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ståle Skare and Harald M. M. Frey


Two male patients aged 36 and 52 years with thyrotoxicosis revealed a serum T3 of 2.8 and 6.5 nmol/l and a serum T4 of 166 and 238 nmol/l, respectively. Both had been exposed to iodine (2–10 mg daily) for 2–12 months before thyrotoxicosis was diagnosed. Urinary iodine excretion was high, 5000 and 10000 nmol/24 h (624–1250 μg). The uptake of 131I in the thyroid glands were low, none had goitre.

Their iodine intake was interrupted, urinary iodine excretion gradually decreased, and T3 and T4 in serum concomitantly normalized. They were clinically and biochemically euthyroid 9 and 11 weeks after withdrawal. After 14 and 22 weeks they had normal thyroid uptake of 131I, and thyroid scans showed glands of normal size and configuration, TRH-stimulation and a T3-suppression tests became normal. ESR was not elevated in any of the cases, thyroid antibodies against thyroglobulin and follicular cell microsomes were absent and TSAb was undetectable during the thyrotoxic stage.

Thus no evidence of any pre-existing and/or pre-disposing pathological condition in the thyroid glands were found. The mechanism for the iodine-induced thyrotoxicosis in such cases remains obscure.

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Irene Gavras and John A. Thomson


The cases of 2 women who had clinical and biochemical evidence of autoimmune thyroiditis, who progressed to develop hypothyroidism and who then, some years later, developed thyrotoxicosis are described. Possible mechanisms for the production of this unusual clinical course are discussed.

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K. Liewendahl, T. Helenius, B.-A. Lamberg, H. Mähönen, and G. Wägar

Abstract. Free thyroxine (FT4) and free triiodothyronine (FT3) concentrations in serum were measured by direct equilibrium dialysis methods in patients receiving thyroxine replacement or suppression therapy. Four of 50 hypothyroid patients euthyroid on replacement therapy (mean thyroxine dose 120 μg/day) had supra-normal FT4 concentrations, whereas the FT3 concentrations were normal in all. Forty-one of 56 operated thyroid carcinoma patients on suppressive therapy (mean thyroxine dose 214 μg/day) had raised FT4 concentrations, whereas the FT3 concentration was elevated in only one patient. There was a large difference in mean FT4 values for hypothyroid and thyroid carcinoma patients (17.2 vs 29.5 pmol/l), whereas the difference in mean FT3 values was small (5.0 vs 6.1 pmol/l), suggesting a decreased peripheral conversion of T4 to T3 with increasing concentrations of FT4. Serum TSH concentrations, as determined by an immunoradiometric assay, varied from < 0.02 to 11.9 mU/l in treated hypothyroid patients; 21 patients (42%) had values outside the reference limits. As a single test, serum TSH is therefore not very useful for the assessment of adequate thyroxine dosage in patients with primary hypothyroidism. In thyroid carcinoma patients, the TSH concentrations were < 0.18 mU/l; 45 patients had values < 0.02 mU/l indicating sufficient suppression of TSH secretion in the majority of cases. On the basis of these results we recommend the combination of FT3 and TSH tests for monitoring thyroxine replacement and suppression therapy. FT4 appears less useful than FT3 for this purpose even if special reference values values were adopted for each patient group.

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J. Mølholm Hansen


Chlorophenoxyisobutyrate (CPIB) added to serum in vitro increases the quantity of dialysable thyroxine. The same effect can be obtained in vivo following large doses of the preparation. After low doses, increase in serum proteinbound iodine (PBI) is observed and with higher doses this increase is not observed, probably because of the thyroxine-displacing effect. Free thyroxine increases in practically all patients investigated. In long-term treated patients the alterations in dialysable thyroxine, serum proteinbound iodine and free thyroxine are transient; pre-treatment values being regained in the course of ½–4 months. 131I uptake in the thyroid gland is influenced irregularly and transiently possibly via inhibition of the thyrotrophin production in the hypophysis. The effect of CPIB on serum cholesterol appears, in long-term therapy, to be completely independent of the effect on these thyroid parameters. This observation is also supported by the fact that the 14C-testosterone metabolism is normal in patients receiving long-term therapy.

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L. Stolte, H. Kock, H. van Kessel, and L. Kock


The utilization of thyroxine was studied in pregnant, non-pregnant and steroid-induced pseudopregnant rhesus monkeys. The PBI concentration in the blood serum was found to be higher during pregnancy and pseudopregnancy than in the non-pregnant state. The turn-over rate of radiothyroxine, following its intravenous injection, was found to be higher during and outside of pregnancy than during pseudopregnancy. The extra-thyroidal thyroxine pool was calculated to be more expanded during pregnancy and (probably) pseudopregnancy than in the non-pregnant state. The utilization of thyroxine per unit time proved to be smaller in the non-pregnant monkey than in the pregnant and (probably) greater than in the pseudopregnant animal. It is concluded that thyroxine utilization during pregnancy is higher than during pseudopregnancy. The increased activity of the thyroid of the pregnant monkey, as judged from the increase in thyroxine utilization, is not only caused by the high level of placental steroids that characterize this state.

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C. Beckers, J. Barzelatto, C. Stevenson, A. Gianetti, A. Pardo, E. Bobadilla, and M. De Visscher


Iodine kinetic studies have been performed in 61 Indians from the Pedregoso goitre endemic in Chile. The daily absolute iodine uptake in the thyroid averaged 98 μg I, with maximal values in the cases of diffuse goitre. The mean thyroxine degradation rate in the same group of patients corresponded to 102 μg I per day, when using the mean thyroxine distribution space and thyroxine (T4) fractional turnover rate obtained from a comparable group of the same population. The output of iodine from the thyroid was calculated by 3 different methods. In each case, the iodine output appears to be higher than the amount of halogen accumulated by the thyroid or metabolized by the tissues.

