EDITORIAL March 09, 2022 March 09, 2022

Inflammatory mediators in polycystic ovary syndrome: the case of interleukin-18

DOI: 10.20945/2359-3997000000455

Polycystic ovary syndrome (PCOS) is a multifactorial condition, characterized by clinical or biochemical hyperandrogenism, ovarian dysfunction, and/or polycystic ovaries. Insulin resistance and central adiposity are often present, and women with PCOS are at higher risk for metabolic comorbidities, such as dyslipidemia, prediabetes, and type 2 diabetes ().

Current evidence suggests that women with PCOS have increased serum pro-inflammatory markers when compared to healthy controls, contributing to a chronic low-grade inflammatory state (). Indeed, major pro-inflammatory cytokines, such as IL-6 and TNFα, may be derived from dysfunctional adipose tissue in PCOS and primarily secreted by resident macrophages (). IL-6 induces the hepatic production of CRP, and women with PCOS exhibit elevated CRP levels, which are correlated with obesity and insulin resistance (). Conversely, some other inflammatory mediators are under investigation in the context of their possible pathophysiological role on the chronic low-grade inflammatory state associated to PCOS. One of these biomarkers of inflammation that are under evaluation is interleukin-18 (IL-18).

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