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ACUTE PITUITARY‐OVARIAN RESPONSE DURING CHRONIC LUTEINIZING HORMONE‐RELEASING HORMONE AGONIST ADMINISTRATION IN POLYCYSTIC OVARIAN SYNDROME
Author(s) -
FAURE NACIA,
LEMAY ANDRE
Publication year - 1988
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1988.tb02889.x
Subject(s) - buserelin , endocrinology , medicine , testosterone (patch) , luteinizing hormone , radioimmunoassay , polycystic ovarian disease , polycystic ovary , agonist , anterior pituitary , gonadotropic cell , hormone , follicle stimulating hormone , receptor , insulin resistance , insulin
SUMMARY The purpose of the study was to evaluate the acute effect of daily subcutaneous injections of the GnRH agonist Buserelin on serum concentration of LH (evaluated by radioimmunoassay (iLH), and by bioassay (bioLH)), FSH, oestradiol and testosterone in 20 women with a diagnosis of polycystic ovarian disease (PCO). Buserelin was administered subcutaneously at the dose of 200 ng three times daily for 7 days followed by 500 fig once daily for a total treatment period of 6 months. Blood samples were drawn immediately before and 2,4 and 6 h after the injection on the first day of treatment as well as after 1,2,3,4,12 and 24 weeks. The first injection of Buserelin induced statistically significant rises of iLH, bioLH and FSH as well as of 17β‐oestradiol. The acute response of gonadotrophins was suppressed after 1 week but a partial recuperation of FSH and iLH responses was observed starting after 2 and 4 weeks of treatment. No significant acute changes of bioLH or of 17β‐oestradiol and testosterone could be seen. The persistence of a small but statistically significant pituitary response in the first hours following the daily injection of the peptide suggests a hyper‐reactive state of the gonadotrophs in PCO patients. Such acute pituitary responses are not seen when a similar treatment is administered to endocrinologically normal women. This observation could be an argument in favour of an initial central defect in the pathogenesis of the syndrome.