The source(s) of estrogen production in hirsute women with polycystic ovarian disease as determined by simultaneous adrenal and ovarian venous catheterization.

To determine the significant source(s) of estrogen production in women with polycystic ovarian disease (POD), 12 women underwent selective adrenal and ovarian vein catheterization, with simultaneous peripheral blood samplings for determination of cortisol, androstenedione (delta 4A), testosterone, estrone (E1), and estradiol (E2). Ovarian vein E2 gradients were observed in 11 of the 12 patients with a mean of 13.4, whereas adrenal blood samples did not demonstrate significant E2 gradients. Seven of 8 patients exhibited ovarian secretion of E1, with a mean gradient of 13.6 times that of peripheral blood, whereas 4 of the 8 adrenal samples showed E1 gradients. The mean value was 1.4 times peripheral levels. No significant correlations were found between peripheral E1 levels and body weight or degree of adiposity, nor was there a relationship between obesity and E1/delta 4A molar ratio in peripheral blood. The subjects with the highest ovarian delta 4A levels had a significant correlation between peripheral delta 4A and E1. Therefore, our data indicate a significant contribution of ovarian E1 secretion to the peripheral E1 pool in addition to the extraglandular conversion of delta 4A to E1. There was general lack of correlation between peripheral E1 concentrations and plasma E2, and these relationships versus body size suggest that the major source of E2 in women with POD was ovarian secretion.

Endometrial damage in acute salpingitis.

Histologic and bacteriologic analyses of endometrium were performed before and on day 15 after minocycline treatment of 20 patients with acute salpingitis. Endometritis was diagnosed in 15 patients before and in nine after treatment. Neisseria gonorrhoeae was recovered from the cervix and endometrium of seven patients but was not isolated after treatment. Chlamydia trachomatis was recovered from the cervix of eight, and from the endometrium of three patients, two of whom had negative cervical cultures. After treatment C. trachomatis was recovered from the cervix of three patients, although two of them had taken aluminum hydroxide for gastric symptomatology during minocycline treatment. Culture of an endometrial specimen revealed no growth of C. trachomatis. The histologic study revealed plasma cell infiltrates in specimens from patients who had cultures positive for C. trachomatis. The results showed that although endometritis is an important manifestation of acute salpingitis, there is no correlation between severity of endometritis and degree of tubal damage.

Determination of the source(s) of androgen overproduction in hirsutism associated with polycystic ovary syndrome by simultaneous adrenal and ovarian venous catheterization. Comparison with the dexamethasone suppression test.

To determine the source(s) of the excessive androgen production in patients with the polycystic ovary syndrome (PCOS), 12 hirsute women with PCOS underwent selective left adrenal and left ovarian venous catheterization. Blood samples were collected simultaneously for determination of cortisol, 17-hydroxy-progesterone, androstenedione (delta), testosterone (T), dehydroepiandrosterone, and dehydroepiandrosterone sulfate. The relative contributions of adrenal secretion rates of T and delta in each patient were estimated by relating their adrenal gradients to those of cortisol. From such calculations we found that in all patients the major source of androgens was the ovary (direct ovarian secretion and/or ovarian secretion of prehormones which then were converted to androgen in the peripheral circulation). After catheterization, 11 of the 12 patients underwent a 5-day dexamethasone suppression test (2 mg/day). In 7 patients studied, plasma delta and/or T levels decreased significantly. Our results indicate that in hirsutism associated with the PCOS, the predominant source of androgens is the ovaries and that glucocorticoid suppression cannot assign adrenal origin as the site of excessive androgens.