Asymmetric dimethylarginine and arginine levels in patients with rheumatoid arthritis

作者：Vatansev Husamettin^*; Ozturk Bahadir; Yilmaz Sema; Sivrikaya Abdullah; Dagli Mehmet; Kiyici Aysel; Unlu Ali

来源：Turkish Journal of Biochemistry, 2013, 38(2): 169-175.

DOI：10.5505/tjb.2013.51523

• ADMA
• arginine
• citrulline
• CRP
• rheumatoid arthritis

Objective: Rheumatoid arthritis (RA) is a chronic inflammatory disease and it is associated with premature atherosclerosis development. RA patients have multiple factors to develop premature atherosclerosis. Enhanced asymmetric dimethylarginine (ADMA) is considered as a risk factor for the development of atherosclerosis by inducing endothelial dysfunction. The aim of this study was to investigate the role of asymmetric dimethylarginine, arginine and citrulline levels in patients with RA and their relation to the disease activity parameters for possible role on the disease activity.
Methods: 92 patients with RA and 34 healthy controls were included the study. Patients and control blood samples collected for ADMA, arginine and citrulline levels. ADMA, arginine and citrulline levels were measured by pre-column derivatization fluorescence HPLC method. CRP and ESR levels examined on the same day were taken from the patient records.
Results: While ADMA levels significantly increased, arginine levels decreased in the patient group. There was no difference in citrulline levels between both groups. Only citrulline and arginine showed a weak positive correlation. ADMA, arginine, and citrulline levels showed no correlation with either biochemical parameters such as CRP or ESR, or disease activity or disease severity.
Conclusion: Our study has shown that an increase in ADMA levels with the decrease in arginine levels suggests an increase in arginine turnover to ADMA. Increased ADMA levels can be used for an increased risk for premature development of atherosclerosis in patients with RA. Since high ADMA levels prevent the NO-dependent vasodilatation, a possible role of ADMA in development of premature atherosclerosis may be independent from inflammation.

• 出版日期2013