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SAT0113 Beta2-Adrenergic Receptors Polymorphisms Increase the Risk of Arteriosclerosis: Clinical-Ultrasound-Genetic Study in Patients with Rheumatoid Arthritis
  1. O. Malysheva1,
  2. H. Barghan1,
  3. K. Muehlberg2,
  4. C. Baerwald1
  1. 1Internal Medicine, Rheumatology
  2. 2Internal Medicine, Cardiology, University Clinic, Leipzig, Germany

Abstract

Background Growing evidence supports the hypothesis that inflammatory systemic response is involved in the pathogenesis of arteriosclerosis. Further progress should be made in defining what kind of additional risk factors may contribute to arteriosclerosis. In recent years it has been identified that some candidate genes, genetic polymorphisms, and susceptibility loci associated with atherosclerotic diseases.

Objectives To further characterize arteriosclerosis risk factors common variants of the beta2-adrenergic receptors (beta2R) were studied in patients with rheumatoid arthritis (RA) and controls.

Methods Classic arteriosclerosis risk factors (lipid status, smoking, hypertension, overweight/obesity, diabetes mellitus), as well RA disease activity (DAS 28, radiographic changes, C-reactive protein level) was studied in 167 RA patients (mean age 62.8±9.3 years) compare with age and sex matched osteoarhritis patients. Ultrasound examination of brain supplying arteries, intima media thickness (IMT) of the carotid arteries, the determination of plaque, as well as the NASCET criteria of carotid artery stenosis was also used to evaluate the arteriosclerosis. An allele-specific polymerase chain reaction was used to determine the common variants of the beta2R at position 16, 27, and 164 in patients with RA (n=156) and ethnically matched patients with osteoarthritis (n=90) and healthy controls (n=305).

Results Plaques were presented 40% RA patients. Moderate- and high-grade stenosis of the carotid artery was registered only in 3% RA patients. The mean IMT was 0.67±0.4 mm. Stratifying classic arteriosclerosis risk factors revealed a statistically significant correlation between overweigt/obesity (p<0.001), triglyceride levels (p=0.028) und plaques. It could be also demonstrated that IMT in RA patients is associated with DAS 28 (p=0.05) and plaques with bone erosions (p=0.026). Otherwise, level of C-reactive protein exerted a significant influence on IMT (p=0.046). There was a highly significant distortion in the distribution of beta2R polymorphisms at codon 16 between RA patients and controls. Arginine (Arg) at codon 16 was present in 89.7% RA patients compared to 66.2% controls (OR 4.43, 95% CI 2.81 to 7.02, p=0.00001). Stratifying RA patients for the genetic at position 16 revealed a statistically significant association between carotid artery stenosis und homozygosity for Arginine (Arg) 16 compared to control group (p=0,046).

Conclusions Classic arteriosclerosis, as well inflammatory disease associated risk factors are involved in arteriosclerosis in RA patients.

Polymorphisms of the beta2AR contribute to the genetic background of RA and are associated with carotid artery stenosis in this group of patients. Further studies are warranted to determine the role of genetic factors on arteriosclerosis.

Disclosure of Interest None declared

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