Could Disease Activity Score In 28 Joints-Gamma-Glutamyl Transferase Use Improve Cardiovascular Disease Risk Management In Rheumatoid Arthritis?

JOURNAL OF RHEUMATOLOGY(2020)

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摘要
Patients with rheumatoid arthritis (RA) experience a markedly increased risk of cardiovascular disease (CVD)1,2,3. Atherogenesis in RA remains poorly elucidated but traditional cardiovascular (CV) risk factors, systemic inflammation and their interactions, as well as genetic components certainly contribute1,2,3. In a recent 13-center study, the population-attributable CV event risk for disease activity as estimated by the Disease Activity Score in 28 joints (DAS28) and positive rheumatoid factor and/or anti cyclic citrullinated peptide antibodies, were both as large as that for lipids in RA4. It is therefore not unexpected that current CVD risk stratification tools calculated based on major traditional CV risk factors, such as the Framingham score and Systematic Coronary Risk Evaluation (SCORE), perform suboptimally in RA1,2,3.\n\nRecently developed disease-specific CVD risk calculators may also not perform better than those developed for the general population in predicting CV events in RA5. In this regard, during the past 2 decades, many population studies revealed that circulating gamma-glutamyl transferase (GGT) concentrations within normal ranges relate to major traditional CV risk factors, systemic inflammation, and incident CV events6,7,8,9,10,11,12. In RA, GGT levels were also found to be associated with disease activity markers13. These reported observations suggest that serum GGT concentrations may be useful in the identification of patients with RA who are at increased CVD risk.\n\nIn this issue of The Journal , Vergneault and colleagues14 explored the associations of circulating GGT levels with CV risk factors in 129 patients with RA. Only patients with unstable hepatic disease and manifestations of liver dysfunction or failure were excluded. GGT concentrations were weakly associated with C-reactive protein … \n\nAddress correspondence to Dr. P.H. Dessein, Departments of Medicine and Physiology, University of the Witwatersrand Medical School, 7 York Road, Parktown, 2193, Johannesburg, South Africa. Email: patrick.dessein22{at}gmail.com.
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