title: Effect of gonadotrophin-releasing hormone agonist treatment on growth hormone secretion in women with polycystic ovarian syndrome.
abstract: The suppression of the pituitary-gonadal axis by the administration of gonadotrophin-releasing hormone agonists (GnRH-a) is used occasionally as an adjunct therapy with gonadotrophins for ovulation induction in women with polycystic ovarian syndrome (PCOS). A number of recent clinical studies have suggested that women with polycystic ovaries (PCO) may have disturbances of normal growth hormone (GH) kinetics and alterations in the GH/insulin-like growth factor (IGF)-I system. The purpose of this study was to determine the effect of GnRH-a administration on GH-releasing hormone (GHRH)-stimulated GH release in women with PCOS. Eight women with PCO and six control women were studied before and after 2 months of treatment with the long acting GnRH-a triptoreline (3.75 mg monthly injections). GHRH was given as a single i.v. injection and blood samples for GH measurements were obtained at -15, 0, 30, 60, 90 and 120 min. The GH responses were expressed as the area under the curve (AUC) or the differences from the basal value (delta(max)). The GH response to GHRH (mean +/- SEM) was lower in women with PCO (AUC 114.9 +/- 43.1 versus 206.2 +/- 28.7 ng/ml/120 min, P < 0.05 and delta(max) 31.6 +/- 8.2 versus 49.4 +/- 5.8 ng/ml, P < 0.05). After treatment with the GnRH-a, the GH response to GHRH was significantly smaller than before treatment in both groups (PCO AUC 34.6 +/- 9.0 ng/ml/120 min and delta(max) 12.4 +/- 3.1 ng/ml; controls AUC 148.8 +/- 28.4 ng/ml/120 min and delta(max) 31.2 +/- 6.1 ng/ml), but the PCO group had a significantly smaller response. These data demonstrate that women with PCO have a reduced GH response to GHRH compared with normal controls and that GnRH-a administration causes a further GH reduction in both groups. Women with PCO have a greater suppression of GH response to GHRH during treatment with GnRH-a. This suggests that a different level of sensitivity in the somatotrophic axis exists in PCOS.
authors.affiliation: Endocrine Clinic, PANAGIA Hospital, Thessaloniki, Greece.
authors.forename: T
authors.initials: T
authors.lastname: Kaltsas
authors.forename: N
authors.initials: N
authors.lastname: Pontikides
authors.forename: G E
authors.initials: GE
authors.lastname: Krassas
authors.forename: K
authors.initials: K
authors.lastname: Seferiadis
authors.forename: D
authors.initials: D
authors.lastname: Lolis
authors.forename: I E
authors.initials: IE
authors.lastname: Messinis
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D006065:Gonadotropins, Pituitary / Q000627:therapeutic use*; D006728:Hormones / Q000378:metabolism; D019382:Human Growth Hormone / Q000378:metabolism*; D006801:Humans; D010062:Ovulation Induction / Q000379:methods*; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy*; D011966:Receptors, LHRH / Q000819:agonists*
chemical_list: D006065:Gonadotropins, Pituitary; D006728:Hormones; D011966:Receptors, LHRH; D019382:Human Growth Hormone