Effect of gonadotrophin-releasing hormone agonist treatment on growth hormone secretion in women with polycystic ovarian syndrome
Autor: | Th. Kaltsas, N. Pontikides, Dimitrios Lolis, K. Seferiadis, Gerasimos E Krassas, Ioannis E. Messinis |
---|---|
Rok vydání: | 1998 |
Předmět: |
Adult
endocrine system medicine.medical_specialty medicine.drug_class media_common.quotation_subject Gonadotropin-releasing hormone Biology Human Growth Hormone/*secretion Ovulation Induction Internal medicine medicine Humans Ovulation media_common Human Growth Hormone Rehabilitation Area under the curve Obstetrics and Gynecology Pituitary gonadal axis Polycystic ovary Hormones Growth hormone secretion Receptors LHRH/*agonists Endocrinology Ovulation Induction/*methods Reproductive Medicine Case-Control Studies Gonadotropins Pituitary Female Hormones/secretion Gonadotropin Receptors LHRH hormones hormone substitutes and hormone antagonists Polycystic Ovary Syndrome Gonadotropins Pituitary/*therapeutic use Polycystic Ovary Syndrome/*drug therapy Hormone |
Zdroj: | Human Reproduction. 13:22-26 |
ISSN: | 1460-2350 0268-1161 |
DOI: | 10.1093/humrep/13.1.22 |
Popis: | 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. Hum Reprod |
Databáze: | OpenAIRE |
Externí odkaz: |