انتهاك الطيف الهرموني في المبايض متعددة الكيسات مع مقاومة الأنسولين. ما هو المحفز: مقاومة الأنسولين أم مرض البويضات متعدد الكيسات؟
محتوى المقالة الرئيسي
الملخص
متلازمة المبيض متعدد التكيسات هي السبب الرئيس للعقم لدى النساء. حيث يناقش البحث دور مقاومة الأنسولين في تطور تكيس المبايض. تم تحليل الطيف الهرموني للمرضى الذين يعانون من متلازمة تكيس المبايض و / أو مقاومة الأنسولين. اشتملت الدراسة على مرضى يعانون من متلازمة تكيس المبايض دون مقاومة الأنسولين (عددهم = 48) ومقاومة الأنسولين (عددهم = 39). كانت مجموعات المقارنة من المرضى الذين ليس لديهم تاريخ من متلازمة تكيس المبايض: مجموعة تحكم بدون مقاومة الأنسولين (عددهم = 46) ومجموعة من المرضى الذين يعانون من مقاومة الأنسولين (عددهم = 45). تم تحديد المعلمات التالية في المرضى: FSH ، LH ، TSH ، T3f ، T4f، PRL ، E2 ، 17-OHd ، Pr ، AMH ، مجموع الاختبار ، Testf ، DHEAS ، DHEAS ، SHBG ، ACTH ، الكورتيزول ، IRI ، IGF-1 ، C- الببتيد ، ومستوى الجلوكوز. تم حساب مؤشر HOMA-IR ونسبة LH / FSH واختبار إجمالي / SHBG. تم إجراء تحليل الارتباط أيضًا بين HOMA IR ومؤشرات المظهر الهرموني و IGF-1 و C-peptide. تم العثور على تغيرات أحادية الاتجاه في مستويات الهرمونات التالية في مقاومة الأنسولين و / أو متلازمة تكيس المبايض و / أو مقاومة الأنسولين بالنسبة لقيم التحكم: استراديول ، هرمون التستوستيرون الكلي ، الكورتيزول ، البرولاكتين ، AMG ، و SHBG. نتيجة لتحليل الارتباط ، تم إنشاء علاقات سلبية بين مؤشر HOMA .IR ومستويات E2 والكورتيزول و AMH في المرضى (باستثناء المجموعة الضابطة) تفترض الدراسة أن تكوين النمط الظاهري للمبيض المتعدد الكيسات مع مزيج من مقاومة الأنسولين يمكن أن يتشكل في المرضى الذين يعانون من مقاومة الأنسولين نتيجة لانخفاض مستوى الاستراديول ، SHBG وزيادة محتوى التستوستيرون الكلي و AMH.
Received 27/5/2021
Accepted 30/12/2021
Published Online First 20/3/2022
تفاصيل المقالة
هذا العمل مرخص بموجب Creative Commons Attribution 4.0 International License.
كيفية الاقتباس
المراجع
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