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Ernst U Frevert, Anja Biester, Manfred J Müller, Heinrich Schmidt-Gayk, Alexander von zur Mühlen, and Georg Brabant

Frevert EU, Biester A, Müller MJ, Schmidt-Gayk H, von zur Mühlen A, Brabant G. Markers of bone metabolism during short-term administration of thyroxine in healthy volunteers. Eur J Endocrinol 1994;131:145–9. ISSN 0804–4643.

We investigated the influence of L-thyroxine (L-T4) treatment over 3 weeks on biochemical markers of bone turnover in 12 healthy young men (age 25.6 ± 1.4 years, BMI: 22.6 ± 2.5 kg/m2). Serum parameters indicating bone formation [bone Gla protein (BGP), carboxyterminal propeptide of type I procollagen (PICP), and bone-specific alkaline phosphatase (BAP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and the urinary excretion of pyridinoline (Pyr) and deoxypyridinoline (D-Pyr)] were measured before and after three weeks of treatment with 300 μg L-T4/d. T3 and T4 significantly increased and TSH decreased to almost undetectable levels even when measured with a third generation TSH assay. Markers of bone formation showed variable responses with a small but significant increase in BGP but not in PICP or BAP. In contrast, all parameters of bone resorption increased significantly with a good correlation between D-Pyr excretion and the serum parameter ICTP (r = 0.78, p < 0.0001). These changes in bone-turnover markers were not necessarily paralleled by comparable increments of other markers of tissue thyrotoxicosis (SHBG, pulse rate, VO2), suggesting a variability in tissue sensitivity. These rapid responding parameters, especially in the easily obtainable serum parameter ICTP, might be valuable tools in the evaluation of several states of thyroxine excess.

G Brabant, Dept. Klinische Endokrinologie, Medizinische Hochschule Hannover, D-30 623 Hannover, Germany

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D. B. Ramsden and D. N. Crossley

Abstract. Some factors influencing serum 3,5,3',5'-tetradiodothyroacetate (T4A) concentrations were examined in hypothyroid, euthyroid and hyperthyroid human subjects. Serum T4A concentration was shown to be correlated with parameters such as serum, total and free thyroxine (T4) concentrations and thyroxine: thyroxine binding globulin ratio, which are indicative of the availability of T4 for peripheral metabolism. The relationship between T4A and these parameters was not a simple linear one; serum levels of T4A tended to show less variation from the normal range than did serum total T4 in hyperthyroid subjects.

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G. Gács and Cs. Bános


The plasma concentrations of thyroxine (T4), free thyroxine (free-T4), triiodothyronine (T3), reverse triiodothyronine (rT3), TSH and thyroxine-binding globulin (TBG) were measured in 19 children suffering from idiopathic growth hormone deficiency. Blood was taken before and one month after growth hormone treatment. Ten patients were hypothyroid (group 1) and 9 were euthyroid (group 2). The basal T3 and rT3 levels correlated well with the T4 concentrations. Free-T4 levels were very low in all the hypothyroid patients and proved to be the most reliable index of TSH deficiency. TBG concentration was high in the hypopituitary patients regardless of their thyroid function.

Following growth hormone treatment T4, free-T4 and rT3 levels fell in both groups. The T3 concentration rose in group 1 but no change was seen in group 2. There was a significant correlation between the changes of T4 and T3, such that the increase in T3 level was greatest in those with only a slight reduction of T4 concentration and no T3 increase was seen with more marked T4 decreases.

The plasma TBG concentration is enhanced in growth hormone deficiency causing relatively high T4 values. Growth hormone treatment reduces T4 secretion and affects the peripheral metabolism of thyroid hormones resulting in an increase of T3 and a reduction of rT3 concentration.

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T. Nakashima, K. Inoue, T. Omae, T. Hisatsugu, and T. Yoshizumi


The thyroid of Hashimoto's disease is unique in its susceptibility to exogenous iodide and the positive perchlorate test. It would be of interest to know if there is any alteration of iodine metabolism in the thyroid.

