Journal ArticleDOI
Cytokine Profiling in the Eutopic Endometrium of Adenomyosis During the Implantation Window After Ovarian Stimulation
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TLDR
Within the implantation window of ovarian stimulation cycles, macrophages,IL-6, IL-10, and MCP-1 are expressed differently in the endometrium of women with adenomyosis, which may correlate with compromised endometrial receptivity.Abstract:
In this study, we aimed to clarify the inflammatory cytokine profile of endometrium in patients with adenomyosis during the implantation window after ovarian stimulation. Eighteen patients with adenomyosis and 24 control patients undergoing in vitro fertilization treatment were included in this prospective case-control study. Regular gonadotropin-releasing hormone antagonist protocol was used for ovarian stimulation. Endometrial samples were obtained 7 days after human chorionic gonadotropin (hCG) injection (hCG + 7). Cytokine levels in endometrium secretions from women with and without adenomyosis were assayed by multiplex immunoassay, levels of interleukin (IL) 6 (25.9 ± 6.6 vs 12.4 ± 3.4 pg/mL; P = .001), IL-10 (10.4 ± 2.9 vs 15.6 ± 4.2 pg/mL; P = .001), IL-17 (11.9 ± 3.0 vs 14.2 ± 3.9 pg/mL; P = .046), interferon-γ (11.7 ± 3.5 vs 8.0 ± 3.4 pg/mL; P = .001), and monocyte chemoattractant protein-1 (MCP-1; 37.1 ± 6.5 vs 16.4 ± 3.2 pg/mL; P = .001) were significantly different between patients with adenomyosis and control groups, respectively. Immunohistochemistry and quantitative real-time polymerase chain reaction showed that CD-68+, IL-6, and MCP-1 expression were higher and IL-10 was lower in adenomyosis endometrium epithelia compared to controls. In conclusion, within the implantation window of ovarian stimulation cycles, macrophages, IL-6, IL-10, and MCP-1 are expressed differently in the endometrium of women with adenomyosis, which may correlate with compromised endometrium receptivity. We postulated that cytokines of endometrial secretions expressed differently in patients with adenomyosis may contribute to impaired endometrium receptivity in these patients.read more
Citations
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Journal ArticleDOI
Uterine polyps, adenomyosis, leiomyomas, and endometrial receptivity
TL;DR: The relationship of these common entities to endometrial receptivity is examined to identify evidence gaps that should be considered when strategizing research initiatives and to examine the mechanisms thought to be involved when these entities are contributing to infertility.
Journal ArticleDOI
Classification and Reporting Systems for Adenomyosis
TL;DR: A systematic review of the available histological and image-based classification systems to determine which, if any, provide clinical utility for prognosis or the selection of appropriate therapeutic interventions found there is inconsistency in histopathological definitions.
Journal ArticleDOI
Role of angiogenesis in adenomyosis-associated abnormal uterine bleeding and subfertility: a systematic review.
Marissa J Harmsen,Caroline F C Wong,Velja Mijatovic,Arjan W Griffioen,Freek Groenman,Wouter J. K. Hehenkamp,Judith A F Huirne +6 more
TL;DR: The level of abnormal vascularization and expression of angiogenic markers is increased in the ectopic and eutopic endometrium of adenomyosis patients in comparison with the endometrial of control patients was investigated through a search of the literature.
Journal ArticleDOI
Immunological changes associated with adenomyosis: a systematic review.
Mathilde Bourdon,Pietro Santulli,Mohamed Jeljeli,Silvia Vannuccini,Silvia Vannuccini,Louis Marcellin,Ludivine Doridot,Felice Petraglia,Frédéric Batteux,Charles Chapron +9 more
TL;DR: A systematic review of published human studies from 1970 to February 2019 found pro-inflammatory cytokines as well as anti-inflammatory or regulatory mediators were found to be elevated in the eutopic and/or ectopic endometrium of the myometrium in women with adenomyosis compared to controls.
Journal ArticleDOI
Endometrial causes of recurrent pregnancy losses: endometriosis, adenomyosis, and chronic endometritis.
TL;DR: In this paper, chronic inflammatory processes affecting the endometrium, as encountered in endometriosis, adenomyosis, and chronic endometritis, alter endometrial receptivity.
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