THERAPEUTIC OBSERVATIONS IN CUSHING'S SYNDROME

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Abstract
Skeletal decalcification has been recognized as a characteristic feature of pituitary basophilism since the syndrome was first described by Cushing, in 1932.1 Such decalcification occurs likewise in those forms of Cushing's syndrome in which hyperplasia or tumor of the adrenal cortexes, rather than basophilic adenoma of the anterior lobe of the pituitary, is the dominant endocrine lesion. The demineralization of bone may be widespread but occurs chiefly in the skull, spine and pelvis. It may be so severe as to result in spontaneous or pathologic fractures, among which compression fractures of the vertebrae are common. Despite the longrecognized prominence of such skeletal demineralization, there have been comparatively few efforts to study the pathologic physiology of the process. Freyberg and Grant2 in 1936 reported detailed observations on a patient with a verified basophilic adenoma of the pituitary on whom studies of calcium, phosphorus and nitrogen metabolism were made under