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.

The adrenal response to a soluble form of beta1-24-corticotropin (tetracosactrin [ACTH]: 250 microgram administered intramuscularly) was studied in 28 patients with meningitis due to Neisseria meningitidis (21 with petechiae and seven without) and in six patients with Salmonella typhi bacteremia. Six normal subjects also were tested for adrenal responsiveness at four different times of the day (8 A.M., 12 noon, 4 P.M., and 10 P.M.) and served as controls. The results showed that, whatever the time of testing, patients with meningococcal infections and typhoid fever had unstimulated (basal) levels of plasma cortisol above the 99% confidence limits for the mean unstimulated cortisol levels for the normal subjects. Furthermore, although patients with meningitis without petechiae and subjects with S. typhi bacteremia responded to ACTH stimulation in a manner similar to that of the normal subjects, most subjects with meningitis with petechiae did not have increased levels of plasma cortisol after treatment with ACTH. This lack of response could not be ascribed entirely to the higher basal levels of plasma cortisol in these patients. Patients with meningitis associated with petechiae may have a relatively decreased adrenal response to stimulation with exogenous ACTH.

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