Background/Purpose: Development of atherosclerosis is accelerated in patients with systemic autoimmune diseases. However, underlying mechanisms of accelerated atherosclerosis remains unknown, and the impact of pharmacotherapies such as glucocorticoid on atherosclerosis is still controversial in these patients. Adipose tissue synthesizes and releases physiologically active molecules that are known as adipokines. It have recently been implicated that they are important regulators of several processes including inflammation and they may also play a role in atherosclerosis. We then prospectively investigated the association of adipokines and glucocorticoid therapy with progression of premature atherosclerosis in patients with systemic autoimmune diseases.

Methods: Thirty-eight patients (27 women, mean age of 49.3 ± 15.2 years old) with systemic autoimmune diseases, including systemic lupus erythematosus (n=16) , polymyositis/dermatomyositis (n=14), vasculitis syndrome (n=6) and adult onset Still’s disease (n=2) were enrolled in this study. All subjects had active disease and started glucocorticoid therapy (prednisolone at 30 mg or more daily). Patients who had previously taken glucocorticoid or other immunosuppressive drugs were excluded.  The carotid arteries were examined by ultrasonography to detect premature atherosclerosis at initiating glucocorticoid therapy and after a follow-up of mean 3 years. Serum levels of 3 adipokines [resistin, leptin, and high molecular weight (HMW)-adiponectin] were measured with respective enzyme-linked immunosorbent assay kit.

Results: Twenty-three of the 38 patients (60.5%) had carotid artery plaques at baseline. Among those without plaque at baseline, 2 patients (5.3%) showed new plaques after follow-up periods. Intima-media thickness (IMT) was significantly increased from median 0.675 (IQR 0.500-0.813) mm at baseline to 0.725 (0.588-0.725) mm at follow-up (p = 0.04). Serum resistin levels decreased [from 7.3 (3.7-16.8) to 6.1 (2.9-8.8), p = 0.013], while serum leptin [from 2.6 (1.9-10.1) to 24.6 (12.4-54.7), p < 0.001] and HMW-adiponectin levels [from 8.3 (3.7-11.8) to 12.4 (7.0-17.8), p < 0.001] increased after glucocorticoid therapy. In multivariate analysis, average yearly change in IMT over follow-up periods was positively associated with male sex, diabetes mellitus, and yearly change in serum resistin levels. In contrast, average yearly change in IMT in this analysis was negatively associated with cumulative prednisolone exposure.

Conclusion: This study showed that premature atherosclerosis was detected at high incidence in patients with systemic autoimmune diseases before glucocorticoid therapy. Overall, these patients had an increased IMT during the follow-up periods, which was positively associated with yearly change of resistin. However, increased IMT was negatively associated with prednisolone therapy. Our findings suggest that glucocorticoid may prevent accelerated atherosclerosis, partly through regulating the balance in concentrations of adipokines such as resistin which might be associated with atherosclerotic progression in systemic autoimmune diseases.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/progression-of-atherosclerosis-might-be-prevented-by-decrease-of-serum-resistin-level-after-glucocorticoid-therapy-in-patients-with-systemic-autoimmune-disease/