We investigated possible abnormalities of Central-nervous-system regulation of luteinizing hormone secretion in the polycystic-ovary syndrome by determining the plasma concentrations of luteinizing hormone over a 24-hour period in five teenage girls with the syndrome; profiles of prolactin and cortisol were also obtained. Four of the five patients had strikingly abnormal plasma luteinizing hormone profiles: whereas normal pubertal girls have a daily surge in secretion of luteinizing hormone that is coterminous with their nocturnal sleep period, our patients had surges that were grossly desynchronized from their sleep period, occurring seven to eight hours later in the daytime than normal. The chronobiologic disturbance involved only luteinizing hormone; the profiles of cortisol and prolactin were normal. This finding points to the central nervous system as the probable locus of the initiating pathophysiology of polycystic-ovary syndrome. (N Engl J Med 1983; 309:1206–9). THE polycystic-ovary syndrome is one of the major causes of infertility and subfertility in women. Although the syndrome was initially defined by a triad of clinical findings (obesity, hirsutism, and secondary amenorrhea) and a specific histologic picture on ovarian biopsy,1 it is currently defined less rigorously, since any or all of the original clinical and histologic criteria may be absent. At present, the polycystic-ovary syndrome is represented by a subset of women with the chronic anovulatory syndrome in whom gonadotropin secretory inadequacy is not present and in whom various specific causes of anovulation (virilizing syndromes, hyperprolactinemia, dysthyroidism, Cushing's syndrome, and.
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