Horm Metab Res 1987; 19(8): 386-388
DOI: 10.1055/s-2007-1011831
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Steroid Biosynthesis in Human Adrenal Tumors

R. D'Agata2 , S. Malozowski1 , A. Barkan3 , F. Cassorla1 , D. Loriaux1
  • 1Developmental Endocrinology Branch, NICHD, NIH, Bethesda, Maryland, U.S.A.
  • 2Endocrinology Unit, Department of Internal Medicine, University of Catania, Catania, Italy
  • 3Division of Endocrinology and Metabolism, University of Michigan, Ann Arbor, Michigan, U.S.A.
Further Information

Publication History

1985

1986

Publication Date:
14 March 2008 (online)

Summary

Patients with adrenal tumors present with varied clinical features which may be related to differing patterns of adrenal steroidogenesis. To explore the mechanism underlying these differences, we studied the in vitro activities of 3β-hydroxysteroid dehydrogenase (3β-HSD), 17-hydroxylase (17-OH), 21-hydroxylase (21-OH),and 17-20 desmolase (17, 20-D) in 6 adrenal tumors, 4 adenomas and 2 carcinomas. Normal human adrenal tissue was also studied for comparison. Adrenal adenomas had increased 21-OH activity compared with normal adrenal tissue (11.4±0.7 vs 5.5±0.5 nmol/mg prot/min, P < 0.002) and with adrenal carcinomas (11.4±0.7 vs 3.3±0.9 nmol/mg prot/min, P < 0.001). Carcinomas had reduced 3β-HSD, 17-OH and 17,20-D activities when compared to controls, but this did not reach statistical significance. These observations suggest less efficient steroidogenesis by adrenal carcinomas, a finding which may explain the large size of these tumors when the symptoms of hypercortisolism first appear.

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