ENDOMETRIOZLARNI IMMUNOGISTOKIMYOVIY O’ZGARISHLARI TAVSIFI

Xomidjon Karimjonov, Avazbek Mamataliyev
In: Международный журнал научной педиатрии · 2023 · pp. 53–59 · doi:10.56121/2181-2926-2023-3-53-59 · W4380342909
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated molecular-biological features of adenomyosis and ovarian endometriosis, finding hormonal disruptions in estrogen and progesterone receptors in 60-90% and 50-70% of cases respectively, correlating with atypical endometrial development and potential malignancy.

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The study used immunohistochemistry on 60 premenopausal (18–51 years) and 20 postmenopausal (51+ years) biopsy samples from women who underwent hysterectomy between 2019 and 2022, including 80 biopsies of adenomyosis and ovarian endometriosis, to characterize molecular features of hormonally regulated activity across the proliferative phase. It reported that progesterone predominated in 60–90% of cases and estrogen in 50–70%, alongside findings of atypical endometrial development with progression toward uterine glandular hyperplasia and transitions described as potentially malignant; Ki-67 and p53 were reported in 20% of postmenopausal patients with a progression to low-differentiated uterine tumors. A stated caveat is that the work was limited to women without other gynecologic pathology and relies on immunohistochemical assessment within a post-hysterectomy biopsy design. This paper is centrally about endometriosis — it describes immunohistochemical molecular alterations in endometriosis (and related adenomyosis) across menstrual-cycle phase context and menopausal status.

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Abstract

Endometriozni etio-patogenezini o’rganishda eutopik va ektopik endometriyaning molekulyar-biologik o’ziga xosligi – esterogen va progestoron resteptorlarini ekspressiyasi, proliferastiyasi, apoptozi, adgeziyasi, angiogenezi, hujayra invaziyasi markerlarini o’rganish perspektiv yo’nalishlardan hisoblanadi. Ishning maqsadi: Reproduktiv yoshdagi ayollarda boshqa ginekologik patologiyalarsiz xayz davrining proliferativ bosqichidagi adenomioz va tuhumdon endometriozidagi molekulyar-biologik xususiyatlarini o’rganish. Material va uslublar: Ushbu tadqiqotda 2019-2022 yillar mobaynida gisterektomiya qilingan menopauzagacha (18-51yosh 60-ta bioptat) va postmenopauza davridagi ayollar bioptatlariga (51 va undan katta yoshdagilar, 20-ta bioptat) immunogistokimyoviy usullarda tekshirildi. Ushbu tadqiqotda 2019-22 yilda AVPAB tekshirilgan 80ta adenomioz va tuhumdonlar endometriozlari bioptatlarini immunogistokimyoviy tekshiruvida estrogen va progesteron gormonal faoliyatni buzilishi 60-90% holatlarda progesteron, 50-70% holatlarda estrogen gormoni bachadon adenomiozi rivojlanishda va bachadonning bezli giperplaziyasiga olib kelishi, buni natijasida bemorlarda bachadon endometriysini atipik rivojlanishi va xavfli o’sma kasalligiga o’tishi kuzatildi. Ki-67 va r53 postmenopauzada davridagi 20% bemorlarda bachadonning boshlang’ich yomon sifatli o’sma holatiga o’tganligi bilan namoyon bo’ldi.
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ОПИСАНИЕ ИММУНОГИСТОХИМИЧЕСКИХ ИЗМЕНЕНИЙ ПРИ ЭНДОМЕТРИОЗЕ Аннотация В изучении этиопатогенеза эндометриоза изучение молекулярно-биологической специфичности эутопического и эктопического эндометрия - экспрессии рецепторов эстрогена и прогестерона, маркеров пролиферации, апоптоза, адгезии, ангиогенеза и клеточной инвазии является одним из перспективных направлений. направления. Цель работы: изучить молекулярно-биологические особенности аденомиоза и эндометриоза яичников в пролиферативную фазу менструального цикла у женщин репродуктивного возраста без другой гинекологической патологии. Материалы и методы. В данном исследовании иммуногистохимическими методами исследованы биоптаты женщин пременопаузального (18-51 год 60 биопсий) и постменопаузального возраста (51 год и старше, 20 биопсий), перенесших гистерэктомию в период с 2019 по 2022 год. В данном исследовании в 2019-2022 гг. АВПАБ исследовано 80 биоптатов аденомиоза и эндометриоза яичников, иммуногистохимическое исследование нарушений гормональной активности эстрогенов и прогестерона показало, что в 60-90% случаев лидирует прогестерон, а в 50-70% случаев гормон эстроген. к развитию аденомиоза матки и железистой гиперплазии матки, наблюдалось атипичное развитие эндометрия и переход заболевания в злокачественную опухоль. Ki-67 и р53 были показаны у 20% пациенток в постменопаузе с переходом в исходное состояние низкодифференцированной опухоли матки. Ключевые слова Об авторах Список литературы Adamyan L.V. et al. The role of proliferation processes in the pathogenesis of endometriosis. Reproduction problems.Technologies of the XXI century in gynecology. Спец Выпуск-М 2008:82. Zairatiants O.V. et al. The role of apoptosis and proliferation in the pathogenesis of simple and proliferating uterine fibroids in combination with adenomyosis / In the book. Uterine fibroids. Edited by corresponding member of the Russian Academy of Sciences Sidorova I.S. M: “MIA” 2002:113–27. Voloshchuk et al. Molecular biological aspects of the pathogenesis of adenomyosis. Pathology Archive 2007:56–61. Sidorova I.S. et al. Molecular and biological features of endometriosis, pathogenetically justified therapy pathways. Abstracts of the reports of the Russian Medical Forum-2006 “Fundamental science and Practice”-M 2006:128. Kogan E.A. et al. Clinical and morphological parallels and molecular aspects of adenomyosis morphogenesis. Archive of pathology 2008:8–12. Matsumoto Y, Iwasaka T, Yamasaki F, Sugimori H. Apoptosis and Ki-67 expression in adenomyotic lesions and in the corresponding eutopic endometrium. Obstet Gynecol 1999;94:71–7. https://doi.org/10.1016/s0029-7844(99)00279-3. KitawakiJ. et al. Expression of aromatase cytochrome P450 protein and messenger ribonucleic acidin human endometriotic and adenomyotic tissues bu tnotin normal endometrium. Biol Reprod 1997;57:514–9. Schmidt С. Endometriosis: Pathogenesis and Treatment. Fertil Steril 1990;53:407–10. Это произведение доступно по лицензии Creative Commons «Attribution-NonCommercial-NoDerivatives» («Атрибуция — Некоммерческое использование — Без производных произведений») 4.0 Всемирная.

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