Jane E. Salmon, MD; Stephen A. Paget, MD; Mary J. Roman, MD
Potential Financial Conflicts of Interest: None disclosed.
Salmon J., Paget S., Roman M.; Carotid Atherosclerosis and Rheumatoid Arthritis. Ann Intern Med. 2006;145:231. doi: 10.7326/0003-4819-145-3-200608010-00015
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Published: Ann Intern Med. 2006;145(3):231.
We, too, expected to find a relationship between markers of systemic inflammation and evidence of carotid atherosclerosis in patients with rheumatoid arthritis. Although our study did not define the mediators of accelerated atherosclerosis or the markers that predict it, we believe our findings support an important role for chronic inflammation. The analyses suggested by Dr. Targher showed no association between autoantibodies (rheumatoid factor or anti-CCP antibodies) and the presence of carotid atherosclerosis in our patients. Carotid plaque was detected in 49% of patients with positive results for rheumatoid factor and in 46% of patients with negative results for rheumatoid factor (P = 0.78), as well as in 42% of patients with anti-CCP antibodies and 44% of those without anti-CCP antibodies (P = 0.84). Furthermore, although titers of anti-CCP antibodies may predict radiographic outcome and disease severity in rheumatoid arthritis (1), they did not predict carotid atherosclerosis. Mean levels (SD) for patients with and without plaque were 388 U/mL (SD, 783) and 480 U/mL (SD, 842), respectively (P = 0.85). However, the cross-sectional design of our study and our single measurements of autoantibodies and inflammatory mediators do not allow us to determine cumulative exposure; therefore, interpretation of our results is limited. These findings contrast with those of our study in patients with lupus (2), in whom the prevalence of atherosclerosis was similar to that in patients with rheumatoid arthritis; however, the presence of certain autoantibodies was inversely associated with carotid plaque. We agree that more focused and effective immunomodulatory therapy may prevent or attenuate morbidity and mortality due to atherosclerosis in rheumatoid arthritis. However, the specific targets for intervention are not yet clear. Indeed, it will be important to determine whether disease-modifying therapies that ameliorate symptoms and prevent joint damage in rheumatoid arthritis will also decrease the prevalence and severity of atherosclerosis in patients with rheumatoid arthritis.
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