Endometrioma may differentially affect eicosanoids in the follicular fluid and serum of infertile women with endometriosis.

IF 1.9
Larissa de Oliveira Koopman, Mayra Beraldo Andozia, Carlos Arterio Sorgi, Lucia Helena Faccioli, Michele Gomes da Broi, Paula Andrea Navarro
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Abstract

Objective: The etiopathogenesis of endometriosis-related infertility remains under investigation, including in women with endometriomas. Oocyte quality is believed to play an important role in the impairment of natural fertility in these patients, with systemic inflammation and oxidative stress acting as mediators of oocyte damage. Eicosanoids are bioactive lipids produced in response to inflammatory or oxidative conditions and are involved in various ovarian processes; their dysregulation may impair oocyte competence. This study aimed to compare the serum and follicular fluid eicosanoid profiles of women with and without endometriosis, including women with and without endometrioma.

Methods: In this prospective cohort study, blood and follicular fluid samples were collected on the day of oocyte retrieval from 18 infertile women with endometriosis (8 with endometrioma and 10 without endometrioma) and 20 patients with tubal and/or male-factor infertility. The eicosanoid profiles of the samples were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS).

Results: No differences were found in serum eicosanoids between the endometriosis and control groups. After subdividing the endometriosis group into women with and without endometrioma, we observed lower serum levels of 5-hydroxyeicosatetraenoic acid (5-HETE) in those with endometrioma (38.47pg/mL vs. 120.45pg/mL; p=0.01). Increased follicular levels of eicosapentaenoic acid (EPA) were found in women with endometriosis (4038.52pg/mL; p=0.03) and in those with endometrioma (5811.50pg/mL; p=0.005) compared with controls (1159.83 pg/mL).

Conclusion: The findings suggest that pelvic disease promotes a systemic pro-inflammatory alteration, whereas endometrioma induces a local anti-inflammatory response. This may represent a mechanism to prevent oocyte damage, highlighting different mechanisms underlying endometriosis-related infertility according to lesion type. Further studies should confirm these findings using appropriate sample sizes and methodology.

子宫内膜异位症不孕妇女卵泡液和血清中的类二十烷醇可能受到不同程度的影响。
目的:子宫内膜异位症相关不孕的发病机制仍在研究中,包括子宫内膜异位症患者。卵母细胞质量被认为在这些患者的自然生育能力受损中起重要作用,全身性炎症和氧化应激是卵母细胞损伤的介质。类二十烷酸是在炎症或氧化条件下产生的生物活性脂质,参与各种卵巢过程;它们的失调可能损害卵母细胞的能力。本研究旨在比较患有和不患有子宫内膜异位症(包括患有和不患有子宫内膜异位症的妇女)的血清和卵泡液类二十烷类蛋白。方法:在这项前瞻性队列研究中,从18名患有子宫内膜异位症的不孕妇女(8名患有子宫内膜异位症,10名没有子宫内膜异位症)和20名输卵管和/或男性因素不孕的患者中采集卵母细胞取卵当天的血液和卵泡液样本。采用液相色谱-串联质谱(LC-MS/MS)分析样品的类二十烷酸谱。结果:子宫内膜异位症患者血清类二十烷酸与对照组无明显差异。在将子宫内膜异位症组细分为有子宫内膜异位症和无子宫内膜异位症组后,我们观察到子宫内膜异位症组血清5-羟基二糖四烯酸(5-HETE)水平较低(38.47pg/mL vs. 120.45pg/mL; p=0.01)。与对照组(1159.83 pg/mL)相比,子宫内膜异位症女性(4038.52pg/mL, p=0.03)和子宫内膜异位症女性(5811.50pg/mL, p=0.005)的卵泡中二十碳五烯酸(EPA)水平升高。结论:盆腔疾病促进全身性促炎改变,而子宫内膜瘤诱导局部抗炎反应。这可能代表了一种防止卵母细胞损伤的机制,根据病变类型突出了子宫内膜异位症相关不孕症的不同机制。进一步的研究应使用适当的样本量和方法来证实这些发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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