IN 1967, new insight into the possible mechanism of thyroid hormone action was suggested by the landmark clinical report of Refetoff et al1 concerning the familial syndrome with goiter and abnormally high serum thyroxine (T4) level despite euthyroid status. Further information was provided by the later extensive metabolic investigation of this sibship with apparent hereditary resistance to the intracellular action of thyroid hormone.2 Not only was the serum T4 level elevated, but the serum triiodothyronine (T3) level as well, owing to increased secretion rate of both hormones from the goitrous thyroid glands. The peripheral tissue conversion of T4 to T3 was found to be normal,2,3 as was the penetration of the thyroid hormones into tissue cells.2 Despite the elevated hormone concentration, euthyroid metabolic status was documented by normal oxygen consumption (basal metabolic rate [BMR]) and other values. Thyroid-stimulating hormone (TSH) concentration
Sterling K, Aranow H. Acquired Refractoriness to Thyroid Hormone Action in Treated Toxic Nodular Goiter. JAMA. 1981;245(13):1339–1340. doi:10.1001/jama.1981.03310380043024
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