The mean serum protein-bound iodine (PBI) level in 36 cases of cerebral disease with seizures treated by administration of diphenylhydantoin was 3.81 ±0.14 (s. E.) jug. per 100 ml. This was significantly lower than the corresponding mean PBI level in 12 cases of cerebral seizure not so treated, viz., 5.39 + 0.16 Hg. per 100 ml. Despite the occurrence of PBI levels as low as 2.4 ng. per 100 ml. in the diphenylhydantoin group, there was no clinical evidence of hypothyroidism in any of the patients and there were no significant alterations in the other parameters of thyroid function. In 7 of 8 euthyroid subjects, diphenylhydantoin also depressed the serum PBI concentration. The mechanism of action of diphenylhydantoin is apparently extrathyroidal, since this drug depressed the PBI level in hypothyroid patients maintained with a constant dosage of desiccated thyroid. Diphenylhydantoin added in vitro consistently increased the uptake of I 131 -labeled 3,5,3'-triiodothyronine by red blood cells incubated with plasma. This effect was progressively diminished by the addition of increasing quantities of stable Z-thyroxine to the incubating mixture. These data are compatible with the thesis that diphenylhydantoin depresses the level of serum PBI by interfering with the binding of thyroxine by plasma proteins.

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Studies have been performed in this laboratory on plasma 17-hydroxycorticosteroid levels in patients with endocrine and non-endocrine diseases (12). During the course of these investigations, it became apparent that there are disease states, particularly primary adrenal insufficiency and hypopituitarism, in which plasma 17-hydroxycorticosteroid levels determined before and after ACTH administration may give a more accurate picture of adrenal capacity than single plasma 17-hydroxycorticosteroid levels. These findings prompted an evaluation of plasma 17-hydroxycorticosteroid response to ACTH in patients with a variety of disorders of the adrenal cortex as compared with normal subjects.

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