Persistent hypokalemia after successful adrenalectomy in a patient with Cushing's syndrome due to ectopic ACTH secretion: Possible role of 11 beta-hydroxysteroid dehydrogenase inhibition

Ectopic ACTH secretion is characterized by a high incidence of hypokalemia. The pathophysiology of hypokalemia has not been totally clarified, althoug h it has been postulated that excessive amounts of adrenal steroids may pla y a role, as well as a possible role of the inhibition of the enzyme 11 bet a-hydroxysteroid dehydrogenase (11 beta-OHSD). This enzyme normally convert s cortisol to cortisone avoiding the mineralocorticoid action of cortisol. We present a patient with ectopic ACTH secretion due to a metastatic carcin oid tumor. The clinical picture was characterized by maintained hypokalemia (1.4 mmol/l) resistant to potassium, spironolactone and ketoconazole admin istration. A bilateral adrenalectomy was performed but the hypokalemia pers isted while he was receiving a physiological dose of cortisol. Eight days a fter adrenalectomy cortisol was replaced by an equivalent dose of dexametha sone. This change was followed by a rapid and persistent normalization of h ypokalemia suggesting a mineralocorticoid effect of cortisol. In conclusion , the origin of hypokalemia in our patient with ectopic ACTH secretion was secondary to cortisol. We postulate that this peculiar effect of cortisol c ould have happened if an inhibition of 11 beta-OHSD occurred. (J. Endocrino l. Invest. 22: 857-859, 1999) (C) 1999, Editrice Kurtis.