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العنوان
Insulin Resistance In Non-Obese (normal weight) and Obese Egyptian Women withPCOS /
المؤلف
Hagag, EslamFetouh Ahmed.
هيئة الاعداد
باحث / Eslam Fetouh Ahmed Hagag
مشرف / Dina Gamal El deen Elkholy
مشرف / Hossam Abdelmohsen Hodeb
مشرف / Hashem Adel Lotfy
الموضوع
Gynecology and Obstetrics.
تاريخ النشر
2023.
عدد الصفحات
106 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
أمراض النساء والتوليد
تاريخ الإجازة
20/3/2024
مكان الإجازة
جامعة طنطا - كلية الطب - امراض النساء واالتوليد
الفهرس
Only 14 pages are availabe for public view

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from 139

Abstract

Polycystic ovary syndrome (PCOS) is a complex hormonal disorder commonly occurring in women of reproductive age. It is characterized by ovulatory dysfunction, hyperandrogenism, and polycystic ovarian morphology (PCOM) under B-ultrasound imaging. The prevalence of PCOS is approximately 5–15%. It is the most common cause of infertility in women[1].According to the Rotterdam criteria, polycystic ovary syndrome (PCOS) is diagnosed if two of 3 criteria present: oligo-anovulation, ultrasonographically defined polycystic ovaries and clinical or biochemical signs of hyperandrogenism with the exclusion of other androgen excess disorders . chronic anovulation is one of. the most common causes of infertility in women with PCOS. Oocyte quality or endometrial and implantation abnormalities also may contribute to the pathogenesis of infertility in PCO [2].Although the etiology of PCOS is still not well known , it seems that insulin resistance is a major pathophysiologic mechanism in developing clinical symptoms and other metabolic complications of PCOS [3]. Resistance to insulin leads to an increase in free androgen availability, and consequently alteration in follicular developmentand granulosa cell function [4, 5]. Insulin resistance is identified as an impaired biologic response to insulin stimulation of target tissues, primarily the liver, muscle, and adipose tissue. Insulin resistance impairs glucose disposal, resulting in a compensatory increase in beta-cell insulin production and hyperinsulinemia. The metabolic consequences of insulin resistance can result in hyperglycemia, hypertension, dyslipidemia, visceral adiposity, hyperuricemia, elevated inflammatory markers, endothelial dysfunction, and a prothrombic state. Progression ofinsulin resistance can lead to metabolic syndrome, nonalcoholic fatty liver disease (NAFLD), type two diabetes and ischemic heart diseases .