These findings suggest an important spillage of iodine (as iodide and/or iodinated tyrosines) by the goitrous gland. Such a disturbance apart from nutritional iodine deficiency may be an important factor in the pathogenesis of endemic goiter.

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Annenienke C van de Ven, Romana T Netea-Maier, Femmie de Vegt, H Alec Ross, Fred C G J Sweep, Lambertus A Kiemeney, Johannes W Smit, Ad R Hermus, and Martin den Heijer


The aim of this study was to investigate the influence of age on the association between thyroid function and mortality.


The Nijmegen Biomedical Study is a population-based study, comprising 5816 randomly selected adults of all age groups without previously known thyroid disease.


TSH, free thyroxine (FT4) and peroxidase antibodies were measured in 2002–2003. The number of deaths were established in 2012 (median follow-up time 9.4 years).


Subclinical thyrotoxicosis was associated with mortality in subjects aged <65 years (hazard ratio (HR) 2.5, 95% CI 1.1–5.7), but not in subjects aged >65 years. As for thyroid function within the normal range: in the 493 participants aged 80 years or older, an FT4 level in the high-normal range (18.5–22 pmol/l) was associated with a higher mortality in comparison with FT4 levels in the middle range (11.5–15.0 pmol/l): HR 1.7 (95% CI 1.0–2.9). In these elderly, TSH levels within the high-normal range (3.0–4.0 mIU/l) were also associated with a higher mortality in comparison with TSH levels within the middle range (1.0–2.0 mIU/l): HR 1.8 (95% CI 1.0–3.1).


The relationship between thyroid function and mortality differs according to age. This finding might (partially) explain the discrepant results of previous studies examining the relationship between thyroid function and mortality in different age groups.

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Jan-Gustaf Ljunggren and Stig Radner


Methods for the biochemical determination of the biosynthesis of thyroxine and thyroglobulin in thyroid specimens, obtained as an outpatient procedure by a new needle biopsy technique, are described. Thyroglobulin and its subunits are analyzed after in vitro incubation of thyroid specimens with 3H-leucine, followed by salt extraction and separation by linear sucrose gradient centrifugation or after salt extraction of the specimen and separation by disc electrophoresis on polyacrylamide gel. The relative amount of thyroxine and its precursors is determined after in vivo administration of 125I or 131I, salt extraction of the thyroid specimen, digestion with pronase and separation by radiochromatography.

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G. D. Chazenbalk, D. L. Kleiman de Pisarev, G. J. Juvenal, and M. A. Pisarev

Abstract. Previous work from our laboratory has shown that iodothyronines have a direct inhibitory action on the thyroid. In the present studies the uptake, metabolism and subcellular distribution of labelled thyroxine were analyzed. The entry of this hormone reaches a plateau after 15–20 min incubation and is temperature-dependent. The T/M values for T4 were much lower than those of labelled T3 and the curve was different from that obtained with [125I]. The influence of a series of compounds on the T/M values for thyroxine was studied. KI, T3, IOP PTU and MMI were without effect. Absence of Ca++ in the buffer, or addition of KClO4 or ouabain caused a slight decrease, while TSH produced a stimulation in the T/M ratio. Calf thyroid slices dehalogenated thyroxine, producing both T3 and rT3. TSH increased the generation of these two compounds. Neither PTU nor IOP altered the production of T3 and rT3 significantly. The lack of effect of IOP on T3 and rT3 generation was confirmed in calf thyroid homogenates. However, and in agreement with previous reports, IOP significantly decreased production of both triiodothyronines in rat liver slices and in rat liver homogenates.

When the subcellular distribution of labelled thyroxine was examined most of the radioactivity appeared in the soluble fraction and less than 1 % was present in purified nuclei. The addition of unlabelled thyroxine to the slices only caused a significant displacement in the radioactivity of purified nuclei. The presence of labelled thyroxine in the nuclei was confirmed by paper chromatography.

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Stephen C. Thorson, Hamish W. McIntosh, and Mary Willms


The binding of 3,5,3'-triiodothyronine (T3) to thyroxine-binding globulin (TBG) was quantitated in pooled serum from normal, hyperthyroid, hypothyroid and pregnant subjects. To aliquots of each pool was added a small quantity of 131I-T3 and varying concentrations of unlabelled T3 or thyroxine (T4). Following countercurrent electrophoresis in both barbital and trismaleate buffers at pH 8.6, the concentration of 131I-T3 bound to TBG was calculated and the displacing effect of unlabelled T3 and T4 compared. The displacement of 131I-T3 from TBG was greater with T4 than with T3 when normal, hypothyroid and pregnancy sera were electrophoresed in barbital buffer (which inhibits thyroid-binding prealbumin (TBPA) binding of T4). The same findings are seen when hyperthyroid serum which is deficient in TBPA is electrophoresed in trismaleate buffer (which does not inhibit TBPA binding of T4). The observed data indicate that T4 has a greater binding affinity for TBG than has T3 but only displaces T3 to significant degree when TBG is saturated and when TBPA binding of T4 is reduced or inhibited. TBG binding capacities for T3 have been derived for each of the 4 clinical groups and appear to be less than corresponding binding capacities for T4.