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Elliott Eisenbud, MD
University of California at Davis

JAMA. 1975;231(13):1339.

	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 recent report by Mataverde et al (230:1014, 1974) is timely in pointing out a commonly encountered but not well recognized problem. A less common problem, but one that may have been a factor in the case presented, is the exacerbation of hypothyroidism during periods of stress.

An early report¹ describes five patients who developed "acute myxedema" following pneumonia. Subsequent work² has shown that during stress thyroxine (T₄) turnover is increased fivefold while plasma T₄ levels were maintained within normal limits, thus suggesting an increase in T₄ secretory rate. It was thought that the increased turnover was the result of an increase in free T₄ caused by a decrease in thyroxine-binding prealbumin (TBPA). More recent work³ has confirmed that TBPA does indeed decrease with acute infections, but this was dissociated in time from changes in free T₄. It was concluded . . . [Full Text PDF of this Article]

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