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EFFECT OF VARIOUS AGENTS ON CALCIUM, PHOSPHORUS AND NITROGEN EXCRETION IN A PATIENT WITH PITUITARY BASOPHILISM

WILLIAM H. PERLOFF, M.D.; EDWARD ROSE, M.D.; F. WILLIAM SUNDERMAN, M.D., Ph.D.

Arch Intern Med. 1943;72(4):494-505.

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

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 . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

From the William Pepper Laboratory of Clinical Medicine, University of Pennsylvania, and the Endocrine Section of the Medical Clinic, Hospital of the University of Pennsylvania.

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