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Raymond C. Mellinger, MD

Arch Intern Med. 1986;146(5):858-860.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Cushing's syndrome has presented clinicians with fascinating diagnostic and therapeutic difficulties for more than half a century. Additional causative mechanisms and different means of treatment continue to be advanced. Although the syndrome usually results from a disordered function originating in the pituitary or the adrenal glands, pathologic hypercortisolism is also well known to result from ectopic secretions. The ectopic corticotropin (ACTH) syndrome, which is characteristic of the latter disorders, is usually associated with very high levels of ACTH secretion, great excesses of cortisol, bilateral adrenal hypertrophy, pigmentation, hypokalemia, hyperglycemia, and hypertension. The very high levels of cortisol accelerate the pace of the disorder, and the underlying malignancy modifies the clinical expression of the endocrine disease. Instead of a classically obese, plethoric patient with Cushing's syndrome, victims are usually severely wasted.¹ In his 1979 review of the Cushing syndromes, Gold² proposed a useful diagnostic algorithm that integrated ACTH assays . . . [Full Text PDF of this Article]

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