Journal of Clinical Endocrinology & Metabolism, Vol 76, 38-43, Copyright © 1993 by Endocrine Society

ARTICLES

Hypoaldosteronism accompanied by normal or elevated mineralocorticosteroid pathway steroid: a marker of adrenal carcinoma

B Aupetit-Faisant, C Battaglia, M Zenatti, N Emeric-Blanchouin and JC Legrand
Service de Biochimie, CHU Pitie-Salpetriere, Paris, France.

In order to find a biochemical marker to assist the physician in the difficult differential diagnosis between malignant and nonmalignant adrenal tumors, plasma levels of the mineralocorticosteroids (deoxycorticosterone, 18-hydroxydeoxycorticosterone, corticosterone, 18- hydroxycorticosterone, and aldosterone) were determined. The same method (RIA which is preceded by a crucial separation step) was used to measure all these steroids including aldosterone. The subjects included 15 adults presenting various clinical signs of adrenocortical tumors (histopathologically: 6 with adrenal carcinoma, 1 with a history of adrenal carcinoma, 1 with adrenal metastasis from other forms of cancer, 6 with adenoma, and 1 with hyperplasia). The results show that both presurgery and during a recurrence of adrenal carcinoma, hypoaldosteronism occurs which contrasts with the normal or even elevated levels of some aldosterone precursors. In the 7 cases of adrenal cortical carcinoma, this dysfunction of the aldosterone pathway was detected regardless of the impairment of the other steroidogenesis pathways, whereas it was never found with a nonmalignant tumor. Despite the limited number of cases so far available, these findings suggest that detection of abnormalities of the aldosterone pathway, and particularly the detection of hypoaldosteronism by an assay method involving a crucial steroid separating step, could contribute to a differential diagnosis between benign and malignant adrenocortical tumor and between adrenal metastasis and other forms of cancer.

This article has been cited by other articles:

				O. Chabre, S. Portrat-Doyen, P. Chaffanjon, J. Vivier, P. Liakos, F. Labat-Moleur, E. Chambaz, Y. Morel, and G. Defaye Bilateral Laparoscopic Adrenalectomy for Congenital Adrenal Hyperplasia with Severe Hypertension, Resulting from Two Novel Mutations in Splice Donor Sites of CYP11B1 J. Clin. Endocrinol. Metab., November 1, 2000; 85(11): 4060 - 4068. [Abstract] [Full Text]

				P. Mulatero, K. M. Curnow, B. Aupetit-Faisant, M. Foekling, C. Gomez-Sanchez, F. Veglio, X. Jeunemaitre, P. Corvol, and L. Pascoe Recombinant CYP11B Genes Encode Enzymes that Can Catalyze Conversion of 11-Deoxycortisol to Cortisol, 18-Hydroxycortisol, and 18-Oxocortisol J. Clin. Endocrinol. Metab., November 1, 1998; 83(11): 3996 - 4001. [Abstract] [Full Text]

				S. Portrat-Doyen, J. Tourniaire, O. Richard, P. Mulatero, B. Aupetit-Faisant, K.M. Curnow, L. Pascoe, and Y. Morel Isolated Aldosterone Synthase Deficiency Caused by Simultaneous E198D and V386A Mutations in the CYP11B2 Gene J. Clin. Endocrinol. Metab., November 1, 1998; 83(11): 4156 - 4161. [Abstract] [Full Text]

				C. Heymes, J.-S. Silvestre, C. Llorens-Cortes, F. Marotte, B. Chevalier, B. I. Levy, B. Swynghedauw, and J.-L. Samuel Cardiac Senescence Is Associated with Enhanced Expression of Angiotensin II Receptor Subtypes Endocrinology, May 1, 1998; 139(5): 2579 - 2587. [Abstract] [Full Text] [PDF]

				J.-S. Silvestre, V. Robert, C. Heymes, B. Aupetit-Faisant, C. Mouas, J.-M. Moalic, B. Swynghedauw, and C. Delcayre Myocardial Production of Aldosterone and Corticosterone in the Rat. PHYSIOLOGICAL REGULATION J. Biol. Chem., February 27, 1998; 273(9): 4883 - 4891. [Abstract] [Full Text] [PDF]