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Sheehan's Disease

JULIUS E. COOK, M.D.; WILLIAM B. BEAN, M.D.; MURRAY FRANKLIN, M.D.; JAMES F. EMBICK, M.D.

AMA Arch Intern Med. 1951;87(4):517-532.

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

ALTHOUGH Simmonds¹ was the first to describe a clear relationship between a destructive lesion of the anterior lobe of the pituitary gland and the clinical syndrome resulting from such a lesion, others² previously had described cases with a similar clinical picture. These writers considered the clinical symptoms to be a result of polyglandular deficiency but failed to recognize that a destructive lesion of the adenohypophysis was primary and that the atrophic change in the adrenal glands, thyroid and gonads was secondary. Clinical panhypopituitarism, long known as Simmonds' disease, follows destruction of the anterior lobe of the pituitary gland. It may be brought about by a variety of pathological lesions, such as an ischemic necrosis occurring during an abnormal delivery or puerperium, by tumors, granulomas, injury, surgical hypophysectomy and "spontaneous" atrophy and fibrosis. The first is by far the commonest cause of Simmonds' disease. Although Simmonds³ and others . . . [Full Text PDF of this Article]

Author Affiliations
IOWA CITY

From the Department of Internal Medicine of the College of Medicine of the State University of Iowa and the University Hospitals.

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