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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}

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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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