lhrh--n-ac-2-nal(1)-4-cl-phe(2)-trp(3)-hci(6)-alanh2(10)- and Ovarian-Hyperstimulation-Syndrome

lhrh--n-ac-2-nal(1)-4-cl-phe(2)-trp(3)-hci(6)-alanh2(10)- has been researched along with Ovarian-Hyperstimulation-Syndrome* in 2 studies

Other Studies

2 other study(ies) available for lhrh--n-ac-2-nal(1)-4-cl-phe(2)-trp(3)-hci(6)-alanh2(10)- and Ovarian-Hyperstimulation-Syndrome

ArticleYear
Gonadotroph adenoma in a premenopausal woman secreting follicle-stimulating hormone and causing ovarian hyperstimulation.
    The Journal of clinical endocrinology and metabolism, 1995, Volume: 80, Issue:2

    The clinical manifestations of gonadotroph adenomas are almost always neurological, consequences of their large size, and are rarely endocrinological. We report an exception, a 39-yr-old woman whose gonadotroph adenoma caused supranormal serum concentrations of FSH, which resulted in the development of multiple ovarian cysts, persistent elevation of her serum estradiol concentration, and endometrial hyperplasia. She initially presented because of amenorrhea at age 30 yr and was treated for an intrasellar mass by transsphenoidal surgery at age 31 yr and again at age 36 yr. Before and after the second operation she had persistently supranormal plasma estradiol concentrations (> 1840 pmol/L) and endometrial hyperplasia. When she was evaluated at age 39 yr, transvaginal ultrasound showed multiple ovarian cysts and endometrial thickening. Her plasma estradiol level was markedly supranormal (2160 pmol/L), FSH was mildly supranormal (17.8 IU/L), and alpha-subunit was markedly supranormal (23.3 micrograms/L). Characteristic of gonadotroph adenomas, her LH beta level increased by 69% in response to TRH. Neither FSH nor alpha-subunit decreased in response to administration of the GnRH antagonist, Nal-Glu-GnRH (5 mg/12 h for 4 weeks). Excised adenoma tissue exhibited morphological features of a gonadotroph adenoma. This patient appears to be unique, in that her gonadotroph adenoma caused slightly, but persistently, supranormal concentrations of FSH, which caused ovarian stimulation, including supranormal plasma estradiol concentrations, multiple ovarian cysts, and endometrial hyperplasia. We propose that gonadotroph adenomas be considered in the differential diagnosis of patients who have this constellation of abnormalities.

    Topics: Adenoma; Adult; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Gonadotropins; Humans; Ovarian Hyperstimulation Syndrome; Pituitary Neoplasms; Thyrotropin-Releasing Hormone; Ultrasonography

1995
Prevention of premature luteinizing hormone and progesterone rise with a gonadotropin-releasing hormone antagonist, Nal-Glu, in controlled ovarian hyperstimulation.
    Fertility and sterility, 1991, Volume: 56, Issue:5

    To report a preliminary study on the efficacy of a gonadotropin-releasing hormone antagonist (Nal-Glu) for preventing premature luteinizing hormone (LH) and progesterone (P) rise in controlled ovarian hyperstimulation using clomiphene citrate (CC) and human menopausal gonadotropin (hMG).. Participants in the study formed two groups. Both groups received CC-hMG and Nal-Glu. Group II differs from group I for receiving human chorionic gonadotropin (hCG) and blood samples for 10 days after the second Nal-Glu injection.. Centre de Fecondation in Vitro, Hôpital Antoine Béclère.. Eleven women 25 to 34 years of age and having normal menstrual cycles using barrier method of contraception not attempting pregnancies participated in the study.. Daily blood samples, pelvic ultrasound, and CC-hMG/Nal-Glu/hCG administration.. (1) Spontaneous LH surge and P rise, follicular growth, and plasma E2 levels in cycles with CC-hMG/Nal-Glu administration and (2) luteal phase after hCG injection in subjects previously treated with CC-hMG/Nal-Glu.. Plasma E2 level increased from 983 +/- 80 pg/mL (mean +/- SEM) on the day of the first Nal-Glu administration to 1,159 +/- 102 and 1,610 +/- 114 pg/mL (mean +/- SEM) 24 and 48 hours later. In 10 women, LH and P remained low for at least 96 hours after the first Nal-Glu administration. In one subject, plasma LH was already elevated at the time of the first Nal-Glu injection. In women who received hCG, plasma E2 and P reached a maximum of 1,258 +/- 313 pg/mL and 50.3 +/- 12.8 ng/mL (mean +/- SEM), respectively, on the 6th day of the luteal phase.. Our results suggest that timely Nal-Glu injections can prevent LH and P rise for at least 96 hours, in spite of increasing levels of plasma E2. Moreover, Nal-Glu had no adverse effect on the kinetic of E2 rise, the follicular growth, or on the post-hCG hormonal profile.

    Topics: Adult; Estradiol; Female; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Menotropins; Menstruation; Ovarian Follicle; Ovarian Hyperstimulation Syndrome; Progesterone; Time Factors

1991