Abstract
A patient with congenital cardiac disease and primary hypogonadism demonstrated a eumetabolic state and normal thyroid function, despite a subnormal protein bound iodine (PBI). Electrophoresis of serum in TRIS-maleate buffer revealed normal binding of thyroxine by pre-albumin, but virtually no binding by the inter-alpha globulin (TBG). Studies of peripheral thyroxine turnover in vivo revealed an increased distribution space, fractional turnover rate and daily clearance rate. Total hormonal removal, however, was within normal limits because of the subnormal PBI. Prolonged administration of large doses of estrogen or of an adrenal corticosteroid failed to restore binding of thyroxine by TBG, excluding the possibility that the decreased TBG was produced by an androgen of testicular or adrenocortical origin. Estrogenic therapy had no significant effect on the kinetics of thyroxine metabolism in vivo. Thyroid suppression by sodium-L-thyroxine did not increase the PBI. The findings are viewed as consistent with the hypothesis that TBG regulates the peripheral metabolism of thyroxine by limiting its cellular penetration and hence its peripheral disposal and peripheral action.