Despite the increased frequency of endometriosis, it remains one of the most enigmatic disorders regarding its effects on pregnancy. Endometriosis adversely affects both natural and assisted conception. Impaired folliculogenesis, which causes follicular dysfunction and low egg quality, as well as luteal phase problems, reduced fertilization, and abnormal embryogenesis, are some of the mechanisms advocated to explain reproductive dysfunction. There is a rising need for a comprehensive study of the potential negative consequences of this condition on pregnancy outcomes, including the postpartum period, as more women with a medical history of endometriosis become pregnant. Obstetrical complications (small for gestational age [SGA], cesarean section [CS], miscarriage, hemorrhage, low placental adhesion, and preterm delivery) are statistically elevated in women with endometriosis. Furthermore, ruptured ovarian endometrioma, appendicitis, intestinal perforation, and hemoperitoneum have been described in pregnancy. Obstetricians are largely unfamiliar with these complications, as they have not been thoroughly investigated. The development and pathogenesis of endometriosis is an important field of study and has not yet been fully elucidated. Finding these mechanisms is crucial for the development of new and more effective strategies to treat this condition. Endometriosis can have an impact on obstetric and neonatal outcomes of pregnancy, in addition to its potential effects on conception. To date, no additional monitoring is recommended for pregnancies with a history of endometriosis. However, more studies are urgently needed to assess the need for the tailored pregnancy monitoring of women with endometriosis.

Objectives: Fibroids cause significant morbidity and are the most common indication for hysterectomies worldwide, delimiting a major public health problem. Uterine artery embolization (UAE) is an alternative therapy to surgical treatment of symptomatic fibroids; it has satisfactory long-time results and is no longer considered investigational for the treatment of symptomatic fibroids. This study was undertaken to evaluate changes in fibroid specific symptom severity and health-related quality of life (HRQOL) after UAE and to optimize the assessment of safety and outcomes measures for participants who receive UAE to objective compare UAE and surgical alternatives for therapy of symptomatic fibroids. Study design: The analysis was based on questionnaires completed by 270 pre-menopausal females with a mean age of 42 years (range, 38–50 years) who underwent UAE for uterine leiomyomas and/or adenomyosis from November 2013 through December 2019. Only symptomatic women were selected whose symptoms were not improving with medication and who did not wish to have children. The primary outcome measure was a change in fibroid symptoms and HRQOL (health related quality of life) after UAE. Secondary outcomes included the decrease in uterine volume after UAE. Results: Questionnaires were completed by 270 women (100%) at a mean of 12.1 months from UAE. The median follow-up period was two years. Uterine fibroid embolization led to a shrinkage at three months for the 90% of the participants. A reduction of bleeding symptoms, pain and bulk-related symptoms was observed in 89.7%, 88.9%, and 89.5% of the patients, respectively. In the long term, there was no significant difference in parameters assessed compared with the midterm follow-up findings. A total of 6 patients (2.3%) underwent fractional curettage an average of 32.1 months after intervention due to necrotic changes in submucosal fibroids. All participants continued to be satisfied with the intervention, and 240 patients (88.9%) answered that they would recommend uterine fibroid embolization to other patients. Conclusions: Women who undergo UAE have a significant decrease in symptom severity and increase in HRQOL which is associated with high levels of satisfaction with the procedure (even when subsequent therapies are pursued).

Programmed frozen embryo transfer (FET) cycles are an integral part of assisted reproductive technologies (ARTs). They rely exclusively on the administration of exogenous estrogens and progesterone to prepare the endometrium, and they are characterized by the absence of a functional corpus luteum (CL). Pregnancies resulting from FET cycles have been associated with an increased risk of complications related to placental dysfunction, such as preeclampsia and fetal growth restriction (FGR). Besides progesterone production, the CL secretes vasoactive and angiogenic factors essential for the regulatory mechanisms that occur during the early stages of pregnancy. Its absence results in a different endocrine environment, which may be associated with differences in normal maternal cardiovascular remodeling. In pregnant women without CL function, reduced vasodilation, increased systemic vascular resistance, altered cardiac output, and inadequate renal adaptation have been reported. In addition, disturbances in angiogenic balance and trophoblast invasion may contribute to abnormal placentation and the development of preeclampsia. Accordingly, the absence of the CL in programmed FET cycles may represent a critical endocrine disorder, predisposing patients to maternal cardiovascular disturbance and adverse obstetric outcomes. Recognition of this potential endocrine and vascular interaction has important implications for cycle selection, risk stratification, and preventive strategies in the implementation of assisted reproduction protocols.

The World Health Organization (WHO) defines infertility as the inability of a couple to conceive after at least 12 months of regular, unprotected sexual intercourse. The male factor appears to be contributing, solely or in combination with other causes, to approximately 50% of all infertility cases. Several etiological factors of male infertility have been identified; however, the exact molecular mechanisms underlying sperm dysfunction are not yet fully understood. Aldehyde dehydrogenases (ALDHs) are multifaceted metabolic enzymes that catalyze the detoxification of several aldehydes, thus acting as antioxidants, while they regulate additional homeostatic functions by contributing to retinoic acid (RA) synthesis. Consequently, they have been identified as crucial factors in various pathogenetic mechanisms. ALDHs hold physiological roles in the testis through supporting the Sertoli cell function, the steroidogenesis in Leydig cells, and the maintenance of sperm integrity. Current evidence supports that dysregulation of specific ALDHs isoforms could be associated with disrupted testicular cell function, including oxidative imbalance and altered RA synthesis. These irregularities could interfere with germ cell development and, subsequently, contribute to decline in reproductive function. In this paper, we are reviewing the role of ALDHs in male reproduction and how their dysregulation could be implicated in male infertility. Unraveling the mechanisms underlying the association of ALDHs with male reproductive function could hold clinical interest regarding the development of novel approaches for enhancing male fertility.