Endometriosis is a benign uterine disorder characterized by menstrual pain and infertility, deeply affecting women’s health. It is a chronic disease and requires a long term management. Hormonal drugs are currently the most used for the medical treatment and are based on the endocrine pathogenetic aspects. Estrogen-dependency and progesterone-resistance are the key events which cause the ectopic implantation of endometrial cells, decreasing apoptosis and increasing oxidative stress, inflammation and neuroangiogenesis. Endometriotic cells express AMH, TGF-related growth factors (inhibin, activin, follistatin) CRH and stress related peptides. Endocrine and inflammatory changes explain pain and infertility, and the systemic comorbidities described in these patients, such as autoimmune (thyroiditis, arthritis, allergies), inflammatory (gastrointestinal/urinary diseases) and mental health disorders.The hormonal treatment of endometriosis aims to block of menstruation through an inhibition of hypothalamus-pituitary-ovary axis or by causing a pseudodecidualization with consequent amenorrhea, impairing the progression of endometriotic implants. GnRH agonists and antagonists are effective on endometriosis by acting on pituitary-ovarian function. Progestins are mostly used for long term treatments (dienogest, NETA, MPA) and act on multiple sites of action. Combined oral contraceptives are also used for reducing endometriosis symptoms by inhibiting ovarian function. Clinical trials are currently going on selective progesterone receptor modulators, selective estrogen receptor modulators and aromatase inhibitors. Nowadays, all these hormonal drugs are considered the first-line treatment for women with endometriosis to improve their symptoms, to postpone surgery or to prevent post-surgical disease recurrence. This review aims to provide a comprehensive state-of-the-art on the current and future hormonal treatments for endometriosis, exploring the endocrine background of the disease.

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These results indicate that RTF is constitutively expressed at endometrial and decidual level and its up-regulation during the secretory phase of the cycle may be relevant in mediating some immune-related aspects of uterine physiology.

Background Acute pancreatitis (AP) caused by gallstones has an increased rate of incidence in young women in the 2 years postpartum. Middle-aged women with longer periods of breastfeeding have less hospitalization for gallbladder disease. Aim To investigate whether breastfeeding or other variables may be associated with AP. Methods We conducted a population-based case-control study among all Sicilian women of childbearing age, and we identified all women who delivered (2013-2016) and had AP within 2 years postpartum. We reviewed their medical records, and for each case we matched four women of the same age (± 5 years), without AP. Univariate and multivariate logistic regression was used to estimate the odds ratios (OR) with their confidence intervals (CI) to assess associations between AP and clinical determinants. Results In the 74 women with AP and 298 controls at univariate analysis, > 6 months oral contraception history (p < 0.01; OR 3.30; 95% CI 1.33-8.16), previous biliary disease (p < 0.001; OR 5.90; 95% CI 1.98-17.57) and smoking (p = 0.035; OR 2.04; 95% CI 1.04-4.0) were predictors of AP; amenorrhea ≥ 3 months (p < 0.001; OR 0.34; 95% CI 0.19-0.59) and breastfeeding ≥ 3 months (p < 0.001; OR 0.07; 95% CI 0.03-0.14) were protective. At multivariate analysis, previous biliary disease (p = 0.011; OR 5.49; 95% CI 1.48-20.38) and breastfeeding ≥ 3 months (p < 0.001; OR 0.06; CI 95% 0.03-0.14) were associated with AP. Conclusions Women who breastfeed for at least 3 months and do not have a history of biliary disorders have reduced risk of developing AP in the 2 years after delivery.

Purpose of the Review The purpose of this review is to provide a synopsis of all the mechanisms involved in the pathogenesis of adenomyosis. It will summarize recent advances in the field, discussing current controversies, and considering potential future directions. Recent Findings Adenomyosis pathogenesis is still a topic under investigation, however advancements in the understanding of disease development and mechanisms have been made. New data coming from new next generation sequencing-based studies and more-in-depth acquisitions on sex hormones imbalance, neuroangiogenesis, inflammation, fibrosis and cell proliferation have been obtained. Summary Adenomyosis is a uterine disorder that affects women of reproductive age, characterized by a benign invasion of the endometrium basalis (glands and stroma) within the myometrium. So far, three theories for the pathophysiology of adenomyosis have been proposed: An invagination of the endometrial basalis into the myometrium by tissue injury and repair. The development from adult stem cells or displaced embryonic müllerian remnants. An “invasion from outside to inside”. In order to invade and develop, endometrial cells require a series of pathogenetic mechanisms which drive to adenomyosis. Altered sex steroids hormones receptors may be the primary event which causes increased endometrial cell proliferations and differentiation from epithelial to mesenchymal cells. Once invaded the myometrium, an inflammatory reaction is displayed, probably driven by local immune changes. The processes of neuroangiogenesis and fibrosis are also involved in the adenomyosis development and may explain some of the associated clinical symptoms (dysmenorrhea, abnormal uterine bleeding, and infertility).