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Philip R. Alper, MD
San Francisco

JAMA. 1970;214(4):761.

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

To the Editor.—

The article on "T₃ Thyrotoxicosis" by Sterling et al (213:571, 1970) illustrates a disease that is probably considerably more frequent than previously appreciated. Because of the relatively greater metabolic potency of triiodothyronine (T₃), than thyroxine (T₄), a thyroid gland that produced a relatively larger quantity of the former than normal would produce a hypermetabolic state in which proteinbound iodine (PBI) or serum T₄ level, T₃ uptake, and radioactive iodine uptake might all be within normal limits. By this simple metabolic alteration, thyroid hyperplasia would not even be necessary to produce a hypermetabolic state. Since hyperthyroidism has long been known to be a remittent disease, the question of whether remission represents a relative change in the production of T₃ vs T₄ rather than total thyroidal activity must be asked.

Although there is a rough correlation between the level of serum T₄ and . . . [Full Text PDF of this Article]

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