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Journal of Clinical Endocrinology & Metabolism Vol. 23, No. 8 737-746
doi:10.1210/jcem-23-8-737
Copyright © 1963 by the Endocrine Society.
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Adrenocortical Hyperfunction and Potassium Metabolism in Patients with "Non-endocrine" Tumors and Cushing's Syndrome

F. T. G. PRUNTY, M.D., F.R.C.P., R. V. BROOKS, PH.D., F.R.I.C., J. DUPRÉ, B.Sc., B.M., M.R.C.P., T. M. D. GIMLETTE, M.D., M.R.C.P., J. S. M. HUTCHINSON, PH.D., R. R. McSWINEY, M.B., M.R.C.P. and I. H. MILLS, M.D., M.R.C.P.

Department of Chemical Pathology, St. Thomas's Hospital Medical School, and Department of Metabolic Diseases, St. Thomas's Hospital London, S.E.I, England

A series of 9 patients with nonendocrine tumors was found to secrete excessive amounts of cortisol (up to 420 mg/day) and to have hypokalemic alkalosis. They are compared with typical cases of Cushing's syndrome, and are found to have more severe and more rapidly advancing adrenocortical hyperfunction. The large cortisol production appeared to be due to corticotropin-like activity in their plasma. There was no indication of an increased aldosterone production. Electrolyte changes, including plasma potassium concentration, exchangeable potassium/kg body wt, and the ratio of exchangeable sodium to exchangeable potassium were more abnormal in the tumor cases. It is concluded that the ratio for exchangeable Na/K gives the earliest indication of a disturbance of potassium metabolism. There was a clear relationship between the height of the cortisol secretion rate and the degree of potassium deficiency. It is concluded that there is no need to postulate unknown factors producing this electrolyte deficit.

Received December 29, 1962.

Accepted April 6, 1963.




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E. M. GOLD
The Cushing Syndromes: Changing Views of Diagnosis and Treatment
Ann Intern Med, May 1, 1979; 90(5): 829 - 844.
[Abstract] [PDF]




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