The prevalence of TSI in Graves' disease was investigated with a radioligand receptor assay using human thyroid membranes and highly purified labeled porcine TSH or bovine TSH in 110 patients before treatment and in 39 patients after successful treatment with antithyroid drugs. In 11 patients, the assay was performed before, during, and after therapy. The results in the radioligand receptor assay were compared to thyroid function tests (TRH test, free T4 index, serum %3 level, and thyroid suppression test). Normal IgG inhibits nonspecifically, but dose dependently, the binding of [125I]TSH to thyroid membranes. IgG samples from patients were only considered to be positive if they reduced the binding of the labeled hormone below the mean value minus 2 SD of the controls. TSI activity was found in 50% of the patients with untreated diffuse toxic goiter, in 3 out of 27 cases who regained suppressible thyroid function, and in 5 out of 12 cases who were off therapy for more than 6 weeks and showed normal TRH tests and normal hormone levels but in whom the suppression test was not performed. Our data cannot prove the hypothesis that only humoral antibodies are responsible for the thyroid stimulation in Graves' disease, but of course they cannot exclude it; furthermore, they suggest the existence of antibodies which bind to the human thyroid cell membrane without necessarily stimulating thyroid cellular activity.

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The isolated perfused rat kidney was used to study renal handling of thyroid hormones. Substrate enriched protein free perfusates were chosen which allowed the kidneys to perform a normal glomerular filtration rate of 1.1 ml/g kidney-min and enabled accurate estimation of filtered load and tubular handling of free thyroid hormones without interference from the presence of hormone binding substances. Under these conditions we found a high tubular reabsorption capacity for both T 3 and T4. This reabsorption capacity was unsaturable, even when the filtered hormone load was far above (x 100) the physiological range.

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