Eutopic endometrium in patients with endometriosis is characterized by aberrant expression of essential genes during the implantation window. It predisposes to disturbance of endometrial receptivity. The pathomechanism of implantation failures in women with endometriosis remains unclear. This paper aims to summarize the knowledge on epigenetic mechanisms in eutopic endometrium in the group of patients with both endometriosis and infertility. The impaired DNA methylation patterns of gene promoter regions in eutopic tissue was established. The global profile of histone acetylation and methylation and the analysis of selected histone modifications showed significant differences in the endometrium of women with endometriosis. Aberrant expression of the proposed candidate genes may promote an unfavorable embryonic implantation environment of the endometrium due to an immunological dysfunction, inflammatory reaction, and apoptotic response in women with endometriosis. The role of the newly discovered proteins regulating gene expression, i.e., TET proteins, in endometrial pathology is not yet completely known. The cells of the eutopic endometrium in women with endometriosis contain a stable, impaired methylation pattern and a histone code. Medication targeting critical genes responsible for the aberrant gene expression pattern in eutopic endometrium may help treat infertility in women with endometriosis.

Endometriosis is the cause of infertility. The eutopic endometrium of women with endometriosis showed an aberrant expression pattern of multitude genes. The role of TET1 protein in the pathogenesis of endometriosis and related infertility is not sufficiently known. Further, knowledge on TET1 transcriptional control still remains incomplete. The aim of the study was assessment of TET1 gene expression, DNA methylation and H3K27me3 level of its promoter region in eutopic endometrium of women with endometriosis and infertility. The study included 44 infertile patients with endometriosis (IWE) and 77 infertile (IW) and fertile (FW) patients without endometriosis. The research material was eutopic endometrium. The TET1 mRNA level was analyzed by qPCR. Western blot was used to evaluate the level of TET1 protein. The level of DNA methylation and H3K27me3 level of TET1 gene's promoter region were assessed using HRM and ChIP qPCR, respectively. The level of TET1 expression (TET1 mRNA; TET1 protein level) was lower in IWE during the implantation window (p < 0.001; p = 0.0329). The level of TET1 DNA methylation was higher in the secretory endometrium in mild and advanced IWE (p < 0.004; p < 0.008). H3K27me3 level did not differ between the study groups. The diminished expression of TET1 gene during the secretory phase, may account for the aberrant process of embryonic implantation in infertile endometriosis patients. DNA hypermethylation of TET1 gene is a potential relevant regulator of its expression. H3K27me3 occupancy does not affect the expression of TET1 gene in our study group.

Endometriosis is a common gynecological condition associated with chronic inflammation, epigenetic dysregulation, and infertility. The TET1 gene, involved in DNA demethylation, may be regulated by repressive histone modifications such as H3K27me3, but its role in endometriosis remains poorly understood. This study aimed to assess H3K27me3 enrichment in the promoter region of TET1 in eutopic endometrium of infertile and fertile women with endometriosis compared to fertile controls. Endometrial biopsies were collected during laparoscopy from 25 women (18 with endometriosis, 7 controls). Chromatin immunoprecipitation (ChIP) was performed to quantify H3K27me3 levels in three promoter regions of TET1. Analyses included stratification based on ChIP efficiency and subgroup comparisons according to fertility status and menstrual cycle phase. In overall comparisons, no significant differences in H3K27me3 levels were observed between endometriosis and control groups. However, after stratification by ChIP efficiency, region 2 showed a significant difference, indicating higher H3K27me3 enrichment in endometriosis samples (p = 0.04), confirmed after correction for multiple comparisons. Analyses by fertility status and cycle phase did not reveal additional significant differences. These findings suggest potential region-specific epigenetic alterations of TET1 in endometriosis. Due to the modest sample size and inconsistent subgroup effects, results should be interpreted with caution. Larger, cell-type-specific studies are warranted to clarify the relevance of H3K27me3-mediated TET1 regulation in endometriosis-related infertility.

