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Research Article Free access | 10.1172/JCI105636

Thyroxine Transport in Thyrotoxicosis and Hypothyroidism

Mitsuo Inada and Kenneth Sterling

Medical Service, Bronx Veterans Administration Hospital and the Department of Pathology, Columbia University College of Physicians and Surgeons, New York

‡

Visiting investigator from the Department of Internal Medicine, Kyoto University School of Medicine, Kyoto, Japan.

§

Address requests for reprints to Dr. Kenneth Sterling, Veterans Administration Hospital, 130 West Kingsbridge Road, Bronx, N. Y. 10468.

*

Submitted for publication 9 February 1967; accepted 25 May 1967.

Supported in part by grant AM-10739-02 from the U. S. Public Health Service.

Find articles by Inada, M. in: PubMed | Google Scholar

Medical Service, Bronx Veterans Administration Hospital and the Department of Pathology, Columbia University College of Physicians and Surgeons, New York

‡

Visiting investigator from the Department of Internal Medicine, Kyoto University School of Medicine, Kyoto, Japan.

§

Address requests for reprints to Dr. Kenneth Sterling, Veterans Administration Hospital, 130 West Kingsbridge Road, Bronx, N. Y. 10468.

*

Submitted for publication 9 February 1967; accepted 25 May 1967.

Supported in part by grant AM-10739-02 from the U. S. Public Health Service.

Find articles by Sterling, K. in: PubMed | Google Scholar

Published September 1, 1967 - More info

Published in Volume 46, Issue 9 on September 1, 1967
J Clin Invest. 1967;46(9):1442–1450. https://doi.org/10.1172/JCI105636.
© 1967 The American Society for Clinical Investigation
Published September 1, 1967 - Version history
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Abstract

(a) The thyroxine-binding proteins were investigated in 23 cases of untreated thyrotoxicosis and 16 cases of untreated hypothyroidism, employing reverse flow paper electrophoresis with the glycine acetate system at pH 8.6 in the Durrum type cell.

(b) In active thyrotoxicosis, all sera exhibited diminished thyroxine-binding prealbumin (TBPA) capacities. however, 17 of the 23 sera also had diminished thryroxine-binding alpha globulin (TBG) capacities, as well as markedly elevated free thyroxine fractions. In contrast, six thyrotoxic sera had normal TBG capacities and normal or slightly elevated free thyroxine fractions.

(c) In hypothyroidism, the TBPA capacities showed no consistent deviation from the normal range. 11 of the 16 sera had elevated TBG capacities as well as markedly diminished free thyroxine fractions. In contrast, five hypothyroid sera had normal TBG capacities and normal or nearly normal free thyroxine fractions.

(d) In thyrotoxicosis and hypothyroidism, the inverse correlation between free thyroxine fraction and TBG was much closer than that with TBPA. When diagnostic categories were considered separately, only TBG bore a significant inverse relation to the free thyroxine fraction. It is therefore suggested that in thyroid diseases TBG may sometimes play a more important role than TBPA in determining the free thyroxine fraction.

(e) The demonstrated variations in the binding proteins were considered sufficient to explain the abnormalities of the free thyroxine fractions in thyroid disease.

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