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Article Type

Original Study

Abstract

Objectives The aim of the study was to evaluate interleukin-18 (IL-18) levels in lean patients with polycystic ovary syndrome (PCOS). Background PCOS is one of the common causes of infertility in women. Several studies have attempted to find the etiology and pathophysiology but with no definitive theory to date. Insulin resistance with obesity was considered a causative factor for a long period of time. In recent times researchers have been considering PCOS as a chronic low inflammatory state with subsequent elevation of inflammatory markers, which were correlated with the disease at different stages as diagnostic, staging, prognostic, or predictor markers. Materials and methods Between September 2015 and May 2016 this multidisciplinary prospective observational study recruited 20 consecutive lean patients (BMI < 25 kg/m2) who presented with infertility disorder at the obstetrics and gynecology clinic and were diagnosed with PCOS according to Rotterdam criteria. Patients with hypertension, diabetes mellitus, and fever within the last 3 weeks, or were currently smokers, or were receiving statins, aspirins, corticosteroids, and insulin-sensitizing drugs were excluded. An endocrinologist assessed the patients, and anthropometric measures were collected. Also, blood samples were collected and sent for estimation of lipid profile, insulin assessment, and IL-18. Results Our study included 20 nonsmoker, nondiabetic, and nonhypertensive lean PCOS patients of a mean age of 24.7 years, mean BMI of 23, and mean waist-to-hip ratio of 0.8. The mean systolic blood pressure was 106.5 and the mean diastolic blood pressure was 70. Glucose homeostasis indices revealed mean fasting blood glucose of 84.9 with a mean fasting insulin of 14.2 and homeostatic model assessment (HOMA-IR) of 2.97. Mean IL-18 was 315. Conclusion Despite previous studies associating high IL-18 levels with obesity related to PCOS, we found that IL-18 is elevated in lean PCOS patients as well, revealing chronic low inflammatory state in those patients, which suggests that the pathophysiology of PCOS is not solely connected to obesity.

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