Background: Endometriosis is a chronic inflammatory disease affecting approximately 10% of women of reproductive age and is commonly associated with pelvic pain and infertility. Increasing evidence indicates that lower urinary tract symptoms (LUTS) are more common in women with endometriosis, even in the absence of direct urinary tract involvement; however, the underlying mechanisms remain poorly understood. This study aimed to compare LUTS in women with surgically confirmed endometriosis and symptomatic women in whom endometriosis was surgically excluded, and to investigate their association with urethral ultrasonographic parameters and lesion localization. Methods: This prospective case–control study included 163 women: 81 with surgically confirmed endometriosis and 82 symptomatic controls in whom endometriosis was surgically excluded. Urinary symptoms were assessed using the validated Urogenital Distress Inventory Short Form (UDI-6). Urethral length and mobility were evaluated by transvaginal pelvic floor ultrasonography at rest, during pelvic floor muscle contraction, and during the Valsalva maneuver. Associations between urinary symptoms, ultrasonographic findings, lesion localization, and selected clinical variables were analyzed using appropriate non-parametric tests and multivariable linear regression. Results: Women with endometriosis demonstrated significantly higher total UDI-6 scores than symptomatic controls (p = 0.002), indicating a greater burden of lower urinary tract symptoms. Significant differences were observed only for pain/discomfort and post-void urine leakage, whereas the remaining UDI-6 domains did not differ between groups. Overall urethral ultrasonographic parameters were comparable between groups. However, among symptomatic women (UDI-6 ≥ 1), urethral mobility during the Valsalva maneuver was significantly lower in women with endometriosis than in controls (p = 0.041). Endometriosis localization was not associated with urinary symptom severity or urethral ultrasonographic findings. In multivariable analysis, previous cesarean section, but not endometriosis itself, was independently associated with higher UDI-6 scores. Conclusions: Women with surgically confirmed endometriosis experienced a greater burden of lower urinary tract symptoms than symptomatic women without endometriosis, particularly pain/discomfort and post-void urine leakage. These symptoms were not associated with lesion localization or major differences in urethral morphology, indicating that structural urethral abnormalities alone do not explain urinary symptom severity in this population. Routine assessment of urinary symptoms using validated questionnaires may facilitate comprehensive evaluation of women with endometriosis. Further prospective multicenter studies incorporating standardized pain assessment, urodynamic evaluation, and longitudinal follow-up are warranted to better elucidate the mechanisms underlying lower urinary tract symptoms in this population.

Fetal and placental growth are influenced by multiple maternal and fetal factors, including fetal sex and maternal parity. Accurate knowledge of these determinants is essential for growth monitoring and perinatal risk assessment. This study aimed to evaluate the effects of fetal sex and maternal parity on birth weight, placental weight, and the fetal-to-placental weight ratio in a large single-center cohort. We conducted a retrospective cohort study of 4,642 singleton live births between 28 and 40 weeks of gestation at a tertiary hospital in the Wielkopolska region, Poland. Birth weight, placental weight, and fetal-to-placental weight ratios were analyzed according to fetal sex and maternal parity. Percentile charts were generated, and differences were assessed using appropriate statistical tests with p < 0.05 considered significant. Male newborns had higher birth weights than females, with significant differences from 36 to 40 weeks. Placental weight increased with gestational age, with males showing higher values at 38-40 weeks. Fetal-to-placental weight ratios were higher in males at 30, 36, 37, and 40 weeks, indicating greater placental efficiency. Multiparous women delivered newborns with higher birth and placental weights compared to primiparas, particularly in late gestation. Correspondingly, fetal-to-placental ratios were higher among multiparas, reflecting enhanced placental efficiency in subsequent pregnancies. Fetal sex and maternal parity significantly influence fetal and placental growth and fetoplacental efficiency. Male newborns and offspring of multiparas had higher birth weights and more favorable fetal-to-placental weight ratios. The provided percentile charts may serve as practical references for obstetric and neonatal care in the Wielkopolska region.

Background: Endometriosis is a chronic inflammatory disease commonly associated with pelvic pain and infertility. Increasing evidence suggests that women with endometriosis may also experience lower urinary tract symptoms (LUTS), even without direct urinary tract involvement. Aim: This study aimed to evaluate LUTS in women with endometriosis and determine whether these symptoms are associated with urethral ultrasonographic parameters or the localization of endometriotic lesions. Materials and Methods: This prospective case–control study included 166 women aged 17–49 years: 83 with confirmed endometriosis and 83 controls without endometriosis. Endometriosis was confirmed laparoscopically, except in patients with cesarean scar endometriosis, where diagnosis was based on imaging and histopathological confirmation. Clinical assessment included standardized questionnaires and transvaginal pelvic floor sonography. Urinary symptoms were assessed using the Urogenital Distress Inventory short form (UDI-6). Urethral length and mobility were evaluated at rest, during contraction, and during the Valsalva maneuver. Results: Women with endometriosis demonstrated significantly higher total UDI scores than controls (27.8 vs. 16.7; p = 0.002), with the greatest differences in pain/discomfort and urine leakage symptoms. No significant differences in urethral anatomy were observed. Among symptomatic patients, urethral mobility during Valsalva was significantly lower in the endometriosis group (p = 0.041). Lesion localization was not associated with symptom severity. Conclusions: Women with endometriosis experience a greater burden of LUTS, particularly bladder storage dysfunction and pain, likely related to functional and neuroinflammatory mechanisms rather than structural abnormalities.