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Ovarian, Fallopian Tube, and Primary Peritoneal Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Robert D. Morgan, Andrew R. Clamp, Gordon C. Jayson
Estrogen secretion is noted in at least 70% of GCTs, and as the median age of diagnosis is between 50 and 55 years old, patients may present with post-menopausal bleeding or irregular menses. In such patients, it is important to exclude a synchronous endometrial cancer caused by hyperestrogenism. Precocious puberty may be the presenting complaint in the case of juvenile GCTs. Patients with Sertoli-Leydig cell tumors may show clinical features of virilization or amenorrhea due to hyperandrogenism. Along with sex hormone secretion, the tumors can also release inhibins, which can be used as tumor markers to monitor the disease. These tumors may also present only when they have reached a large size, with symptoms related to tumor bulk, such as abdominal pain and distension. Due to their vascular nature, emergency presentation with an acute abdomen due to intraperitoneal bleeding is also not uncommon.
Autocrine and Paracrine Actions of Prolactin in Uterine Neoplasia
Published in Nagasawa Hiroshi, Prolactin and Lesions in Breast, Uterus, and Prostate, 2020
Jungi Kimura, Teruhiko Tamaya, Hiroji Okada
Chronic anovulation is one of the characteristic features of polycystic ovary syndrome (PCO) and related disorders categorized as “chronic anovulation syndrome”. Sustained hyperestrogenism and a state of progesterone deficiency are frequently observed in patients with these disorders. A category of chronic anovulation syndrome includes diagnoses or signs and symptoms such as PCO, Stein-Leventhal syndrome, oligomenorrhea, amenorrhea, dysfunctional uterine bleeding, hirsutism, anovulation, ovarian dysfunction, and irregular menses. Patients are considered to have chronic anovulation syndrome if they fulfill one or more of the following criteria:24 (1) histologic findings consistent with those reported by Stein and Leventhal; (2) an oyster-like appearance of the ovaries; and (3) clinical diagnosis made on the basis of chronic anovulation, with evidence of estrogen production determined by endometrial biopsy, progesterone withdrawal bleeding, or by estrogen assay.
Assessment and Diagnosis of the Male Infertility Patient
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Muhannad M. Alsyouf, Cayde Ritchie, David Kim, Edmund Ko
Hyperestrogenism should be suspected in infertile males found to have gynecomastia. Significant seminal alterations can occur when the estradiol levels are elevated. Infertile men with a low serum testosterone-to-estradial ratio can be treated with an aromatase inhibitor. The increase in testosterone-to-estradial ratio results in improved semen parameters [21].
Rapid reduction of adenomyosis coexisting with leiomyoma volume during treatment with Relugolix
Published in Gynecological Endocrinology, 2023
Keitaro Yamanaka, Keiichi Washio, Akiko Uchida, Yuki Sasagawa, Masashi Nishimoto, Yui Yamasaki, Satoshi Nagamata, Yoshito Terai
Our study is the first report of a reduction in uterine volume and adenomyotic lesion for adenomyosis with REL, which was also effective in mitigating symptoms (menorrhagia and pelvic pain). Especially, adenomyotic lesion volume showed the most marked reduction compared to uterine volume and fibroid volume. In our study, uterine volume was reduced more in patients with adenomyosis compared with fibroids only, even though the reduction of fibroids with REL didn’t differ between the two groups. This result can be attributed to the fact that adenomyosis shrinks earlier than the normal myometrium. In fact, adenomyosis is marked by elevated levels of estrogen caused by the enhanced expression of estrogen receptors [4,6]. The condition causes a reduction in the effectiveness of progesterone receptors, resulting in the development of progesterone resistance [17]. Some studies have also reported that uterine adenomyosis has estrogen dependence and progesterone resistance [5,18–20]. Hyperestrogenism is thought to be involved in neoangiogenesis and growth factors and inflammation in adenomyosis [5]. It has already been reported that GnRH agonist therapy for adenomyosis affects inflammation, angiogenesis, and apoptosis [21]. From the above, the overexpression of estrogen receptors in adenomyosis may have made the effect of GnRH antagonists more pronounced, thus resulting in a significantly reduced uterine volume in adenomyosis coexisting with fibroids.
Adenomyosis: is an endocrine-related uterine dysfunction?
Published in Gynecological Endocrinology, 2022
Silvia Vannuccini, Felice Petraglia
Pathogenesis of adenomyosis is mainly characterized by estrogen/progesterone imbalance and inflammation, which in turn facilitate the ectopic localization of endometrial cells into the myometrium by disrupting the endometrial–myometrial interface. In particular, an increase of local estrogens in the lesions and reduced progesterone receptor activity within adenomyotic lesions has been observed [6]. Thus, local rather than systemic hyperestrogenism contributes to the development of the disease: a) increased estrogen synthesis (by aromatase); b) reduced estrogens metabolism (by 17ß-hydroxysteroid dehydrogenase type 2 and sulphatase); and c) increased estrogen receptor (ER) activity [6]. Furthermore, some epigenetic aberrations of ER and progesterone receptor (PR) genes may lead to the endocrine-related background, with an hyperestrogenic state enhanced by the lack of progesterone counteracting activity. Specifically, ERβ expression is significantly elevated in adenomyotic glands during the proliferative phase and throughout the myometrium across the menstrual cycle. In addition, while the PR isoform B promoter is hypermethylated with a concomitant PR isoform B downregulation, a PR isoform A dominant state becomes present (progesterone resistance) [7].
The effect of adenomyosis on endometrial cancer: a university hospital-based cohort study
Published in Journal of Obstetrics and Gynaecology, 2022
Engin Celik, Hale Goksever Celik, Hamdullah Sozen, Semen Onder, Ozgur Aydin Tosun, Samet Topuz, Mehmet Yavuz Salihoglu
The relationship between adenomyosis and EC is still contradictory despite several limited studies in the literature. Some studies argue that adenomyosis has a good prognostic predictor for EC (Taneichi et al. 2014), while others advocate that the patients with adenomyosis are more likely to have deeper MI (Ismiil et al. 2007; Musa et al. 2012). Johnatty et al. (2020) reported the incidence of adenomyosis and EC coexistence as 4% in their recent publication. The link between adenomyosis and EC depends on some common molecular and mechanical basis of these two diseases (Matsuo et al. 2014). There are also similar genetical mutations including PTEN, KRAS, PIK3CA and BCL2 in adenomyosis and EC. Unopposed hyperestrogenism has been proposed as the main underlying theory, although common epidemiological factors have not yet identified in both diseases (Habiba et al. 2018).