An i.v. infusion dexamethasone (Dex) test was used to investigate the ACTH feedback response in 9 normal subjects, 12 obese patients, and 11 patients with Cushing's syndrome. Dex phosphate was infused iv for 4 h, starting at 1100 h (1 mg/h). Plasma concentrations of beta-lipotropin (beta LPH) and cortisol were measured every 20 min between 0900 and 1600 h, then every 2 h until midnight and at 0900 h the next day. In normal subjects and obese patients, plasma beta LPH and cortisol concentrations fell rapidly to less than 40 ng/liter and 3 micrograms/dl, respectively, at the end of Dex infusion. Subsequent values remained low through 0900 h the next day. In 7 patients with Cushing's disease, basal plasma beta LPH and cortisol concentrations declined by greater than 50% during the Dex infusion. In these patients, rapid escape from suppression occurred between 1600 and 2400 h; by 0900 h the following day, beta LPH and cortisol levels were higher than 100 ng/liter and 10 micrograms/dl, respectively. In 3 patients with adrenal tumors, beta LPH concentrations were low, and cortisol concentrations did not decline during the Dex infusion. In 1 patient with ectopic ACTH secretion, beta LPH concentrations were high and were not suppressed by the Dex infusion. We conclude that the iv infusion Dex suppression test can distinguish patients with Cushing's syndrome from normal or obese subjects and can aid in the etiological diagnosis of Cushing's syndrome.

In two of eight premenopausal women with somatotropic adenomas, galactorrhea was the earliest clinical feature, associated in one patient with amenorrhea. These two patients did not have clinically evident acromegaly. Mean basal serum GH levels were elevated and did not decrease after glucose ingestion. Both patients had modest hyperprolactinemia. Histological and immunocytological studies of the adenomas showed numerous adenomatous somatotropic cells and some alpha-subunit- and PRL-containing cells. In these patients, the origin of the hyperprolactinemia was not clear. In one patient, elevated GH secretion was probably responsible for the galactorrhea, since it disappeared after surgical treatment despite persistence of hyperprolactinemia. In conclusion, galactorrhea, isolated or associated with amenorrhea, can be the only clinical manifestation of a somatotropic adenoma.

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