Endometrioid ovarian cysts: a rationale for post-operative hormonal therapy

A.I. Davydov, L.D. Belotserkovtseva, M.B. Tairova
In: Voprosy ginekologii, akušerstva i perinatologii · 2019 · vol. 18(2) , pp. 122–128 · doi:10.20953/1726-1678-2019-2-122-128 · W2966227223
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Endogenous estradiol enhances progestogen's antiproliferative effect on endometrioid cysts by inducing progesterone receptors, supporting combined hormonal contraceptives with dienogest.

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This paper discusses the rationale for post-operative hormonal therapy for endometrioid ovarian cysts by focusing on how endogenous and exogenous estradiol (EE) influences endometriosis tissue growth and how progestogens exert antiproliferative effects. It argues that endometrioid tissue can produce estradiol from inactive precursors and that EE may enhance the inhibitory effect of progestogens by inducing progesterone receptor (PR) expression, with simultaneous EE and progestogen promoting rapid maximal PR induction. The authors use this mechanistic framing to support the concept that combined hormonal contraceptives with strong antiproliferative progestogenic activity, specifically dienogest, could be preferred after surgery. The paper’s limitation is that it is largely a theoretical/biological rationale rather than a report of original empirical clinical outcomes. This paper is centrally about endometriosis—specifically endometrioid ovarian cysts and a mechanistic rationale for post-operative hormonal therapy involving dienogest-containing combined regimens.

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Gynecology, Obstetrics and Perinatology - Gynecology, Obstetrics and Perinatology - 2019 volume 18 issue 2 Endometrioid ovarian cysts: a rationale for post-operative hormonal therapy Authors / Institutions Aleksandr I. Davydov / Larisa D. Belotserkovtseva / Marina B. Tairova / The role of endogenous and exogenous estradiol (EE) in the morphogenesis and therapy of endometriosis has been discussed in literature over the past years. As has been found, the endometrioid tissue itself produces estradiol from inactive precursors, synthesised in the adrenal glands. Hence EE cannon influence the growth of endometriosis in principle. On the contrary, EE enhances the inhibitory effect of progestogens (PG) on cellular growth of the ovarian endometrioma. This mechanism is based on induction of the progesterone receptor (PR) expression with subsequent enhancement of the PG effect. Simultaneous introduction of EE and PG promotes rapid PR induction, ensuring the maximal antiproliferative effect of PG. This can basically change the understanding of hormone therapy in patients with endometriosis, giving preference to combined hormonal contraceptives containing PG with the maximal antiproliferative activity – dienogest. Key words: dienogest, combined hormonal contraception, endometriosis, endometrioid ovarian cyst, ethinylestradiol For citation: Davydov A.I., Belotserkovtseva L.D., Tairova M.B. Endometrioid ovarian cysts: a rationale for post-operative hormonal therapy. Vopr. ginekol. akus. perinatol. (Gynecology, Obstetrics and Perinatology). 2019; 18(2): 122–128. (In Russian). DOI: 10.20953/1726-1678-2019-2-122-128 Key words: dienogest, combined hormonal contraception, endometriosis, endometrioid ovarian cyst, ethinylestradiol For citation: Davydov A.I., Belotserkovtseva L.D., Tairova M.B. Endometrioid ovarian cysts: a rationale for post-operative hormonal therapy. Vopr. ginekol. akus. perinatol. (Gynecology, Obstetrics and Perinatology). 2019; 18(2): 122–128. (In Russian). DOI: 10.20953/1726-1678-2019-2-122-128

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