Endometriosis is a gynecological disorder characterized by the growth of endometrial tissue (glands and stroma) outside the uterus, mainly in the peritoneal cavity, ovaries, and intestines. This condition shows estrogen dependency and progesterone resistance, and it has been associated with chronic inflammation, severe pain, and infertility, which negatively affect the quality of life in reproductive women. The molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood; however, inflammation plays a key role in the pathophysiology of the disease, mainly by altering the function of immune cells (macrophages, natural killer, and T cells) and increasing levels of pro-inflammatory mediators in the peritoneal cavity, endometrium, and blood. These immune alterations inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells, as well as angiogenesis and neurogenesis in endometriotic lesions. It has been demonstrated that hormonal alterations in endometriosis are related to the inflammatory unbalance in this disease. Particularly, steroid hormones (mainly estradiol) promote the expression and release of pro-inflammatory factors. Excessive inflammation in endometriosis contributes to changes of hormonal regulation by modulating sex steroid receptors expression and increasing aromatase activity. In addition, dysregulation of the inflammasome pathway, mediated by an alteration of cellular responses to steroid hormones, participates in disease progression through preventing cell death, promoting adhesion, invasion, and cell proliferation. Furthermore, inflammation is involved in endometriosis-associated infertility, which alters endometrium receptivity by impairing biochemical responses and decidualization. The purpose of this review is to present current research about the role of inflammasome in the pathogenesis of endometriosis as well as the molecular role of sex hormones in the inflammatory responses in endometriosis.

Polycystic ovary syndrome (PCOS) is the leading endocrine and metabolic disorder in premenopausal women characterized by hyperandrogenism and abnormal development of ovarian follicles. To date, the PCOS etiology remains unclear and has been related to insulin resistance, obesity, type 2 diabetes mellitus, cardiovascular disease and infertility, among other morbidities. Substantial evidence illustrates the impact of genetic, intrauterine and environmental factors on the PCOS etiology. Lately, epigenetic factors have garnered considerable attention in the pathogenesis of PCOS considering that changes in the content of DNA methylation, histone acetylation and noncoding RNAs have been reported in various tissues of women with this disease. DNA methylation is changed in the peripheral and umbilical cord blood, as well as in ovarian and adipose tissue of women with PCOS, suggesting the involvement of this epigenetic modification in the pathogenesis of the disease. Perhaps, these defects in DNA methylation promote the deregulation of genes involved in inflammation, hormone synthesis and signaling and glucose and lipid metabolism. Research on the role of DNA methylation in the pathogenesis of PCOS is just beginning, and several issues await investigation. This review aims to provide an overview of current research focused on DNA methylation and PCOS, as well as discuss the perspectives regarding this topic.

Endometriosis is one of the most frequent gynecological diseases in reproductive age women, but its etiology is not completely understood. Endometriosis is characterized by progesterone resistance, which has been explained in part by a decrease in the expression of the intracellular progesterone receptor in the ectopic endometrium. Progesterone action is also mediated by nongenomic mechanisms via membrane progesterone receptors (mPRs) that belong to the class II members of the progesterone and adipoQ receptor (PAQR) family. The aim of the present study was to evaluate the expression at mRNA and protein levels of mPR members in the eutopic and ectopic endometrium of women with endometriosis. Total RNA and total protein were isolated from control endometrium (17 samples), eutopic endometrium (17 samples), and ectopic endometrium (9 samples). The expression of PAQR7 (mPRα), PAQR8 (mPRβ), and PAQR6 (mPRδ) at mRNA and protein levels was evaluated by RT-qPCR and Western blot, whereas PAQR5 (mPRγ) gene expression was evaluated by RT-qPCR. Statistical analysis between comparable groups was performed using one-way ANOVA followed by Tukey’s multiple comparisons test with a confidence interval of 95 %. The analysis of gene expression showed that PAQR7 and PAQR5 expression was lower in both eutopic and ectopic endometrium as compared to the endometrium of women without endometriosis, whereas the expression of PAQR8 and PAQR6 was only reduced in eutopic endometrium. Furthermore, mPRα and mPRβ protein content was decreased in the ectopic endometrium of women with endometriosis. Our results demonstrate a decrease in the expression and protein content of mPRs in eutopic and ectopic endometrium of patients with endometriosis, which could contribute to the progesterone resistance observed in patients with this disease.

ObjectiveTo evaluate fasting plasma glucose (FPG) as a screening test for gestational diabetes mellitus (GDM) among Mexican adolescents using International Association of Diabetes and Pregnancy Study Groups criteria.DesignRetrospective cohort study.SettingLevel-three medical institution in Mexico City.ParticipantsThe study population comprised 1061 adolescent women aged 12–19 years with singleton pregnancies, who underwent a 75 g oral glucose tolerance test (OGTT) between 11 and 35 weeks of gestation.Primary and secondary outcome measuresThe sensitivity (Sn), specificity (Sp), positive and negative predictive values (PPV and NPV, respectively), and positive and negative likelihood ratios LR (+) and LR (−), respectively) with 95% CIs for selected FPG cut-off values were compared. Secondary measures were perinatal outcomes in women with and without GDM.ResultsGDM was present in 71 women (6.7%, 95% CI 5.3% to 8.4%). The performances of FPG at thresholds of ≥80 (4.5 mmol/L), 85 (4.7 mmol/L) and 90 mg/dL (5.0 mmol/L) were as follow (95% CI): Sn: 97% (89% to 99%), 94% (86% to 97%) and 91% (82% to 95%); Sp: 50% (47% to 53%), 79% (76% to 81%) and 97% (95% to 97%); PPV: 12% (9% to 15%), 23% (18% to 28%) and 64% (54% to 73%); NPV: 99% (98.5% to 99.9%) for all three cut-offs; LR (+): 1.9 (1.8 to 2.1), 4.3 (3.8 to 5.0) and 26.7 (18.8 to 37.1) and LR (−): 0.06 (0.02 to 0.23), 0.07 (0.03 to 0.19) and 0.09 (0.04 to 0.19), respectively. No significant differences in perinatal outcomes were found between adolescents with and without GDM.ConclusionsAn FPG cut-off of ≥90 mg/dL (5.0 mmol/L) is ideal for GDM screening in Mexican adolescent women. An FPG threshold of 90 mg/dL would miss 6 (8.5%) women with GDM, pick up 34 (3.4%) women without GDM and avoid 962 (90.7%) OGTTs.