Elevated thyroxine-binding globulin (TBG) capacity has been found in 3 generations of a family. Two male and 7 female members of the family had elevated TBG, proteinbound iodine (PBI) and serum thyroxine content. The resin T3 uptake was decreased. The free thyroxine, the 24-hr thyroidal per cent 13lI-uptake and clinical status were normal. Also normal were serum cholesterol, serum free amino acids, total serum protein, serum protein electrophoresis, and corticosteroid-binding globulin (CBG) concentration. Measurements of radio-thyroxine turnover in 2 affected family members yielded normal thyroxine degradation rates of 50 and 55 μg T4 iodine/day. Administration of estrogen to 1 male and 2 female affected family members resulted in a further increase in TBG activity. The mode of transmission of the trait was consistent with x-chromosome linked codominant inheritance. A genetic mechanism in terms of gene duplication is suggested for the phenomenon of TBG elevation and its further increase with estrogen treatment.
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Jones et al. (1967) studied this question.