Bromocriptine response in normoprolactinemic patients with polycystic ovary disease: a preliminary report

Recent work has suggested that a central deficiency or defect of dopamine may contribute significantly to the inappropriate gonadotropin secretion commonly associated with polycystic ovary disease. To evaluate this hypothesis, 2.5 to 5 mg of the dopamine agonist bromocriptine was administered daily to patients with polycystic ovary disease. Prolactin (PRL) levels were normal in all cases and there was no evidence of galactorrhea. All patients had failed to conceive while on clomiphene citrate. Seven patients were treated for a total of nine cycles. Ovulation occurred in four cycles, and two of these patients conceived. In five cycles, no ovulation occurred. Among ovulatory cycles, PRL levels declined, but not to undetectable levels. There was also a periovulatory drop in dehydroepiandrosterone sulfate. Levels of luteinizing hormones rose initially and then dropped to below baseline postovulation. Among anovulatory cycles, PRL fell to undetectable levels and dehydroepiandrosterone sulfate was unaffected. Luteinizing hormone levels rose initially and then dropped slightly. In both ovulatory and anovulatory cycles, follicle-stimulating hormone (FSH) levels remained low. These preliminary data suggest: 1) bromocriptine appears capable of altering gonadotropin secretion in polycystic ovary disease, and 2) variable results on ovulation in polycystic ovary disease may reflect the diverse etiology of the pathophysiology of polycystic ovary disease and/or choosing inappropriate dosages of bromocriptine.