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(Hypertension. 2008;52:1001.)
© 2008 American Heart Association, Inc.

Hypertension Grand Rounds

Cushing’s Disease, Hypertension, and Other Sequels

Eugenia Singer; Sebastian Strohm; Ursula Göbel; Markus Bieringer; Dierk Schmidt; Wolfgang Schneider; Ralph Kettritz; Friedrich C. Luft

From the Medical Faculty of the Charité, Franz-Volhard Clinic, HELIOS Klinikum-Berlin, Berlin, Germany; and the Experimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine, Berlin, Germany.

Correspondence to Friedrich C. Luft, Experimental and Clinical Research Center, Building 84, Max Delbrück Center, Robert-Rössle Str 10, 13125 Berlin, Germany. E-mail: luft@charite.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
In his biography of Harvey Cushing, Michael Bliss¹ discusses Cushing’s perhaps most lasting scientific contribution as follows: "The old man’s hunch had played out. After all those years of gathering information and misinformation about the pituitary, Cushing had correctly identified basophil pituitary adenomas as one significant cause of hypersecretion from the adrenal cortex.² In those cases, Cushing’s syndrome becomes Cushing’s disease." In his report, which was actually a lecture at the Yale Medical School, Cushing mentioned, "painful adiposity, particularly of the trunk and chest, without involvement of the extremities, rounded shoulders, amenorrhea, purple colored striae on the abdomen, hypertension, a tendency toward spontaneous ecchymoses and epistaxis, rough, dry skin, blue and dusky in appearance, pressure headaches with low-grade chocked discs, fragility of the bones, and excessive growth of hair on the lips and elsewhere over the body."² Cushing also observed that the tumors were too small to cause changes in the sella turcica that could be observed roentgenographically. Although Cushing’s disease is not common, patients with the condition almost invariably are hypertensive, often severely so. Cushing mentioned all of the cardinal features, save for psychiatric manifestations; depression and even psychosis are also commonly present.³ Associated laboratory abnormalities include neutrophilic leukocytosis, hyperglycemia, hypokalemia, and hypercholesterolemia. Every medical student faithfully learns the above. Most have already observed the features of iatrogenic Cushing’s syndrome as a sequel to long-term therapeutic glucocorticoid exposure. Faculty-attending physicians have all encountered Cushing’s disease at some point in their careers and are, therefore, attuned. Nonetheless, when finally confronted, . . . [Full Text of this Article]