Abstract
BackgroundRheumatoid arthritis is a risk factor for early mortality due to cardiovascular disease. Interleukin-33 appears to protect against the development of atherosclerosis. The purpose of this study was to investigate the relationship between serum levels of interleukin-33 and its soluble receptor with the presence of subclinical carotid atherosclerosis in rheumatoid arthritis patients.MethodsRheumatoid arthritis patients without atherosclerotic disease were subjected to clinical and laboratory assessments, including carotid ultrasound. Interleukin-33 and its soluble receptor serum levels were measured by ELISA.Results102 patients were included. The prevalence of carotid plaques was 23.5% and the median intima-media thickness was 0.7 mm. The median interleukin-33 and its soluble receptor concentration was 69.1 and 469.8 pg/ml. No association was found between serum interleukin-33 or its soluble receptor and intima-media thickness or plaque occurrence. Each 0.1 mm increase of intima-media thickness raised the odds of plaque occurrence by 5.3-fold, and each additional year of rheumatoid arthritis duration increased the odds of plaque occurrence by 6%. Each additional year in patients age and each one-point increase in the Framingham Risk Score were associated with a 0.004 mm and 0.012 mm increase in intima-media thickness. Methotrexate use was associated with a 0.07 mm reduction in intima-media thickness.ConclusionsInterleukin-33 and its soluble receptor were not associated with subclinical atherosclerosis. Traditional risk factors for atherosclerosis and rheumatoid arthritis duration were associated with intima-media thickness and plaque occurrence; methotrexate use was associated with a lower intima-media thickness.
Highlights
Rheumatoid arthritis is a risk factor for early mortality due to cardiovascular disease
Our study investigated the possible association between serum interleukin 33 (IL-33) and soluble ST2 (sST2) levels and subclinical carotid atherosclerosis in Rheumatoid arthritis (RA) patients
Based on their Framingham Risk Scores [24], 64 (62.7%) participants were at high cardiovascular risk, and only 22 (21.6%) patients met the low-density lipoprotein (LDL) therapeutic goal established by the Brazilian Society of Cardiology Guideline [23] (Table 1)
Summary
Rheumatoid arthritis is a risk factor for early mortality due to cardiovascular disease. The purpose of this study was to investigate the relationship between serum levels of interleukin-33 and its soluble receptor with the presence of subclinical carotid atherosclerosis in rheumatoid arthritis patients. Rheumatoid arthritis (RA) is an autoimmune inflammatory disease that can lead to articular destruction. Fibroblast-like synoviocytes are local producers of inflammatory interleukins, including interleukin 33 (IL-33). IL-33 is a member of the IL-1 family that modulates the immune response by inducing cytokine production by type 2 T helper lymphocytes (Th2). Increased levels of soluble ST2 (sST2) were found in inflammatory conditions, and it is involved in the attenuation of the Th2-induced inflammatory response, probably via IL-33 sequestration. The active form of IL-33 is released after cell damage and it promotes macrophage activation, neutrophil migration to articular sites and production of metalloproteinases and cytokines by fibroblast-like synoviocytes.
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