1. Whole-body retention and plasma values of 131I after a test dose were measured for up to 32 days in patients previously rendered athyreotic by surgery and 131I treatment for thyroid carcinoma, and who were without detectable functioning tissue at the time of study.

2. About 99·8% of the administered 131I was rapidly excreted, consistent with renal iodide excretion. The remainder (about 0·2%) was eliminated slowly, with mean half-life 15 days; we call this the slow-turnover component.

3. By the sixth day after the 131I dose, very little [131I]iodide remained in the plasma. The average protein-bound 131I was only 0·0035% of dose/l, with mean half-life 14·1 days; 90% was non-extractable in butanol. Labelled albumin accounted for about 80% of the non-extractable fraction.

4. The distribution space estimated from the slow-turnover component and protein-bound 131I was 34 1, indicating that most of the slow-turnover component is extravascular.

5. Stable potassium iodide administration, starting 2 days after giving 131I, had no observable effect on the variables measured.

6. Impairment of renal function delayed [131I]iodide excretion and increased both slow-turnover component and plasma protein-bound 131I.

7. A simple model describing iodine kinetics in athyreotic individuals is suggested. It predicts that the slow-turnover component contains only about 4 μg of iodine and, since this is distributed widely in body tissues, it is unlikely to be of biological significance.

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