Evaluation of Stimulation and Suppression Tests in the Etiological Diagnosis of Cushing's Syndrome

  1. EDWARD R. WEISS, M.D.;
  2. SUAD S. RAYYIS, M.D.;
  3. DON H. NELSON, M.D., F.A.C.P.; and
  4. JOHN E. BETHUNE, M.D., F.A.C.P.
  1. Los Angeles, California
  1. Requests for reprints should be addressed to John E. Bethune, M.D., University of Southern California School of Medicine,
    2025 Zonal Ave., Los Angeles, Calif. 90033

SUMMARY

An evaluation of dexamethasone suppression, metyrapone and adrenocorticotrophic hormone (ACTH) stimulation, plasma radioimmunoassayable ACTH, and retrograde adrenal venography in the differential diagnosis of the causes of Cushing's syndrome is presented in 26 patients studied at the Los Angeles County/University of Southern California Medical Center. Dexamethasone was confirmed as a reliable indicator of adrenal hyperplasia in that all but 1 of the 17 patients with this pathology showed the expected suppression of urinary 17-ketogenic steroids to less than 50% of control values. All seven patients with adrenal adenoma responded to ACTH. In contrast to the patients with adrenal hyperplasia, these patients did not respond to metyrapone stimulation. Metyrapone appeared to be a very helpful diagnostic aid in general and in these cases where confirmation of dexamethasone suppression was required. Plasma ACTH as measured by radioimmunoassay may be a reliable indicator of the underlying pathology. Adrenal venography in conjunction with simultaneous measurement of the adrenal venous effluent content of 17-hydroxycorticoids may because of its simplicity supplant the above techniques in the final diagnosis of Cushing's syndrome.

Article and Author Information

  • From the Department of Medicine, University of Southern California School of Medicine; and the Los Angeles County/University of Southern California Medical Center; Los Angeles, Calif.

  • Supported in part by research grants AM 05176 and AM 04131, U. S. Public Health Service, Washington, D. C.; and by grant FR-43, The General Clinical Research Centers, National Institutes of Health, Bethesda, Md.

    • Received April 25, 1969.
    • Accepted July 8, 1969.
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