THE DISTURBANCES in electrolytic equilibrium, in water balance and in the metabolism of carbohydrates and pigments which are observed in Addison's disease are known to reflect adrenocortical hypofunction. This, in turn, is dependent on severe retrogressive changes in the adrenal glands, often terminating in extensive bilateral destruction. Various etiologic processes have been incriminated in the production of the structural alterations.
Review of 2,550 autopsy protocols by Philpott1 in 1928 (University Hospital, Ann Arbor, Mich.) disclosed 14 cases with morphologic features providing a basis for chronic adrenal insufficiency. In 7 the lesions were due to tuberculosis and in 4 to metastatic carcinoma. Of the remaining 3 cases, 1 was ascribed to mycosis fungoides, 1 to simple atrophy and 1 to amyloidosis. Today, twenty-two years later, it seems worth while to study the subsequent 9,000 postmortem records to determine whether the same etiologic factors are operative and, if so, to learn
O'DONNELL WM. CHANGING PATHOGENESIS OF ADDISON'S DISEASE: With Special Reference to Amyloidosis. Arch Intern Med (Chic). 1950;86(2):266–279. doi:10.1001/archinte.1950.00230140102009
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