Preservación de fertilidad con análogos agonistas de la hormona liberadora de gonadotropinas hipofisiarias (GnRH) en pacientes sometidas a tratamiento médico oncológico / Fertility preservation with agonist analgos of pituitary gonadotropin-relasing hormone (GnRH) in patients undergoing medical oncological treatment

Evaluar el potencial que tiene la utilización de los análogos de GnRH en la conservación de la función ovárica a mediano y largo plazo en pacientes sometidas a quimioterapia. Se evaluó la recuperación de la función ovárica de 6 pacientes sometidas a tratamiento oncológico que fueron tratadas concomitantemente con análogo de GnRH, mediante la medición de FSH, estradiol sérico y presencia de menstruaciones. En la Clínica Santa Sofía y Salud Chacao, Caracas. Cinco de las seis pacientes evaluadas (83,3 por ciento), recuperaron su función ovárica posterior al tratamiento oncológico y con análogo de GnRH. El uso de análogos de GnRH durante el tratamiento médico oncológico pareciera ser una alternativa válida para la protección de la función ovárica

To evaluate the potential of GnRH analogs use during chemotherapy in the preservation of short and long term ovarian function. Evaluation of ovarian function by measuring FSH, seric estradiol and menses, in six patient after use of GnRH analogs during chemotherapy. Clinica Santa Sofia y Salud Chacao, Caracas. Five of six patients (83,3 percent) reassumed their ovarian function after chemotherapy plus GnRH analog. The use of GnRH seems to be a good alternative to protect ovary function during chemotherapy

Agonist-specific Ca2+ signaling systems, composed of multiple intracellular Ca2+ stores, regulate gonadotropin secretion.

Ca2+ signals regulate many cellular functions, including hormone secretion. Agonist-specific Ca2+ signaling may arise from the differential mobilization of multiple Ca2+ stores. Although they act through the same receptor subtype, two gonadotropin-releasing hormones (sGnRH and cGnRH-II) generate quantifiably different Ca2+ signals in goldfish gonadotropes, suggesting that their Ca2+-dependent signaling cascades may differ. We combined electrophysiology, Ca2+ imaging, and radioimmunoassay detection of gonadotropin (GTH-II) secretion to determine the role of intracellular Ca2+ stores in GnRH-stimulated exocytosis. Our findings suggest that voltage-gated Ca2+ channels do not mediate acute GnRH-signaling. Instead, both sGnRH- and cGnRH-II-stimulated GTH-II releases are dependent on Ca2+ mobilized from TMB-8/CPA-sensitive compartments. However, sGnRH, but not cGnRH-II, utilizes intracellular stores sensitive to caffeine and xestospongin C. We also identified a homeostatic mechanism where reduced extracellular Ca2+ availability increase GTH-II release by mobilizing Ca2+ stores. Our results are the first to suggest that several classes of intracellular Ca2+ stores differentially participate in agonist signaling and homeostasis in gonadotropes.