Endometriosis and Infertility

Nesbitt‐Hawes, Erin; Ledger, William

doi:10.1007/978-1-4471-4953-8_3

Cited by 4 publications

(2 citation statements)

References 43 publications

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“…Cells involved in the immune response such as monocytes, macrophages, natural killer cells, T and B cells, regulatory T cells, as well as secreted cytokines and chemokines, participate in inflammation. Their role in endometriosis has been extensively studied, as cell numbers and cytokine concentrations were higher or altered in the peritoneal fluid of the endometriosis patients (Nesbitt-Hawes & Ledger 2004, Podgaec et al 2012, Gupta et al 2016.…”

Section: Introductionmentioning

confidence: 99%

Interleukin in endometriosis-associated infertility-pelvic pain: systematic review and meta-analysis

Malvezzi¹,

Hernandes²,

Piccinato³

et al. 2019

Reproduction

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The objective is to study the significance of altered interleukin levels in endometriosis-related infertility or pelvic pain. The present systematic review and meta-analysis includes a discussion on the roles of interleukin in the physiopathology of endometriosis-associated infertility and/or pelvic pain. We included all studies in which interleukins in peritoneal fluid, follicular fluid or serum from patients were measured and that correlated the findings with either peritoneal or deep endometriosis-associated infertility or pelvic pain. For the meta-analysis, we selected studies on the following cytokines: interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-8 (IL-8). Endometriosis is a chronic inflammatory disease. Inflammatory processes clearly participate in the etiology of endometriosis. Cytokines are mediators of inflammation, and increase in their concentration in plasma or other body fluids signals the presence and extent of tissue lesions. A number of studies have reported on the association between higher cytokine levels and progression or maintenance of endometriosis and coexisting infertility or pelvic pain. The results of the analyses support that an association exists between elevated serum IL-6 and/or IL-8 concentrations and the occurrence of endometriosis-associated infertility. Such association was not found for endometriosis-associated pain. In spite of accumulated evidence on the association of pro-inflammatory cytokines and endometriosis, it still is not clear if and how these mediators participate in the physiopathology of endometriosis-associated infertility or pelvic pain, in part due to poor quality of the evidence established in the vast majority of interleukins and challenges in endometriosis research reproducibility. In summary, the results of the analyses support that an association exists between elevated serum IL-6 and/or IL-8 concentrations and the occurrence of endometriosis-associated infertility.

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Section: Introductionmentioning

confidence: 99%

Interleukin in endometriosis-associated infertility-pelvic pain: systematic review and meta-analysis

Malvezzi¹,

Hernandes²,

Piccinato³

et al. 2019

Reproduction

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“…Endometriosis is a common disorder that is believed to affect 6-10% of women of reproductive age estimated to be ~176 million women worldwide (Bulletti et al 2010). An increased prevalence is commonly found in women with infertility, pelvic pain or both, with values ranging from 30 to 50% (Eskenazi & Warner 1997, Giudice & Kao 2004.…”

Section: Introduction Prevalence Characteristics and Socioeconomic Imentioning

confidence: 99%

SULFATION PATHWAYS: Contribution of intracrine oestrogens to the aetiology of endometriosis

Piccinato

Malvezzi

Gibson

et al. 2018

Journal of Molecular Endocrinology

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Endometriosis is an incurable hormone-dependent inflammatory disease that causes chronic pelvic pain and infertility characterized by implantation and growth of endometrial tissue outside the uterine cavity. Symptoms have a major impact on the quality of life of patients resulting in socioeconomic, physical and psychological burdens. Although the immune system and environmental factors may play a role in the aetiology of endometriosis, oestrogen dependency is still considered a hallmark of the disorder. The impact of oestrogens such as oestrone and particularly, oestradiol, on the endometrium or endometriotic lesions may be mediated by steroids originating from ovarian steroidogenesis or local intra-tissue production (intracrinology) dependent upon the expression and activity of enzymes that regulate oestrogen biosynthesis and metabolism. Two key pathways have been implicated: while there is contradictory data on the participation of the aromatase enzyme (encoded by ), there is increasing evidence that the steroid sulphatase pathway plays a role in both the aetiology and pathology of endometriosis. In this review, we consider the evidence related to the pathways leading to oestrogen accumulation in endometriotic lesions and how this might inform the development of new therapeutic strategies to treat endometriosis without causing the undesirable side effects of current regimes that suppress ovarian hormone production.

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Peritoneal fluid of women with endometriosis reduces SOD1 in bovine oocytes in vitro maturation

et al. 2018

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Studies have demonstrated oxidative stress in peritoneal fluid (PF) from women with endometriosis and the importance of enzymatic antioxidant machinery to avoid oocyte oxidative damage. Considering that PF constantly surrounds the ovaries and has direct contact with the oocyte at ovulation, we wonder if PF from women with endometriosis may affect antioxidant enzyme gene expression. Thus, the present study aims to evaluate the PF impact from infertile women with minimal and mild endometriosis and from fertile control women without endometriosis on SOD1, CAT, GSR gene's expression in experimental bovine oocytes matured in vitro. Samples of PF were obtained from women who underwent videolaparoscopy-7 infertile with EI/II and 7 fertile without endometriosis. Immature bovine oocytes underwent in vitro maturation in the absence of PF and in the presence of three concentrations (1, 5 and 10%) of PF from fertile and from infertile women with EI/II. After 22 to 24 h of IVM, oocytes were denuded and stored for analysis of SOD1, CAT and GSR by real-time polymerase chain reaction. Oocyte SOD1 expression was significantly lower in the 10% endometriosis group (0.67 ± 0.32) when compared with no-peritoneal fluid (1.05 ± 0.24, p < 0.008) and 10% control groups (1.06 ± 0.22, p < 0.006). These findings raise the possibility of a deleterious influence of PF from women with EI/II on the oocyte, not only after ovulation but also during the maturation process, which could contribute to worsening oocyte quality, being one of the mechanisms related to infertility in patients with endometriosis.

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Endometriosis and Infertility

Cited by 4 publications

References 43 publications

Interleukin in endometriosis-associated infertility-pelvic pain: systematic review and meta-analysis

Interleukin in endometriosis-associated infertility-pelvic pain: systematic review and meta-analysis

SULFATION PATHWAYS: Contribution of intracrine oestrogens to the aetiology of endometriosis

Peritoneal fluid of women with endometriosis reduces SOD1 in bovine oocytes in vitro maturation

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