In most aldosterone-producing adenomas (APA) dedifferentiation occurs
with formation of transitional cells, bearing characteristics of both
glomerulosa and fasciculata cells: These cells are able to produce cor
tisol, and their aldosterone production follows the circadian rhythm o
f ACTH. Usually, no clinical signs of cortisol excess develop, since t
he cortisol production remains under ACTH feedback control. Only a few
cases have been described with autonomous cortisol secretion, not sup
pressible by low dose dexamethasone. We present a patient with an APA,
synthesizing enough cortisol to cause the typical clinical expression
of Gushing's syndrome. Possible etiopathological mechanisms are discu
ssed.