Case Study 6
Cushing Syndrome
A 22-year-old nurse complained of weakness, tiredness, easy bruising, leg edema, recent
acne, and hirsutism. Her menses became irregular. Her family commented that she was
emotionally labile. They also believed that her face had become fuller. On physical
examination she was found to be mildly hypertensive with a moon facies, buffalo hump,
truncal obesity, diffuse cutaneous striae, and +2 pitting pretibial edema. The results of a
recent chest X-ray study performed at work were normal.
Studies Results
Routine laboratory work Within normal limits (WNL) except glucose: 240
mg/dL (normal: 60-120 mg/dL)
Urine test for 17-hydroxycorticosteroids
(OHCS), p. 926
28 mg/24 hours (normal: 4.5-10.0 mg/24 hour)
Urine test for 17-ketosteroids, p. 929 14 mg/24 hours (normal: 4-15 mg/24 hour)
Plasma cortisol test, p. 179
8 AM 88 mg/dL (normal: 6-28 mg/dL)
4 PM 78 mg/dL (normal: 2-12 mg/dL)
Plasma cortisol level after 2 mg/day 60 mg/dL (normal: <10 mg/dL)
Plasma cortisol level after 8 mg/day 8 mg/dL (normal: <10 mg/dL)
Plasma adrenocorticotropic hormone
(ACTH) test, p. 34
140 pg/mL (normal: 15-100 pg/mL)
Plasma cortisol level after ACTH
stimulation test, p. 179
140 mg/dL (normal: >40 mg/dL, <60 mg/dL)
Urine 17-OHCS level after metyrapone
stimulation test, p. 36
Stimulated excretion of 17-OHCS tripled
(normal: doubled) baseline values
Computed tomography (CT) scan of
head, p. 1026
No pituitary tumor
Adrenal CT scan, p. 1020 Bilaterally enlarged adrenal gland; no tumor
Diagnostic Analysis
This patient had the classic signs and symptoms of Cushing syndrome (adrenal gland
hyperactivity). Her elevated urinary 17-OHCS level and the elevation and loss of normal
diurnal variation in her plasma cortisol levels substantiated the diagnosis. The underlying
pathologic condition causing the adrenal gland hyperfunctioning had to be determined to
permit appropriate therapy. The causes could have been bilateral adrenal hyperplasia, adrenal
adenoma or carcinoma, a pituitary tumor, or an ACTH-secreting tumor. Lack of adrenal
gland suppression with 2 mg of dexamethasone, combined with complete suppression with 8
mg of dexamethasone, strongly indicated that adrenal hyperplasia (abnormally high secretion
of ACTH), rather than an adrenal tumor, was causing the Cushing syndrome. The patient’s
elevated levels on the plasma ACTH, metyrapone suppression, and ACTH stimulation tests
were all consistent with bilateral adrenal hyperplasia. The CT studies of the head and the
Case Studies 2
Copyright 2014 by Mosby, Inc., an imprint of Elsevier Inc.
adrenal glands eliminated the possibility of pituitary and adrenal tumors. The CT scan of the
adrenal glands was compatible with adrenal hyperplasia. The patient underwent bilateral
adrenalectomy and became asymptomatic. She was given physiologic steroid-replacement
medications and had no further difficulties.
Critical Thinking Questions
1. If the patient did not have adrenal hyperfunction, metyrapone could instigate an adrenal
crisis. How might that present clinically?
2. What nonpathologic factors might influence ACTH levels?