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AB0216 Activation of the renin angiotensin sistem in a population of patients with rheumatoid arthritis and low severity comorbidity in therapy with dmards and/or anti-tnf alfha
  1. C. Bentivenga1,
  2. E. R. Rinaldi1,
  3. F. Santi1,
  4. E. Cosentino1,
  5. S. Corvaglia1,
  6. G. Vukatana1,
  7. N. Malavolta1,
  8. C. Borghi1
  1. 1Reumatology Unit and Internal Medicine Borghi, University of Bologna-S. Orsola Malpighi Hospital, Bologna, Italy


Background Rheumatoid arthritis(RA) is a chronic autoimmune inflammatory disease. The inflammatory process causes joint destruction and disability. Patients have a shorter life expectancy and a relative risk of cardiovascular (CV) disease ranging from 1.5 to 4.0 with an increase in CV morbidity and mortality of 1.5 fold compared with the general population. The chronic inflammation seen in RA have its main effectors in factor alfa tumor necrosis (TNF) and interleukin 6 (IL-6) that, in addition to playing a key role in the initiation of joint damage and progression of atherosclerotic disease, are also potent inducers of the renin angiotensin system (RAS). The latter could contribute in these patients to the development of an early and accelerated CV damage.

Objectives To evaluate the possible presence of hyperactivation of RAS and its association with the activity parameters of RA, with traditional risk factors and premature CV organ damage

Methods there were evaluated 17 (F) patients (pts) with RA receiving stable therapy (3 months) with DMARDs or anti-TNF alpha, in the absence of previous CVevents and/or traditional risk factors. All pts underwent a visit with rheumatologic evaluation of patient history, activity of RA (DAS28), pain (VAS), quality of life (HAQ), patient GH. Blood samples were collected for the evaluation of: lipid profile, indices of insulin resistance (HOMA-IR), indices of activity of rheumatoid arthritis (autoantibodies, inflammatory markers) and CV risk according to risk charts based on the Framinghamstudy. The CV organ damage was assessed by imaging techniques such as Pulse Wave Velocity (PWV) and Augmentation Index (AIx), Intima-media thickness (IMT) and ankle-brachial index (ABI). From a sample of the patient’s blood leukocytes were separated and subsequently extracted RNA to perform Real time qPCR to verify the expression of Angiotensin II and AT1 and AT2 receptors. The mean disease duration was 9 ±7 years; the mean age (pts all female) was 55 ± 12 years. FR was positive in 49%, antiCC and ANA respectively in 64% and 59%

Results data, though preliminary, showed a statistically significant correlation between the density of receptors for angiotensin II (AT1R and AT2R) and, respectively, the values of ABI(p <0.05, p 0.043), serum uric acid values (p <0,014, p <0016) and the index of insulin resistance (HOMA-IR) (p <0,034, p <0.033). This seems to indicate a very strong correlation between markers of early atherosclerosis and expression of the RAS, although the sample did not have additional CV risk factors.

Conclusions The results obtained so far make attractive and plausible the initial assumption and could, if confirmed in further continuation of the study, help to explain the paradoxical development of vascular disease in patients with RA and apparent low CV risk with important therapeutic implications

Disclosure of Interest None Declared

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