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Abstract Number: 1296

Associations of Metabolic Syndrome and Adipokines in SLE

Diane Apostolopoulos1, Fabien Vincent2, Rachel Koelmeyer2, Alberta Hoi1 and Eric Morand3, 1Monash University, Melbourne, Victoria, Australia, 2Monash University, Clayton, Victoria, Australia, 3Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Australia

Meeting: ACR Convergence 2020

Keywords: autoimmune diseases, Systemic lupus erythematosus (SLE)

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Session Information

Date: Sunday, November 8, 2020

Title: SLE – Diagnosis, Manifestations, & Outcomes Poster II: Comorbidities

Session Type: Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Metabolic syndrome (MetS) is a chronic pro-inflammatory and pro-thrombotic state associated with increased atherosclerosis, cardiovascular events and type 2 diabetes. It is diagnosed in the presence of at least 3 of 5 metabolic risk factors (obesity, hypertension, hypertriglyceridemia, low high-density lipoproteins (HDL) and insulin resistance [1]). The pathophysiology of MetS remains incompletely understood, but may share mechanisms with inflammatory states such as SLE. Visceral adiposity is known as a source of pro-inflammatory cytokines by adipocytes, the so-called adipokines. The contribution of glucocorticoids to the development of MetS in SLE is not clear, even though their use is associated with cardiovascular comorbidities [2]. We aim to characterize the prevalence and associations of MetS, including serum levels of adipokines, in a multi-ethnic cohort of patients with SLE.

Methods: Using a standardised protocol, baseline demographics, per visit disease activity (SLEDAI2K) and treatment data, and annual recording of organ damage accrual (SLICC damage index (SDI)) were prospectively captured on SLE patients from a single tertiary centre. The presence of MetS,defined using the updated joint consensus criteria [1], was assessed retrospectively at the last recorded visit. Serum levels of adipokines (resistin, lipocalin-2, TNF, MCP-1) and insulin were measured by Quantibody.

Results: 116 patients (median (IQR) age at enrolment 39.5 (31.4-51.1) years, median disease duration 6.1 (1.4-12) years) were followed for a median of 6.7 (4.1-8.1) years. 80% of patients were exposed to glucocorticoids (median time-adjusted mean dose 3.7 (0.5-7.0) mg/day and 50% accrued organ damage during follow-up. The prevalence of MetS in this cohort was 29%. The prevalence of the components of MetS included: hypertension (59%), low-HDL (51%), hypertriglyceridemia (32%), obesity (16%) and hyperglycaemia (22%). In univariable analysis, MetS was associated with baseline organ damage (SDI) (OR 4.34; 95% CI 1.80-10.48; P< 0.01) and organ damage accrual (OR 2.34; 1.02-5.36; P=0.04). The association between MetS and baseline organ damage remained significant in multivariable analysis (adjusted OR 3.36; 95% CI 1.32-8.59; P=0.01). Unexpectedly, glucocorticoid use was not associated with MetS or any of its five components. High serum levels of resistin were significantly negatively associated with MetS (OR 0.17; 95% CI 0.04-0.70; P=0.014); no other adipokine were associated with MetS.

Conclusion: MetS is common in SLE patients, with the most frequent components being hypertension and low-HDL. An independent association was found of MetS with baseline organ damage, and low serum resistin, but not glucocorticoid exposure or disease activity.


Disclosure: D. Apostolopoulos, None; F. Vincent, None; R. Koelmeyer, None; A. Hoi, None; E. Morand, AstraZeneca, 2, 5, 8, Bristol-Myers Squibb, 2, 5, Eli Lilly, 2, 5, GlaxoSmithKline, 2, 5, Janssen, 2, 5, Merck Serono, 2, 5, Neovacs, 5, Sandoz, 5, Novartis, 8, AbbVie, 5, Amgen, 5, Biogen, 5.

To cite this abstract in AMA style:

Apostolopoulos D, Vincent F, Koelmeyer R, Hoi A, Morand E. Associations of Metabolic Syndrome and Adipokines in SLE [abstract]. Arthritis Rheumatol. 2020; 72 (suppl 10). https://acrabstracts.org/abstract/associations-of-metabolic-syndrome-and-adipokines-in-sle/. Accessed .
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