THE EFFECT OF CORTISONE ON THE IODINE ACCUMULATING FUNCTION OF THE THYROID GLAND IN EUTHYROID SUBJECTS*

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Abstract
THIRTY years ago Marine and Baumann (1) noted that adrenal insufficiency in rabbits led to an increase in heat production and respiratory exchange and to the appearance of a symptom complex resembling exophthalmic goiter. Marine (2) subsequently reviewed the evidence pointing to the importance of a primary adreno-gonadal insufficiency as a possible fundamental cause of Graves' disease. The occurrence of Graves' disease following roentgen ray damage to the adrenal cortex in 2 cases reported by Oppenheimer (3) provided a direct clinical example in support of this concept. The pathologic changes observed in patients who have died of thyrotoxicosis—enlargement of the thymus, diffuse lymphoid hyperplasia and small adrenal cortices—have been cited as evidence suggestive of adrenal cortical insufficiency (2). The endocrine antithesis to the hyperthyroid-hypoadrenocortical state is well demonstrated by the frequent occurrence of an atrophied thyroid gland in Cushing's syndrome (4). The high concentration of serum cholesterol, the dry skin, and the low BMR frequently present in this disease (5) are clinically suggestive of hypothyroidism.