NDLI: Symmetric Dimethylarginine Is Not Associated with Cumulative Inflammatory Load or Classical Cardiovascular Risk Factors in Rheumatoid Arthritis: A 6-Year Follow-Up Study

Content Provider	PubMed Central
Author	Dimitroulas, Theodoros Hodson, James Aamer, Sandoo Smith, Jacqueline P. Douglas, Karen M. Kitas, George D.
Copyright Year	2015
Abstract	Symmetric dimethylarginine (SDMA) indirectly inhibits nitric oxide (NO) synthesis and predicts cardiovascular and all-cause mortality in high-risk patients. The aim of our study was to investigate the associations of cumulative inflammatory burden (assessed by serial measurements of inflammatory markers) and classical cardiovascular (CV) disease risk factors with SDMA in RA patients. 201 RA patients (155 females, median age 67 (59–73)) were assessed at baseline (2006). Classical CV disease risk factors were recorded and systemic inflammation was determined by the measurement of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). At follow-up (2012) SDMA levels were measured by enzyme-linked immunosorbent assay. Mean SDMA levels in RA population were 0.40 (0.40–0.53) μmol/L. No significant association between SDMA and cumulative inflammatory load was established in the analysis. SDMA levels were not found to be significantly related to CV disease risk factors. We explored the potential relationship between SDMA and cumulative inflammatory burden in patients with RA and obtained negative results. SDMA did not relate to CV disease risk factors in our population and its clinical significance as a surrogate marker of endothelial dysfunction in patients with RA remains to be determined.
Related Links	http://dx.doi.org/10.1155/2015/796562
Starting Page	796562
File Format	PDF
ISSN	09629351
e-ISSN	14661861
Journal	Mediators of Inflammation
Volume Number	2015
Language	English
Publisher	Hindawi Publishing Corporation
Publisher Date	2015-01-01
Access Restriction	Open
Rights Holder	Hindawi Publishing Corporation
Subject Keyword	Immunology Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Immunology

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