Aldosterone-producing
adenomas (APAs) demonstrate exquisite sensitivity to endogenous
ACTH. We previously showed an
ACTH receptor overexpression in APAs compared with the other adrenal
tumors. To evaluate the meaning of such findings, we investigated the response of
aldosterone,
cortisol, and 17OH
progesterone (17OHP) to 1 microg
ACTH in 42 patients with adrenocortical
tumors (23 NHAs, 9 APAs, and 10 CPAs) and 10 normal subjects (C). All 52 subjects were responsive to
ACTH, and
hormone peak levels were reached at 30 min. The
aldosterone peak level was significantly higher in APAs [mean +/- SEM: 84.3 +/- 13.1 ng/dl (2335.1 +/- 362.9 pmol/liter)] than in other
tumors and control (C).
Cortisol peak levels was higher in CPAs [37.1 +/- 3.9 microg/dl (1023.9 +/- 107.6 nmol/liter)] than in NHAs (P < 0.01), in C (P < 0.01) and in APAs (P = n.s.). 17OHP peak levels were significantly higher in patients with adrenocortical
tumors toward C. In summary: 1) low-dose
ACTH induces an important stimulation in all
tumors, suggesting preservation of high responsiveness to
ACTH; 2) this is especially true for
aldosterone in APA and could be of primary importance when performing diagnostic tests for
hyperaldosteronism; and 3) 17OHP-hyperresponsiveness to low-dose
ACTH is the most common alteration both in functional and nonfunctional
tumors.