THE existence of decreased or absent thyroxine-binding globulin in the serums of certain asymptomatic subjects has been recognized since 1959, when the first case was described by Tanaka and Starr.1 In addition to a low serum protein-bound iodine concentration, serums from persons affected demonstrate a decrease or absence of thyroxine-binding globulin on paper electrophoresis, a normal binding capacity for thyroxine by thyroxine-binding prealbumin and an increase in the in vitro resin uptake of radioactive tri-iodothyronine. The disorder presents no clinical symptoms and causes no discernible ill-effects. The low concentration of protein-bound iodine is accompanied by an accelerated turnover of thyroxine, . . .
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Marshall et al. (1966) studied this question.
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