E. Glaz et al., MINERALOCORTICOID PRODUCTION OF ADRENAL-CORTICAL ADENOMAS, Journal of steroid biochemistry and molecular biology, 45(1-3), 1993, pp. 57-64
We studied in vitro and in vivo corticosteroid production as well as t
he presence of symptoms of an increased mineralocorticoid effect in pa
tients with 'silent' adrenal cortical adenomas, and compared these res
ults to those found in patients with classical mineralocorticoid exces
s syndromes. We found that under in vitro conditions, cells from 'sile
nt' adrenal cortical adenomas (n = 19) produced substantial amounts of
both zona glomerulosa and fasciculata steroids, although the producti
on of steroids in these cells was lower compared to that in mineraloco
rticoid-producing adenoma cells (n = 26). Patients with aldosterone-pr
oducing and 'silent' adenomas had significantly increased plasma atria
l natriuretic peptide levels, which remained non-suppressible after up
right posture and furosemide administration. Of the 25 patients with '
silent' adenomas, 11 had low and non-stimulable plasma renin activity
(PRA) before but, in most cases, not after adrenal surgery. When compa
red to those with normal PRA (n = 14), patients with low PRA 'silent'
adenomas (n = 11) had higher blood pressure which was significantly re
duced after surgery, and a mild hypokalemia before but not after surge
ry. Although basal plasma concentrations of aldosterone, 18-hydroxy-co
rticosterone, corticosterone, deoxycorticosterone, 18-hydroxy-DOC, cor
tisol, 11-deoxycortisol and 17-hydroxy-progesterone (17-OH-P) were not
increased in either groups of 'silent' adenomas, ACTH stimulation pro
duced a hyperreactive response for all measured steroids, of which an
extremely high 17-OH-P seemed to be one of the most intriguing finding
s. We consider that these observations in 'silent' adrenal cortical ad
enomas may justify surgical intervention, irrespective of the size and
potential malignancy of these adenomas.