Metabolic syndrome and systemic lupus erythematosus: the connection

ABSTRACT

Introduction: The metabolic syndrome (MetS) is now recognized as a chronic proinflammatory and prothrombotic state that aggravates insulin resistance, oxidative injury, and cardiovascular risk. MetS is more prevalent in patients with systemic lupus erythematosus (SLE), a prototype of systemic autoimmune disease associated with premature atherosclerosis that cannot be accounted by traditional vascular risk factors alone. Dysregulation of the cytokines and adipokines is a common feature in both SLE and MetS, suggesting a complex relationship among autoimmunity, obesity, inflammation, and atherosclerosis.

Areas covered: This review summarizes the prevalence of MetS and its effect on cardiovascular outcome and organ damage in patients with SLE. The pathophysiology of MetS and its relevance to SLE is also briefly discussed.

Expert opinion: Imbalance of adipokine production in MetS contributes to inflammation and atherosclerosis. MetS predisposes SLE patients to new cardiovascular events and vascular mortality, as well as the development of chronic kidney disease and diabetes mellitus. However, conflicting results have been reported in the literature regarding the levels of the proinflammatory leptin and anti-inflammatory adiponectin, and their relationship with disease activity in SLE patients. While lifestyle modifications and targeting dyslipidemia, hypertension and diabetes mellitus is essential, there is little information on the efficacy and safety of metformin and hydroxychloroquine in alleviating insulin resistance in SLE or MetS. Further research on adipokines in SLE and the role of anti-obesity medications and probiotics in MetS is necessary.

KEYWORDS:

• Obesity
• cardiovascular
• lupus
• metabolic syndrome
• adipokine

Article Highlights

• MetS is a chronic inflammatory and pro-thrombotic state related to dysregulation of obesity-related adipokines, insulin resistance, and oxidative stress.

• SLE is characterized by premature atherosclerosis that cannot be explained solely by traditional risk factors. Systemic inflammation and other non-traditional risk factors, including autoantibodies and glucocorticoid therapy, may contribute.

• MetS is more frequent in SLE patients and aggravates the risk of subclinical and clinical atherosclerotic vascular disease, diabetes mellitus, and chronic kidney disease.

• Given the elevation of proinflammatory cytokines is a common mechanism of lupus activity and obesity, MetS may be an important factor bridging chronic systemic inflammation and accelerated atherosclerosis in SLE.

• The role of adipokines such as leptin and adiponectin in SLE remains unclear.

• Further research on the efficacy and safety of hydroxychloroquine, metformin, anti-obesity medications and probiotics in alleviating insulin resistance in SLE or MetS is necessary.

Declaration of interest

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.