If the patient did not have adrenal hyperfunction, metyrapone could instigate an adrenal crisis. How might that present clinically?

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 patients 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 2. What nonpathologic factors might influence ACTH levels?

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