Serum Resistin Level and Progression of Atherosclerosis during Glucocorticoid Therapy for Systemic Autoimmune Diseases.

Nahoko Tanaka,Shinichi Kawai,Natsuko Kusunoki,Shotaro Masuoka,Toshihiro Nanki

doi:10.3390/metabo6030028

Nahoko Tanaka, Shinichi Kawai + Show 3 more

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https://doi.org/10.3390/metabo6030028

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Journal: Metabolites	Publication Date: Sep 16, 2016
Citations: 74	License type: CC BY 4.0

Affiliation: Toho University

Abstract

Adipokines are important regulators of several processes, including inflammation and atherosclerosis. In patients with systemic autoimmune diseases, atherosclerosis is accelerated with higher cardiovascular morbidity and mortality. We prospectively investigated the association of adipokines and glucocorticoid therapy with progression of premature atherosclerosis in 38 patients starting glucocorticoid therapy for systemic autoimmune diseases. To detect premature atherosclerosis, carotid ultrasonography was performed at initiation of glucocorticoid therapy and after a mean three-year follow-up period. The ankle-brachial pressure index and cardio-ankle vascular index (CAVI) were measured. Serum adipokine levels were determined with enzyme-linked immunosorbent assay kits. Twenty-three patients (60.5%) had carotid artery plaque at baseline. The carotid artery intima-media thickness (IMT) increased significantly during follow-up. Glucocorticoids reduced the serum resistin level, while increasing serum leptin and high molecular weight-adiponectin. There was slower progression of atherosclerosis (carotid IMT and CAVI) at follow-up in patients with greater reduction of serum resistin and with higher cumulative prednisolone dose. In conclusion, progression of premature atherosclerosis occurred at an early stage of systemic autoimmune diseases before initiation of glucocorticoid therapy. Since resistin, an inflammation and atherosclerosis related adipokine, is reduced by glucocorticoids, glucocortidoid therapy may not accelerate atherosclerosis in patients with systemic autoimmune diseases.

Highlights

Adipose tissue synthesizes and releases various physiologically active molecules that are known as adipokines or adipocytokines, including resistin, leptin, and adiponectin, as well as interleukins (IL-1, IL-1 receptor antagonist, IL-6, and IL-10) and tumor necrosis factor (TNF)-α [1]
We have previously reported that adipokines, especially resistin, may be associated with inflammatory processes in rheumatoid arthritis (RA) [15], Kawasaki disease [16], and other systemic autoimmune diseases [17]
We demonstrated that premature atherosclerosis was already progressing in patients with systemic autoimmune diseases at an early stage before initiation of glucocorticoid therapy

Summary

Introduction

Adipose tissue synthesizes and releases various physiologically active molecules that are known as adipokines or adipocytokines, including resistin, leptin, and adiponectin, as well as interleukins (IL-1, IL-1 receptor antagonist, IL-6, and IL-10) and tumor necrosis factor (TNF)-α [1]. Adipocytes have an established important role in regulating the systemic energy balance and glucose homeostasis [2]. It has been suggested that they adipokines are important regulators of several processes including immunity and inflammation, and may even play a role in atherosclerosis [1,3]. Patients with systemic autoimmune diseases show accelerated development of atherosclerosis with an increased risk of cardiovascular morbidity and mortality compared to the general population [4,5,6,7,8,9,10,11]. It has been suggested that autoimmunity/inflammation might contribute to accelerated atherosclerosis in these patients

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