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Research Article Free access | 10.1172/JCI105827
St. Elizabeth's Hospital and Department of Medicine, Tufts Medical School, and the Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Find articles by Braverman, L. in: JCI | PubMed | Google Scholar
St. Elizabeth's Hospital and Department of Medicine, Tufts Medical School, and the Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Find articles by Foster, A. in: JCI | PubMed | Google Scholar
St. Elizabeth's Hospital and Department of Medicine, Tufts Medical School, and the Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Boston, Massachusetts
Department of Medicine, Harvard Medical School, Boston, Massachusetts
Find articles by Ingbar, S. in: JCI | PubMed | Google Scholar
Published June 1, 1968 - More info
Multiple indices of thyroid hormone binding have been studied in sera obtained from patients with thyrotoxic Graves' disease, before and after treatment, and in sera from a group of carefully matched normal controls. Specimens from patients with thyrotoxicosis displayed a decrease in the thyroxine (T4)-binding capacities of T4-binding globulin (TBG) and T4-binding prealbumin (TBPA), an increase in serum protein-bound iodine (PBI), and an increase in both the proportion and absolute concentration of free T4. In addition, a smaller than normal proportion of 131I-labeled T3 was associated with TBG during filter paper electrophoresis. After treatment of thyroxicosis, the only residual abnormality detected was a very slight persistent decrease in the T4-binding capacity of TBPA, which did not appear to influence the overall thyroid hormone-plasma protein interaction significantly, regardless of whether this was assessed under basal conditions or after enrichment of specimens with stable T4. It is concluded that the persistent abnormalities in the peripheral metabolism of T4, previously reported to occur in some patients with treated Graves' disease, probably do not stem from residual abnormalities in the transport of T4 in the plasma but must arise from abnormalities in T4 accumulation or metabolism within the tissues themselves.