4.7 Article

No significant change in arterial stiffness in RA after 6 months and 1 year of rituximab treatment

Journal

RHEUMATOLOGY
Volume 51, Issue 6, Pages 1107-1111

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/kes006

Keywords

rheumatoid arthritis; arterial stiffness; cardiovascular risk markers; rituximab

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Funding

  1. Abbott
  2. Wyeth

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Objective. The excess cardiac risk, found in RA has been attributed to biological inflammation. Effective control of inflammation may be of benefit in reducing cardiovascular risk in RA patients. The aim of this study is to investigate the effects of 24 and 52 weeks of rituximab treatment on arterial stiffness and cardiovascular risk factors. Methods. Arterial stiffness was measured by augmentation index (AIx) and pulse wave velocity (PWV), and other cardiovascular risk factors (lipid profile, blood pressure) were collected in active RA patients. Results. Thirty-three patients, of whom 29 were females, with a mean age of 60.9 (12.0) years were included. Thirty patients had positive RFs, 27 had positive anti-CCP antibody and 93.9% (n = 31) were erosive. Nineteen patients were non-responders to anti-TNF-alpha treatments. After rituximab treatment, no change was observed in arterial stiffness, neither after 6 nor after 12 months [PWV 8.1 (3.1) m/s at baseline, 8.1 (2.8) at 6 months, 8.0 (2.7) at 1 year, P = 0.924; and AIx 30.4 (8.2)% at baseline, 28.6 (7.6) at 6 months, 29.4 (6.7) at 1 year, P = 0.216]. Total and low-density lipoprotein cholesterol levels increased significantly but high-density lipoprotein (HDL) and triglyceride levels were unchanged. The atherogenic index (total cholesterol/HDL cholesterol) was increased, but not to a level of significance. No change was found in other cardiovascular risk factors. DAS-28 according to levels of ESR and CRP and biologic inflammation were significantly improved. Conclusion. Arterial stiffness did not improve after 6 and 12 months of rituximab therapy. The treatment had a beneficial effect on biologic inflammation and disease activity, but caused a pro-atherogenic lipid profile.

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