OCTREOTIDE EFFECT ON OVARIAN MORPHOLOGY IN INSULIN-RESISTANT PCOS PATIENTS FOLLOWING 6-MONTH DECAPEPTYL TREATMENT

PROBLEM: Regulation of ovarian folliculogenesis involves bidirectional communication between the immune and endocrine systems. Somatostatin analogues have been reported to acutely suppress elevated androgens in polycystic ovary syndrome (PCOS). The aim of our study was to analyze the morphologic and hormonal-metabolic response to octreotide therapy for one month in insulin-resistant PCOS patients in whom luteinizing hormone (LH) effect had formerly been separated by a six-month GnRH-ag onist (GnRH-a) course. METHOD: Fifteen PCOS patients were studied two months after completing a six-month GnRH-a (decapeptyl 3.75 mg monthly injection) course. Seven of the patients (group A), who were insulin- resistant and gave hyperinsulinemic response to a glucose challenge, r eceived a 50-mu g subcutaneous injection of octreotide twice a day for one month. The nonhyperinsulinemic patients (group B) received placeb o injections. Hormonal measurements, oral glucose tolerance test (OGTT ), and transvaginal ovarian ultrasound were performed before and towar d the end of the treatment period. RESULTS: After octreotide ovarian v olume dropped significantly in group A (x +/- SD) (19.2 +/- 5.1 versus 14.7 +/- 5.5 cc, P = .02). LH levels increased (3.25 +/- 1.22 versus 5.95 +/- 4.34 mu/ml, P = .05) as did E(2) levels (38.0 +/- 11.4 versus 55.1 +/- 12.7 pg/ml, P = .005). There was no change in follicle-stimu lating hormone, 17-hydroxy-progesterone, free testosterone, or androst enedione levels. Insulin secretion during OGTT dropped significantly ( 555 +/- 294 versus 68 +/- 29 mu u/ml/hr, P = .002). Glucose tolerance was not affected. In contrast, the placebo-treated group B patients sh owed an increase in ovarian volume (10.9 +/- 3.5 versus 14.8 +/- 3.3 c c, P = .001) while their gonadotropin and steroid profile relapsed, si milarly to our patients receiving octreotide.CONCLUSIONS: Octreotide h as an adjunctive beneficial effect to GnRH-a on ovarian morphology alt hough, at the dose used, there was no suppression of gonadotropin or o varian steroid levels. The changes in ovarian morphology are probably mediated through suppression of insulin levels and/or other ovarian gr owth factors.