cetrorelix and Ovarian-Diseases

Topics: Adolescent; Adult; Antineoplastic Agents; Female; Gonadotropin-Releasing Hormone; Hematologic Neoplasms; Hormone Antagonists; Humans; Ovarian Diseases; Retrospective Studies; Treatment Outcome; Young Adult

Ovarian torsion (OT) in IVF is rare, however, the consequences are significant, which include ovariotomy. In the present study, it was aimed for the first time to compare the incidence of OT between hCG triggered cycles with ICSI and fresh transfer and GnRH-agonist triggered cycles with the ICSI-freeze-all and frozen embryo transfer (FET). In total, 15,577 ICSI cycles performed between 2001 and 2016 were categorised into two groups (Group 1, n: 9978): cycles with controlled ovarian stimulation (COS) and hCG-triggered (Group 2, n: 5599) and COS, with GnRH-agonist only triggered and freeze-all. Thirteen patients (0.13%) were diagnosed with OT and corrected by laparoscopy (12) and laparotomy (1) in Group 1. One patient (0.018%) was diagnosed with OT and corrected by laparotomy in Group 2 (Group 1 vs. Group 2, p = .049). The incidence of severe ovarian hyperstimulation syndrome (OHSS) was 2.4% in Group 1 and 0.05% in Group 2 (p < .001). The use of freeze-all with GnRH agonist trigger in ART significantly reduced the incidence of OT and concomitantly OHSS, with no effect on the reproductive outcome. Impact Statement What is already known on this subject? Adnexal ovarian torsion (OT) is a well-known gynaecological event that constitutes a surgical emergency. Assisted reproduction technologies (ART) may result in ovarian conditions that predispose patients to ovarian hyperstimulation syndrome (OHSS) and torsion. What the results of this study add? The combined use of GnRH agonist trigger for final oocyte maturation after OS with freeze-all and frozen embryo transfer (FET) significantly reduces the incidence of OT, as well as OHSS. What the implications are of these findings for clinical practice and/or further research? The treatment strategy of GnRH agonist trigger with freeze-all significantly reduces the risks of adverse complications.

Topics: Adult; Birth Rate; Chorionic Gonadotropin; Embryo Transfer; Female; Gonadotropin-Releasing Hormone; Humans; Ovarian Diseases; Ovulation Induction; Retrospective Studies; Torsion Abnormality

We investigated the potential of gonadotropin-releasing hormone (GnRH) agonists and GnRH antagonists to inhibit cell proliferation in endometriotic and endometrial stromal cells.. Twenty patients with ovarian endometriomas and 18 patients with uterine fibromas were recruited. Endometriotic and endometrial stromal cells were obtained from the ovarian chocolate cyst linings and the eutopic endometria of premenopausal women with uterine fibromas, respectively.. GnRH agonist or antagonist treatment attenuated tumor necrosis factor (TNF)-α-induced cell proliferation in the endometrial stromal cells, whereas endometriotic stromal cells did not respond to treatment. The endometriotic stromal cells exhibited a decreased expression of the type I GnRH receptor compared with the endometrial stromal cells. GnRH agonists or antagonists did not repress TNF-α-induced IL-8 production in endometriotic stromal cells.. GnRH agonists and antagonists have similar effects in slowing the growth of endometrial stromal cells. Endometriotic stromal cells resist the antiproliferative effect of GnRH agonists and antagonists.

Topics: Adult; Blotting, Western; Buserelin; Cell Proliferation; Endometriosis; Endometrium; Enzyme-Linked Immunosorbent Assay; Female; Gene Expression; Gonadotropin-Releasing Hormone; Humans; Interleukin-8; Leiomyoma; Ovarian Diseases; Premenopause; Receptors, LHRH; Stromal Cells; Tumor Necrosis Factor-alpha; Uterine Neoplasms

The aim of the current study was to examine the effects of gonadotropin-releasing hormone agonist (GnRH-a) and antagonist (GnRH-ant) on the expression of GnRH receptor-I (GnRHR-I) in pituitary and ovaries in cyclophosphamide (CTX) chemotherapeutic rats and to investigate the possible mechanism of interventions of GnRH-a and GnRH-ant in CTX-induced ovarian damage. In total, 36 female rats were distributed into 6 groups at random: normal saline (NS) group, CTX group, GnRH-a + NS group, GnRH-a + CTX group, GnRH-ant + NS group, and GnRH-ant + CTX group. After the rats were killed, the expression of GnRHR-I messenger RNAs (mRNAs) and proteins in pituitary and ovaries were examined by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot, respectively. The distribution of GnRHR-I in various compartments of the ovaries was observed by immunohistochemistry. Significant downregulation of GnRHR-I mRNA and protein expression in the pituitary were observed after treatment with GnRH-a or GnRH-ant. Moreover, GnRH-ant was more potent for this direct and fast inhibition. In ovary, GnRHR-I expression was significantly downregulated by GnRH-a. Although GnRH-ant slightly decreased the ovarian expression of GnRHR-I mRNA, the protein level was only weakly changed. In the ovarian compartment, GnRHR-ant groups had markedly GnRHR-I expression in early and late growing follicles compared to GnRHR-a groups that exhibited decreased expression of GnRHR-I, especially in late growing follicles. In summary, this study presents evidence for the different regulating effects of GnRH-a and GnRH-ant on the expression of GnRHR-I in pituitary and ovaries, which may provide insight into the mechanism of GnRH-a and GnRH-ant interventions on chemotoxic ovarian damage.

