Thyroid function was studied for 42 days in 58 patients, 28 of whome had euthyroid goiter, after urography (diatrizoic acid), cholangiography (ioglycamic acid), and cholecystography (Naiopanoate). After urography and cholangiography short-lived increases of the serum thyroxine occurred in a few patients, but the mean thyroxine and triiodothyronine concentration did not change. By contrast, 7 days after oral cholecystography serum thyroxine had risen consistently by 22% with a concomittant rise of the free thyroxine, while triiodothyronine declined by 15%. The thyroxine metabolite 3,3',5'-triiodo-1-thyronine (reverse T3) rose by 50% and serum thyrotropin concentration doubled. After 42 days thryoxine and triiodothyronine had returned to baseline, and none of the 58 patients developed clinical hyperthyroidism. In patients with severe myxoedema kept on a constant replacement dose with 1-thyroxine NA-iopanoate produced similar changes with the exception of the rise of the serum thyroxine. The primary event after Na-iopanoate seems to be a fall of the serum triiodothyronine, which in turn augments thyrotropin and indirectly thyroxine secretion. the marked and sometimes sustained rose of serum thyroxine after cholecystography may lead to the erroneous diagnosis of hyperthyroidism.

Among patients with differentiated thyroid carcinoma (diffTCa), the rare hyperfunctioning or toxic TCa (ToxTCa) was diagnosed when scintigraphic hot thyroid areas were attributable only to diffTCa (diameter >1 cm by pathological examination) and/or total thyroidectomy failed to induce hypothyroidism. Of 924 cases of all TCa (papillary diffTCa 47.3%, follicular diffTCa 44.2%, others 8.5%), 19 had ToxTCa (2.1%, 15 of 19 follicular, 4 of 19 papillary, P = 0.008). These received a more intensive radioiodine therapy (average cumulated (131)I activities 21.8 vs. 15.2 GBq, P < 0.01). Five-year survival rates for ToxTCa (n = 19, 56%) and diffTCa (n = 545, 94.5%) differed [hazard ratio 4.8, 95% confidence interval (CI) 2.8-8.1, P = 0.001]. However, the differences were attenuated by matching ToxTCa and diffTCa (n = 57, 5-yr survival rate 74%) for age, sex, and histopathologic type (hazard ratio 2.1, 95% CI 1.13-3.9, P = 0.02). Correcting statistically for M(1) against M(0) stage distribution resulted in a further reduction of the hazard ratio (hazard ratio 1.8, 95% CI 0.93-3.48, P = 0.08). An M(1) stage is an important prognostic factor in ToxTCa patients. Thus, ToxTCa, treated with higher activities of (131)I, has a survival prognosis close to that of matched diffTCa cases, both groups consisting mainly (79%) of follicular subtypes.

In the Bernese region, where goiter was formerly endemic, alimentary salt has been supplemented by increasing amounts of potassium iodide (KI): 5, 10, 20 mg KI/kg in 1922, 1965 and 1980 respectively. Ioduria rose from < 30 micrograms I/g creatinine in 1920 to > 100 micrograms I/g creatinine in the 1980s. In 1992 ioduria was estimated in 55 healthy volunteers (group A and individual B) and 234 thyroid carcinoma patients after thyroidectomy: hypothyroid patients with (C) and without thyroid remnants (D) and euthyroid patients on T4 substitution (E). The arithmetic mean iodine excretion of the healthy volunteers in group A and individual B was found to be 87 +/- 40 micrograms I/g creatinine. This is insufficient according to the recommendations of the WHO. In all groups, the iodine excretion reached the recommended level only in some members: 24% (A, B), 19% (C), 38% (D) and 81% (E). It was thought in the 1980s that in a formerly iodine-deficient society, iodinated salt would continue to provide an adequate supply of iodine. However, iodine intake in this affluent society has proved to be unstable. This can be attributed to modifications of eating habits, which include a reduction of total salt consumption, combined with a growing consumption of manufactured food of cosmopolitan origin, prepared using salt containing little or no iodine.