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Endocrine Disorders, Contraception, and Hormone Therapy during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Gonadotropin-releasing hormone (GnRH) agonists are widely used in clinical gynecologic practice for the treatment of endometriosis and uterine leiomyomas. Leuprolide acetate (Lupron) is an agent that is frequently used for these conditions. Although no epidemiological studies are published of infants born following Lupron therapy, it is unlikely that the risk of congenital anomalies is high following exposure to this drug during pregnancy (Friedman and Polifka, 2006). Chronic administration of agonists downregulates the pituitary gonadotropin receptors, thereby suppressing release of LH and FSH, leading to a hypoestrogenic state. The likelihood of pregnancy occurring while a woman is given GnRH agonists is extremely low. However, GnRH agonists may also be used prior to HMG therapy in infertile women undergoing in vitro fertilization cycles. Typically, administration is begun in the luteal phase of the cycle, when a patient may be in the early stage of a pregnancy. No epidemiologic studies are published on the risk malformations in the offspring of women treated with this drug during pregnancy.
Prostate Cancer
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Karl H. Pang, James W.F. Catto
ADT aims to lower/block androgen activity:Lowering testosteroneBilateral orchidectomy to remove testosterone-producing Leydig cells.GHRH agonist: downregulates GnRH receptors.GHRH antagonist: blocks GnRH receptors.CYP17A1 inhibitor (Abiraterone): inhibits androgen synthesis.Blocking androgen effectNon-steroidal anti-androgens (Bicalutamide): block androgen receptors.
Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
GnRH antagonists can suppress release of luteinizing hormone and follicle-stimulating hormone from the pituitary by blocking the GnRH receptors and preventing their stimulation. Therefore, they can act very rapidly compared to the GnRH agonists which can take weeks to lower testosterone to castration levels. For example, clinical trials of the GnRH antagonist degarelix (FirmagonTM) have demonstrated complete ablation of testosterone within three days of treatment. The other significant advantage is that this mechanism of action avoids the tumor flare effect observed with GnRH agonists, thus avoiding the need for anti-androgen medication at the beginning of treatment, as is the case with GnRH agonists.
Meta-analysis of the relation between irritable bowel syndrome and antibodies against endogenous gonadotropin-releasing hormone and its receptor
Published in Baylor University Medical Center Proceedings, 2023
Karam R. Motawea, Joseph Varney, Mohamed Gamal, Kirellos Said Abbas, Fatma A. Monib, Mhd Kutaiba Albuni, Elias Battikh, Bisher Sawaf, Lina Taha Khairy, Agyad Bakkour, Ali Hadi Hussein Muwaili, Fatima Abubaker Abdalla Abdelmajid, Eman Mohammed Sharif Ahmed, Dhuha Hadi Hussein Muwaili, Safaa M. A. Ahmed, Sarya Swed
Little research has been done on the role of GnRH in gastrointestinal function. In a study using immunochemistry, Huang et al16 discovered that GnRH-R and leuprolide acetate, which do not act through GnRH receptors, were detectable in the intestinal epithelium and myenteric ganglia of small and large rats. This revealed enhanced motor activity in the rodents’ gut muscle cells.17 GnRH is known as a 9-residue gonadotropin-releasing hormone analog. GnRH could explain why IBS is an immunological disease, with patients developing autoantibodies against endogenous GnRH located in intestinal neurons, resulting in IBS.8 According to some studies, antibodies to GnRH have been associated with autoimmune diseases such as primary Sjögren’s syndrome, inflammatory bowel disease, celiac disease, and diabetes, as the antibodies were found in sera.9 The presence of GnRH was revealed in the human enteric nervous system.18
Effectiveness of gonadotrophin-releasing hormone agonist therapy to improve the outcomes of intrauterine insemination in patients suffering from stage I-II endometriosis
Published in Annals of Medicine, 2022
Kemei Zhang, Shisi Huang, Haiyan Xu, Jiaou Zhang, Ensheng Wang, Yang Li, Changling Zhu, Jing Shu
The most common side effects of GnRH-a therapy included hot flash (7.32%), sexual hypoactivity (2.44%) and vaginal dryness (9.77%), which were mild and temporal. No other severe side effects were observed in all subjects. As shown in Table 1, more patients with stage II endometriosis were given GnRH-a therapy (75.86% vs 24.14%), while fewer patients with stage I were treated with GnRH-a (27.94% vs 72.06%). The r-AFS score of patients with or without GnRH-a therapy were 7.56 ± 3.81 and 2.88 ± 1.95, respectively. The differences were both significant (p = .000). There were no statistical differences in terms of female age, body mass index (BMI), Antimullerian hormone (AMH), basal hormones before laparoscopy surgery, duration of infertility, female education, unhealthy lifestyle and medical history between the two groups.
The LH endocrine profile in gonadotropin-releasing hormone analogue cycles
Published in Gynecological Endocrinology, 2022
Lara Janssens, Ella Roelant, Diane De Neubourg
To understand LH suppression by GnRH analogues, one needs to understand the difference between the GnRH agonist and the GnRH antagonist. Both cause a transient suppression of endogenous LH to prevent premature ovulation, but the mode of action of both analogues differs. In 1978, it was discovered that the administration of GnRH agonists causes an initial flare up effect, characterized by a transient increase in LH levels [13]. After one to three weeks, desensitization and downregulation of the pituitary lead to the loss of GnRH receptors. GnRH antagonists on the other hand, competitively block the GnRH receptor, providing a direct suppression of LH levels for a period of 24 to 72 h. By preserving pituitary gland responsiveness, GnRH antagonists ensure a fast recovery after cessation [9, 14].