1967The Journal of Clinical Endocrinology & MetabolismRequires access

Effect of Small Doses of Carrier Iodide Upon the Organic Binding of Radioactive Iodine by the Human Thyroid Gland

R. D. H. Stewart, I. P. C. Murray

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Abstract

The effect of small doses of carrier iodide (127I′) upon the organic binding of radioactive iodine (131I) by the thyroid gland has been studied by performing 123 perchlorate discharge tests in normal persons and patients with abnormal thyroid function. In 86 tests, 100–2000 μg 127I′ was given with the iv 131I dose; the remaining 37 tests without carrier served as controls. In 60 of the 86 tests in which carrier iodide was administered, there was a positive perchlorate discharge of 131I from the thyroid gland, indicating that organic binding of iodine was impaired. In the 37 control tests, perchlorate discharge was observed only in 2 patients with untreated thyrotoxicosis. Although there was considerable individual variation, the minimum carrier dose of 127I′ required to cause demonstrable block of organic binding in normal persons appeared to be of the order of 750 μg, which resulted in a serum iodide level of 30–38 μg/1. However, a positive perchlorate discharge was observed in 1 of 3 TSH-treated normals given only 350 μg 127I′ (serum iodide concentration 15 μg/1), in 4 of 7 patients with nontoxic goiter given 500 μg 127I′ (serum iodide concentration 18-28 μg/I), in 6 of 7 patients with untreated thyrotoxicosis given 125–250 μg 127I′ (serum iodide concentration 7–17 μg/1) and in 7 of 11 patients with thyrotoxicosis treated by radioactive iodine or thyroidectomy given 100–250 μg 127I′ (serum iodide concentration 7–17 μg/1) Analysis of all the results showed a significant correlation between perchlorate discharge value and serum iodide concentration. This correlation was also present in the normal individuals, the TSH-treated normals, the patients with nontoxic goiter and those with untreated thyrotoxicosis when these diagnostic groups were considered separately. Inhibition of organic binding of iodine by the thyroid has been demonstrated with smaller carrier doses of iodide than has previously been recognized, and the results indicate that the presence and degree of block in organic binding is to a considerable extent dependent upon serum iodide concentration. The increased sensitivity of the patients with abnormal thyroid function to iodide inhibition is probably due to a higher thyroid/serum concentration gradient for iodide in these individuals.

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The effect of small doses of carrier iodide (127I′) upon the organic binding of radioactive iodine (131I) by the thyroid gland has been studied by performing 123 perchlorate discharge tests in normal persons and patients with abnormal thyroid function. In 86 tests, 100–2000 μg 127I′ was given with the iv 131I dose; the remaining 37 tests without carrier served as controls. In 60 of the 86 tests in which carrier iodide was administered, there was a positive perchlorate discharge of 131I from the thyroid gland, indicating that organic binding of iodine was impaired. In the 37 control tests, perchlorate discharge was observed only in 2 patients with untreated thyrotoxicosis. Although there was considerable individual variation, the minimum carrier dose of 127I′ required to cause demonstrable block of organic binding in normal persons appeared to be of the order of 750 μg, which resulted in a serum iodide level of 30–38 μg/1. However, a positive perchlorate discharge was observed in 1 of 3 TSH-treated normals given only 350 μg 127I′ (serum iodide concentration 15 μg/1), in 4 of 7 patients with nontoxic goiter given 500 μg 127I′ (serum iodide concentration 18-28 μg/I), in 6 of 7 patients with untreated thyrotoxicosis given 125–250 μg 127I′ (serum iodide concentration 7–17 μg/1) and in 7 of 11 patients with thyrotoxicosis treated by radioactive iodine or thyroidectomy given 100–250 μg 127I′ (serum iodide concentration 7–17 μg/1) Analysis of all the results showed a significant correlation between perchlorate discharge value and serum iodide concentration. This correlation was also present in the normal individuals, the TSH-treated normals, the patients with nontoxic goiter and those with untreated thyrotoxicosis when these diagnostic groups were considered separately. Inhibition of organic binding of iodine by the thyroid has been demonstrated with smaller carrier doses of iodide than has previously been recognized, and the results indicate that the presence and degree of block in organic binding is to a considerable extent dependent upon serum iodide concentration. The increased sensitivity of the patients with abnormal thyroid function to iodide inhibition is probably due to a higher thyroid/serum concentration gradient for iodide in these individuals.

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Available abstract

The effect of small doses of carrier iodide (127I′) upon the organic binding of radioactive iodine (131I) by the thyroid gland has been studied by performing 123 perchlorate discharge tests in normal persons and patients with abnormal thyroid function. In 86 tests, 100–2000 μg 127I′ was given with the iv 131I dose; the remaining 37 tests without carrier served as controls. In 60 of the 86 tests in which carrier iodide was administered, there was a positive perchlorate discharge of 131I from the thyroid gland, indicating that organic binding of iodine was impaired. In the 37 control tests, perchlorate discharge was observed only in 2 patients with untreated thyrotoxicosis. Although there was considerable individual variation, the minimum carrier dose of 127I′ required to cause demonstrable block of organic binding in normal persons appeared to be of the order of 750 μg, which resulted in a serum iodide level of 30–38 μg/1. However, a positive perchlorate discharge was observed in 1 of 3 TSH-treated normals given only 350 μg 127I′ (serum iodide concentration 15 μg/1), in 4 of 7 patients with nontoxic goiter given 500 μg 127I′ (serum iodide concentration 18-28 μg/I), in 6 of 7 patients with untreated thyrotoxicosis given 125–250 μg 127I′ (serum iodide concentration 7–17 μg/1) and in 7 of 11 patients with thyrotoxicosis treated by radioactive iodine or thyroidectomy given 100–250 μg 127I′ (serum iodide concentration 7–17 μg/1) Analysis of all the results showed a significant correlation between perchlorate discharge value and serum iodide concentration. This correlation was also present in the normal individuals, the TSH-treated normals, the patients with nontoxic goiter and those with untreated thyrotoxicosis when these diagnostic groups were considered separately. Inhibition of organic binding of iodine by the thyroid has been demonstrated with smaller carrier doses of iodide than has previously been recognized, and the results indicate that the presence and degree of block in organic binding is to a considerable extent dependent upon serum iodide concentration. The increased sensitivity of the patients with abnormal thyroid function to iodide inhibition is probably due to a higher thyroid/serum concentration gradient for iodide in these individuals.

Key concepts: Iodide, Perchlorate, Iodine, Thyroid, Chemistry, Radioactive iodine, Internal medicine, Endocrinology

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