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Oral GnRH antagonists have become an important advancement in the medical management of endometriosis and are increasingly being explored for adenomyosis. These agents work by directly blocking GnRH receptors in the pituitary gland, producing an immediate decrease in LH and FSH and therefore suppressing ovarian estrogen production without causing the “flare effect” seen with older GnRH agonists.
Endometriosis is classically defined as the presence of endometrial tissue both endometrial glands and stroma (connective tissue), in ectopic locations outside of the uterus, primarily the ovaries, fallopian tubes, pelvic peritoneum and rectovaginal septum. Affecting 6-10% of women of reproductive age, endometriosis is characterized by dysmenorrhea, chronic pelvic pain, irregular uterine bleeding and/or infertility and is occasionally accompanied by painful intercourse, bowel movements and/or urination.
Endometriosis is a significant factor contributing to infertility in women, primarily due to its impact on the reproductive organs and functions. The presence of endometriotic tissue outside the uterus causes chronic inflammation, which can interfere with normal ovarian and tubal function, disrupting the process of ovulation, fertilization, and embryo implantation.
The medical treatment of endometriosis focuses on managing symptoms, particularly pain, and improving fertility outcomes by addressing the hormonal imbalances and inflammation associated with the condition. A common first-line treatment involves hormonal therapy aimed at reducing estrogen levels, which fuel the growth of endometriotic lesions. Oral contraceptives, containing a combination of estrogen and progestin, help regulate hormonal fluctuations and reduce menstrual flow, thereby alleviating symptoms.
Endometriosis and PCOS are the Yin and Yang of reproductive medicine. Endometriosis is driven by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis.
Endometriomas are cystic ovarian masses filled with old blood and tissue, stemming from endometriosis, a condition where tissue from the lining of the uterus, the endometrium grows outside the uterus. Endometriomas are often referred to as "chocolate cysts" due to the dark, reddish-brown fluid they contain. Endometriomas are a common finding in women with endometriosis and can indicate a more advanced stage of the disease. About 10% of young women will develop endometriosis, and about 17% to 44% of these women will also develop ovarian endometriomas and 28% of these women will have bilateral endometriomas.
Endometriosis is driven by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis (defined below), and at low levels and it can result in an altered trajectory of reproductive and physiological phenotypes that can mediate the symptoms of endometriosis. A phenotype is defined as a person’s observable characteristics resulting from the interaction of their genetic makeup and the environment. Polycystic ovary syndrome, by contrast, is known to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes that are diametrically opposite to those found in endometriosis.
Epigenetics plays an important role in the development of many metabolic diseases and since these alternations to the underlying DNA are reversible, restoring the DNA to normal provides opportunities for developing pharmacotherapies for many metabolic diseases.
Summary
Although endometriosis is a common disease affecting up to 15% of women of reproductive age, the mechanisms underlying the disease are not fully understood. Retrograde menstruation is a widely accepted cause of endometriosis. However, not all women who experience retrograde menstruation develop endometriosis, suggesting that other factors might contribute to its development. A recent study demonstrated a pathogenic role of Fusobacterium in the formation of ovarian endometriosis. In a cohort of women, 64% of patients with endometriosis but less than 10% of controls were found to have Fusobacterium infiltration in the endometrium (the lining of the uterus). This data supports an additional mechanism for the pathogenesis of endometriosis via Fusobacterium infection and suggests that eradication of this bacterium could be an approach to treat endometriosis
Summary
At mid-cycle, uterine contractions are predominantly cervical-fundal (from the bottom of the uterus to the top), specifically toward the fallopian tubes. The amplitude and frequency of the contractions increase significantly as ovulation approaches. There is evidence that this facilitates sperm ascension towards the distal (far) end of the fallopian tubes, where fertilization occurs. Women with endometriosis display marked uterine hyperperistalsis that differs significantly from the contractions of women without endometriosis. At mid-cycle, uterine contractions in women with endometriosis became dysperistaltic (abnormal), arrhythmic, and convulsive, while in controls, peristalsis continues to show long and regular cervical-fundal (normal) contractions. This may explain the high incidence of infertility even in women with only mild endometriosis.