Apoptotic Pathways and Anti-Müllerian Hormone affects the Ovarian Tissue Damage during Endometrioma Cystectomy

Tanzil Al Hair, Wachyu Hadisaputra, Soegiharto Soebijanto, Primariadewi Rustamadji

Research output: Contribution to journalArticlepeer-review

Abstract

Background: Endometriomas are cysts caused by endometriosis that can impair ovarian function and fertility. Anti-Müllerian hormone (AMH) is an important marker for ovarian reserve. This study aimed to determine the optimal timing of operative management for endometrioma by evaluating the impact of cyst size on ovarian tissue damage and hormone levels. Methods: The study included 32 endometrioma patients who underwent laparoscopic cystectomy between February 2018 and December 2019 at Women and Children’s YPK Hospital, Jakarta. Patient characteristics were recorded, including age, parity, BMI, and cyst diameter. Serum AMH levels were measured using ELISA before and one month after cystectomy. Immunohistochemical examination assessed apoptotic factor gene expression on the inner surface epithelium of endometriomas. Results: AMH levels declined post-cystectomy in both endometriomas ≤4 cm and >4 cm, with significant differences in the latter group. Additionally, there was increased Bax expression in >4 cm endometriomas. Correlation tests revealed a strong positive relationship between TNFR1 and Caspase-3 in both groups. Multivariate analysis suggested a connection between apoptotic factor gene expression and reduced AMH levels. Conclusion: TNF-α appears to initiate apoptosis in endometriomas through the intrinsic pathway. It is advisable to perform endometrioma surgery when the diameter is ≤4 cm and before the age of 30 to achieve optimal outcomes.

Original languageEnglish
Article number9690
JournalJournal of Angiotherapy
Volume8
Issue number5
DOIs
Publication statusPublished - 2024

Keywords

  • AMH
  • apoptosis
  • Bcl-2/Bax ratio
  • caspase-3
  • caspase-8
  • caspase-9
  • cytokine TNF-α
  • endometrioma
  • gene expression
  • intrinsic pathway
  • P53

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