Kinetic analysis of iodine metabolism.

Abstract

Iodide kinetic studies were performed on 24 subjects, including normal controls (4), patients with multinodular goiter (8), thyro toxicosis (4), and a variety of other thyroid diseases (8). Rates of iodine metabolism were calculated by more than one technique when possible. The resulting observations are at variance with traditional concepts of iodide metabolism in some instances. AIU (absolute iodine uptake) agrees well with estimates of hormone degradation derived from isotope labeled thyroxine turnover studies. Estimates of thyroid hormone secretion, calculated by 3 different techniques, were uniformly higher than AIU. It is believed that the discrepancy may be attributed to (a) incomplete isotope equilibrium, and (b) a valid difference reflecting spillage of thyroidal iodine as iodide or iodotyrosine, in addition to hormone secretion. Thyroid clearance, as usually measured, probably represents a “net clearance,” and does not include iodide bound and again released as iodotyrosine during the observation period. Initial apparent “clearance” rates may be seen to exceed steady state “clearance” rates in hyperplastic glands. A “leak” of iodide from the thyroid, as iodide or iodotyrosine, occurs in normal and abnormal glands. The evidence for this is (a) a discrepancy between AIU and thyroid iodine secretion; (b) a marked disparity between predicted and observed urinary iodide excretion; (c) the obvious tendency for urinary iodide excretion curves to parallel thyroid iodine content rather than plasma PB131I content; and (d) the high ratios of urinary iodide specific activity to PBI specific activity. Characteristic variations from normal iodide kinetics were present in thyroid disease. Of these the most striking were: (a) A tendency toward high thyroid iodine pool in multinodular goiter, with retention of a normal thyroid iodine secretion rate, resulting in elevated iodide release. Many of these thyroids secreted an abnormal butanol-insoluble iodoprotein in addition to thyroid hormone, (b) High iodide clearance, low thyroid iodide stores, and vastly accelerated thyroid iodine secretion rates are present in thyrotoxicosis. Apparent thyroid “clearance” of iodide may be as high as 2 1/min. (c) In 3 of 4 patients with the butanol-insoluble iodine defect iodide clearance was augmented, thyroid iodine was normal or low, and secretion rates were elevated. Calculated thyroid iodine release was in some instances higher than that observed in thyrotoxicosis. An abnormal iodoprotein was secreted by these glands, (d) Augmented thyroid iodine release rates allowed 2 patients with Hashimoto's thyroiditis to secrete normal or increased amounts of stable iodine despite markedly reduced thyroid iodine pools. A large portion of the iodine secretion product was a butanol-insoluble iodoprotein.