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Department of Medicine, Endocrinology Division, West Virginia University Medical Center, Morgantown, West Virginia, and the Research Service, V. A. Hospital Minneapolis, Minnesota 55417
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.
This study was supported in part by USPHS Grant AM-05578 AMP (Clinical Center for Metabolic Studies) and by USPHS Grant CA-05993 from the National Cancer Institute and by the V. A. Cooperative Urological Research Project.
Received March 6, 1967.
Accepted July 13, 1967.
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G. C. BORST, C. EIL, and K. D. BURMAN Euthyroid Hyperthyroxinemia Ann Intern Med, March 1, 1983; 98(3): 366 - 378. [Abstract] [PDF] |
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