Cushing’s Disease, Hypertension, and Other Sequels

tion 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 actu-ally 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. Al-though 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 psychi-atric manifestations; depression and even psychosis are also commonly present.3 Associated laboratory abnormalities include neutrophilic leukocytosis, hyperglycemia, hypokalemia, and hy-percholesterolemia. 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 glu-cocorticoid exposure. Faculty-attending physicians have all en-countered Cushing’s disease at some point in their careers and are, therefore, attuned. Nonetheless, when finally confronted, clinical reality often does not follow textbook rules. We recently encountered such a patient