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April 1980

In Reply.—

Author Affiliations

Tampa, Fla

Arch Intern Med. 1980;140(4):583-584. doi:10.1001/archinte.1980.00330160143057

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We, too, considered the pathophysiologic explanation offered by Drs Phillips and Pain for our case, and this was discussed as the second of three explanations in the "Comments" section. The marked thyroidal response to TSH, however, clearly militated against a diagnosis of primary hypothyroidism. In addition, we remain convinced that the adrenal insufficiency is not owing to hypothalamic dysfunction secondary to hypothyroidism. First, the latter has not been described (the case report cited by Phillips and Pain was one of pituitary dysfunction), although admittedly theoretically possible. Second, our patient was only receiving 25 mg of cortisone each morning, and this should not have impaired the cortisol response to insulin hypoglycemia 48 hours after stopping such therapy.1 The suggestion to gradually reduce steroid therapy further for subsequent retesting seems hazardous and may invite a medical catastrophe.

As a final note, we are not sure that common diseases with uncommon

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