential in determining PON1 activity values. …

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    Footnotes

    • RL-M and FG contributed equally.

    • MAG-G and JM shared senior authorship in this study.

    • Contributors RL-M and FG performed the study, contributed to the elaboration of the protocol of study, helped in the interpretation of data and in the elaboration of the manuscript. AC and CG-J performed the carotid ultrasound studies. BU performed the PCR studies and helped in the interpretation of data. JL contributed to the elaboration of the protocol of study, helped in the interpretation of data and the elaboration of the manuscript and performed the statistical analysis. JAM-F, TP and RB recruited patients for the study, contributed to the elaboration of the protocol of study and helped in the interpretation of data. SC contributed to the elaboration of the protocol of study, helped in the interpretation of data and in the final drafting and elaboration of the manuscript. JM contributed to the elaboration of the protocol of study, helped in the interpretation of data and was responsible of the final drafting and elaboration of the manuscript. MAG-G recruited patients, contributed to the elaboration of the protocol of study, helped in the Interpretation of data and was responsible of the final drafting and elaboration of the manuscript.

    • Funding European Union FEDER funds, FIS (PI06/0024, PS09/00748 and PI12/00060), RETICS Programs RD12/0009/0013 and RD12/0009/0004 and the European IMI BTCure Program. RL-M is a recipient of a Sara Borrell postdoctoral (CD12/00425). FG and BU are supported by funds from the RETICS Program.

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval Local institutional committee approval was obtained.

    • Provenance and peer review Not commissioned; externally peer reviewed.