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Activity of autoantibodies to the thyrotropin receptor in the serum of patients with active Graves's disease was compared when the patients' IgG was purified by three different procedures: ammonium sulfate precipitation (I), a modified batch diethylaminoethyl cellulose method (II), and affinity chromatography on Protein A-Sepharose CL-4B (III). IgG extracted by I was significantly less potent in inhibiting binding of 125I-labeled thyroid membranes than that prepared by either II or III, and was significantly less effective than II in stimulating adenyl cyclase activity in thyroid membrane. Thyroglobulin, a serum protein whose concentration is increased in patients with various thyroid diseases, was coprecipitated in amounts sufficient to significantly inhibit binding only when method I was used, but not with either of the other two procedures. Evidently method I is inferior to either of the other two when used for purification of autoantibodies to the thyrotropin receptor. Method II used in this study, being faster and more economical than I and of equivalent efficacy, is a feasible alternative method for clinical use.

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Thyrotropin (TSH)-receptor autoantibodies were assessed by measurement of 125I-bTSH binding inhibition in 32 patients with juvenile-onset Graves' disease (one of whom was studied twice) and 16 normal control subjects. Thirteen (76.5%) of 17 thyrotoxic patients had significantly elevated TSH binding-inhibitory immunoglobulin (TBII) activity compared with eight (50%) of 16 patients who were in clinical remission and none of the control subjects. Mean TBII activity was significantly greater in thyrotoxic patients than in individuals in remission, except in one unusual patient in whom there was a discordance between TBII activity and in vitro thyroid-stimulatory activity. In eight euthyroid patients who were followed up for at least five months while not receiving treatment, assessment of TBII activity did not predict who would or would not suffer relapse at a later date. Thus, TBIIs are secreted in excess in juvenile Graves' disease, the titer decreasing as the disease remits. The TBII assay cannot be used as the sole predictor of when antithyroid medication can be withdrawn safely, however.

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The iodinated contrast agents used in oral cholecystography impair peripheral iodothyronine-5'-deiodinase activity, resulting in a transient decrease in serum 3,5,3'-triiodothyronine (triiodothyronine, T3) and in increases in serum 3,3',5'-triiodothyronine (reverse T3, rT3) and thyroxine (T4) concentrations. A related iodinated contrast agent, diatrizoate, is employed in coronary angiography. The effect of diatrizoate (Renografin-76) on serum T4, T3, rT3, and thyroid stimulating hormone (thyrotropin, TSH) concentrations and the TSH and T3 responses to thyrotropin releasing hormone (TRH) were evaluated in seven euthyroid patients before and on the fifth day following coronary angiography. No significant changes were observed. Thus, diatrizoate, in contrast to the oral cholecystographic agents, appears to have little or no clinically important effect on thyroid hormone metabolism in man.

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Oral cholecystographic agents induce a decrease in serum T3 and an increase in serum T4 and rT3 concentrations in normal subjects. However, their effect on TSH secretion in man is unclear. In the present study, the serum TSH concentration was increased above baseline values 5 days after the administration of 3 g iopanoic acid (IA) in five of six euthyroid volunteers (an increase of borderline significance), and the TSH response to TRH was significantly augmented after IA administration. In four other euthyroid subjects who had received IA 3 days earlier, the administration of T3 (5 microgram, five times daily) for the next 2 days restored the serum T3 concentration toward baseline values and prevented the IA-induced increase in TRH-stimulated serum TSH concentrations. It is concluded from the present study that IA enhances pituitary thyrotroph sensitivity to TRH and that this effect may be related, at least in part, to the IA-induced decrease in circulating T3 as well as the previously demonstrated inhibitory effect of IA on the pituitary conversion of T4 to T3. This decrease in the serum T3 concentration after IA administration is due primarily to inhibition of peripheral 5-monodeiodination of T4 and, possibly, to a direct inhibitoy effect of excess iodide on the release of T3 from the thyroid.

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Two patients with extrathyroidal anterior neck abscesses are discussed. Normal thyroid scans ruled out acute, suppurative thyroiditis.

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