Polycystic ovary syndrome and circulating inflammatory markers

71Citations
Citations of this article
66Readers
Mendeley users who have this article in their library.

Abstract

Background: Human and experimental studies suggest that the sympathetic regulatory drive in the ovary may be unbalanced (hyperactivity) in polycystic ovary syndrome (PCOS). Dysfunctional secretion of interleukin (IL) -1 (α & β) or related cytokines may thus be related to abnormal ovulation and luteinization. Objective: The aim of this study was the evaluation of cytokines’ pattern in PCOS women and discussion about the explanation of cross-talk between two super systems: sympathetic and immune systems and explanation sympatho-excitation and relationship with interleukins. Materials and Methods: In this study, 171 PCOS women aged between 20-40 years were studied. Their body mass index was <28. The patients were divided into two groups: study group (n=85, PCOS women) and control group (n=86 normal women). The blood sample was obtained on the 3rd day of menstruation cycle. IL-17, IL-1α, IL-1β, and Tumor necrosis factor-alpha (TNF-α) concentrations were determined in both groups. Results: The median serum level of IL-1α in the PCOS group was higher than the control group (293.3 and 8.0, respectively, p<0.001). Also, the median serum level of IL-1β was higher than the control group (5.9 and 3.1 respectively). But the median serum of level IL-17 in women with PCOS was significantly lower than the control group (p<0.001). Conclusion: Our results confirm that PCOS is a low-level chronic inflammation.

Cite

CITATION STYLE

APA

Zangeneh, F. Z., Naghizadeh, M. M., & Masoumi, M. (2017). Polycystic ovary syndrome and circulating inflammatory markers. International Journal of Reproductive BioMedicine, 15(6), 375–382. https://doi.org/10.29252/ijrm.15.6.375

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free