RESUMEN
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.
RESUMEN
BACKGROUND: Hysteroscopy is the best approach for the management of Asherman syndrome with reproductive purposes, since it allows a quick diagnosis and treatment of partial or total uterine adhesions. However, there are a few studies on the reproductive outcome in patients with Asherman's syndrome. OBJECTIVE: Evaluate the results of adherenciolisis hysteroscopy in women with Asherman's syndrome. PATIENTS AND METHODS: We performed a cohort study of thirty-nine patients diagnosed with Asherman's syndrome and who underwent surgical hysteroscopic adherenciolisis by bipolar energy through the period from 2006 to June 2011. RESULTS: Thirty-nine cases were reviewed. All patients restored their menstrual cycle in the course of the first three months after surgery. The pregnancy rate after hysteroscopic treatment was 71.7% (28/39), with a son living at home in 28.2% of the cases (11/39). There was no statistical difference to achieve term pregnancy based on a cut-off point at 35 years of age. A history of menstrual pattern before hysteroscopy was associated with perinatal success. All pregnancies were achieved spontaneously within the first year after the procedure. CONCLUSIONS: Spontaneous pregnancy is possible after hysteroscopic adherenciolisis in Asherman's Syndrome. It confirms the viability of using bipolar energy to restore the size and shape of the uterine cavity with minimal endometrial damage and with an exclusive reproductive purpose.