Topics: Analysis of Variance; Animals; Blotting, Western; Cyclophosphamide; Female; Gonadotropin-Releasing Hormone; Hormone Antagonists; Immunohistochemistry; Luteolytic Agents; Ovarian Diseases; Ovary; Pituitary Gland; Random Allocation; Rats; Rats, Sprague-Dawley; Receptors, LHRH; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Triptorelin Pamoate

GnRH antagonist cetrorelix could reserve the ovarian follicles during chemotherapy, but the mechanism remains unclear. The objectives of this study were to examine the overall effect of cetrorelix against ovarian failure and to define if the apoptotic process was involved.. Female SD rats were injected with cetrorelix before and after administration of saline, or cyclophosphamide (Cy), or oral etoposide (VP). Main outcome measures were the number of ovarian follicles, serum hormones, ovary histology and apoptotic markers.. The females exposed to Cy or VP had reduced body and ovary weights, which could be restored by cetrorelix pretreatment. Single cetrorelix treatment could increase the number of primordial follicles, but reduce the number of growing and mature follicles. As a consequence, the ovaries exposed to cetrorelix prior to Cy or VP showed significantly higher numbers of follicles at all developing stages than those exposed to Cy or VP alone. Meanwhile, the ovarian apoptotic indexes as shown by TUNEL assay were reduced by cetrorelix pretreatment and the ovary expressed less caspases-3 and more Bcl-2 compared with chemotherapy alone. Moreover, the rats regained normal hormonal profile after cetrorelix pretreatment without any alterations in ovarian expression of estrogen receptor (ER)alpha, ERbeta, or progesterone receptor (PR).. Cetrorelix could reduce the chemotherapy-induced ovarian damage through regulating the expression of Bcl-2 and caspases-3 in the ovary, without any expressional alterations of nuclear receptors, suggesting the apoptosis pathway involved.

Topics: Animals; Antineoplastic Agents; Apoptosis; Caspase 3; Cyclophosphamide; Etoposide; Female; Gonadotropin-Releasing Hormone; Immunohistochemistry; Ovarian Diseases; Ovarian Follicle; Proto-Oncogene Proteins c-bcl-2; Random Allocation; Rats; Rats, Sprague-Dawley

To report a case of empty follicle syndrome (EFS) after human error occurring in hCG administration and discuss the specific management of this event in a GnRH antagonist cycle.. Case report.. A university hospital.. A 27-year-old woman admitted for a first oocyte retrieval resulting in empty follicle syndrome. The cause was the lack of administration of hCG injection 36 hours earlier.. Serial measurements of hCG, LH, and P.. Because no injection of GnRH antagonist had been given for 2 days, the occurrence of endogenous LH surge was assessed by measurement of serum LH, P, and E(2). In the absence of any spontaneous LH surge, EFS was successfully treated by administering 250 microg of recombinant hCG in the evening of the first failed ovarian puncture and rescheduling the second oocyte retrieval 36 hours later. Four oocytes were retrieved and two resulting embryos were transferred. Pregnancy was obtained and patient gave birth to a healthy male baby at term.. Our case is the first report of pregnancy obtained after a successful treatment of EFS in a GnRH antagonist cycle. In contrast to GnRH agonist down-regulated cycles, the management of EFS in GnRH antagonist cycles has to take into account the possible occurrence of spontaneous endogenous LH surge.

Topics: Adult; Female; Gonadotropin-Releasing Hormone; Humans; Medical Errors; Oocyte Retrieval; Ovarian Diseases; Pregnancy; Pregnancy Outcome; Syndrome

Inhibin and activin are structurally related dimeric peptide hormones and are members of the TGF-beta superfamily of proteins. In the accompanying paper, we describe transgenic mice that overexpress the inhibin alpha-subunit gene from a metallothionein-I promoter (MT-alpha) and examine the effects of the MT-alpha transgene on gonadotropin levels and fertility. To characterize the effects of increased inhibin alpha-subunit on gonadal morphology and function, in this report we investigate gonadal histology, steroid hormone levels, and the basis of ovarian cyst formation in MT-alpha transgenic mice. MT-alpha transgenic female mice develop large fluid-filled ovarian cysts of follicular origin as early as 3 months of age. By 12 months of age, more than 92% of female MT-alpha transgenic mice develop ovarian cysts compared with less than 25% of wild-type littermates. Ovarian cysts form unilaterally or bilaterally, and cystic ovaries often have a greatly expanded bursal sac. Additionally, the ovaries of MT-alpha transgenic mice contain polyovular follicles and have fewer mature antral follicles and corpora lutea. MT-alpha female mice exhibit abnormal steroid hormone production, with increased serum T levels and reductions in serum E with corresponding reductions in uterine mass. In the MT-alpha transgenic males, testis size was decreased by 20-40% compared with control males, and there is a corresponding reduction in seminiferous tubule volume. After a chronic treatment with a GnRH antagonist, MT-alpha female mice continued to develop ovarian cysts and bursal sac expansions, although the cysts were markedly reduced in size. These results indicate that the expression of the rat inhibin alpha-subunit in mice results in significant ovarian pathology, reduced testicular size, and altered ovarian steroidogenesis. The antagonist studies are consistent with a direct ovarian effect of the alpha-subunit transgene product mediated by changes in the inhibin-to-activin ratio in these mice.

Topics: Animals; Cysts; Estrogens; Female; Genital Diseases, Female; Genital Diseases, Male; Gonadotropin-Releasing Hormone; Hormone Antagonists; Inhibins; Male; Mice; Mice, Transgenic; Ovarian Diseases; Ovary; Rats; Testis; Testosterone