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

Arteaga, E; Fardella, C.; Campusano, C; Cardenas, I; Martinez, P

Keywords: dehydrogenase, insulin, inhibition, enzyme, chile, chemotherapy, liver, disease, tumor, dexamethasone, spironolactone, humans, protocols, potassium, human, male, doxorubicin, metastasis, combined, pathophysiology, outcome, neoplasms, adult, glucocorticoids, adrenalectomy, article, production, cyclophosphamide, antineoplastic, hypokalemia, hydrocortisone, mineralocorticoid, acth, vincristine, ketoconazole, dehydrogenases, etoposide, carcinoid, syndrome, Syndrome,, case, report, cushing, ectopic, Fatal, hydroxysteroid, corticotropin, 11beta, 11-beta-Hydroxysteroid

Abstract

Ectopic ACTH secretion is characterized by a high incidence of hypokalemia. The pathophysiology of hypokalemia has not been totally clarified, although it has been postulated that excessive amounts of adrenal steroids may play a role, as well as a possible role of the inhibition of the enzyme 11?-hydroxysteroid dehydrogenase (11?-OHSD). This enzyme normally converts cortisol to cortisone avoiding the mineralocorticoid action of cortisol. We present a patient with ectopic ACTH secretion due to a metastatic carcinoid tumor. The clinical picture was characterized by maintained hypokalemia (1.4 mmol/l) resistant to potassium, spironolactone and ketoconazole administration. A bilateral adrenalectomy was performed but the hypokalemia persisted while he was receiving a physiological dose of cortisol. Eight days after adrenalectomy cortisol was replaced by an equivalent dose of dexamethasone. This change was followed by a rapid and persistent normalization of hypokalemia 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 could have happened if an inhibition of 11?-OHSD occurred. (J. Endocrinol. Invest. 22: 857-859, 1999) (C) 1999 Editrice Kurtis.

Más información

Título de la Revista: JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
Volumen: 22
Número: 11
Editorial: EDITRICE KURTIS S R L
Fecha de publicación: 1999
Página de inicio: 857
Página final: 859
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-0033380897&partnerID=q2rCbXpz