PERIPHERAL AND OVARIAN STEROIDS IN OVARIAN HYPERTHECOSIS

  • 1 January 1976
    • journal article
    • research article
    • Vol. 47  (5) , 581-586
Abstract
Serum levels of cortisol (F), pregnenolone (.DELTA.5-P), 17-hydroxypregnenolone (17-.DELTA.5-P), progesterone (P), 17-hydroxyprogesterone (17-P), androstenedione (A), testosterone (T), 5.alpha.-dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), its sulfate (DHEA-S), estrone (E1) and estradiol-17.beta. (E2) were measured in 2 virilized patients with ovarian hyperthecosis. Daily morning blood samples were obtained for 6 consecutive days. Dexamethasone (Dex) 2 mg/day was administered orally starting after venipuncture on the 2nd day and continued for 5 days. Human chorionic gonadotropin (hCG) was administered i.m. on the afternoon of the 4th and 5th days. Following the suppression-stimulation test, both patients underwent abdominal hysterectomy and bilateral salpingo-oophorectomy. At the time of surgery, samples of peripheral and ovarian vein blood were obtained for steroid measurements. Blood samples were also obtained postsurgery to evaluate the effect of ovariectomy on the steroid levels. Although both patients were eumenorrheic, no corpus luteum or corpus albicans was seen on histologic examination of the ovaries. Of the androgens measured, only peripheral T and DHT were elevated and did not suppress upon Dex treatment, but decreased to low levels following ovariectomy, pointing toward the ovary as the source of excess T and DHT. Both patients had elevated T and DHT in the ovarian vein samples. In 1 patient the ovarian vein samples showed elevated F levels with a significant ovarian-peripheral venous gradient for this steroid, an indication of ovarian secretion of F in this patient. The levels of 17-P were elevated in both patients, did not suppress upon administration of Dex, and increased markedly following hCG, suggesting the ovary as the source of excess 17-P. Since A levels were normal and did not increase concomitantly with 17-P levels following hCG, it is likely that the patients had a decreased activity of the ovarian C17-20 desmolase, the enzyme responsible for the conversion of 17-P to A.

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