The results obtained in 9 cases with untreated Hashimoto's disease were compared with those in 9 normal thyroids; 5 cases were investigated for iodine metabolism and 4 cases for the peroxidase study.

The thyroglobulin content in thyroid wet weight showed lower values 1.6 ± 1.2 % compared to 8.0 ± 1.5 % in normal. Thyroglobulin represented 18.9 ± 9.3 % of total soluble protein and was significantly lower than normal, 66.9 ± 5.4 %. Iodine content of thyroglobulin was extremely low, 0.10 ± 0.05 % compared to 0.49 ± 0.03% in normal. The thyroglobulin with low degree of iodination showed a low sedimentation coefficient of 18.1 ± 0.1. Distribution of iodo-amino acid-iodine was 8.1 ± 2.8% for thyroxine (T4) and 14.4 ± 9.7 % for triiodothyronine (T3), resulting in a much higher T3/T4 ratio than in normal thyroids. Monoiodotyrosine/diiodotyrosine (MIT/DIT) ratio was higher and T4/DIT ratio was apparently lower than normal. These results resemble the pattern of that found in iodine deficiency. T3/T4 ratio was increased in the blood of patients with Hashimoto's disease. Consequently the alteration of distribution of iodo-amino acids in the thyroid may contribute to the increase in T3/T4 ratio in the blood of this disease.

Peroxidase activity showed 103 ± 51 U/mg particulate protein and was significantly lower than values in normal thyroids, 299 ± 85 U/mg protein.

On the other hand, the total amount of thyroglobulin was not significantly decreased in this disease. The total amount of organified iodine, however, was apparently lower than normal.

These results suggest that the low degree of iodination of thyroglobulin is an essential alteration in the thyroid of Hashimoto's disease.

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Erik Moltke

Previous investigations have shown that d,l-thyroxine reduces the tensile strength of healing wounds in guinea pigs (Moltke, 1955). This effect is apparently mediated by an inhibition of an important – but not indispensable – factor promoting the healing process (Moltke, 1956). This factor might be identical with the thyroid stimulating hormone of the pituitary gland (TSH) (Moltke & Ebbesen, 1957). It has been shown that both isomers of thyroxine markedly inhibit the pituitary release of TSH (Griesbach et al., 1949, and Moltke, 1957). d-Thyroxine, however, exerts only a very slight effect on the oxygen consumption of tissues and on tadpole metamorphosis (Pitt-Rivers & Lerman, 1948, and Reineke & Turner, 1945) while 1-thyroxine is highly active in this respect. By using the dextro-isomer, d-thyroxine, it should, therefore, be possible to show whether the marked inhibitory effect of d,l-thyroxine on wound healing is caused by a direct action on the tissues or

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J. A. Franklyn, M R. Wilkins, R. Wilkinson, D. B. Ramsden, and M. C. Sheppard

Abstract. Circulating concentrations of total and free thyroid hormones and thyroid hormone binding proteins were measured in thyrotoxic and euthyroid subjects treated with propranolol. In the thyrotoxic group, total triiodothyronine (T3) concentration fell after propranolol therapy, suggesting an effect of the drug on the peripheral conversion of thyroxine (T4) to T3. In euthyroid subjects, a rise in circulating concentrations of free T4 and reverse T3 (rT3) was observed, while only a small decrease in free T3 was evident. Thyroxine binding globulin (TBG) concentration fell during propranolol treatment while thyroxine binding prealbumin (TBPA) concentration rose. The changes observed in the euthyroid state are consistent with inhibition of peripheral deiodination of T4 and rT3; an additional effect of propranolol on binding protein metabolism was evident.

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M Ludgate

Graves' disease (GD) is an autoimmune condition in which goitre and hyperthyroidism are induced by thyroid stimulating antibodies (TSAB) which mimic the action of thyrotrophin (TSH). The target of the autoimmune response is the thyrotrophin receptor (TSHR) and, since its cloning, a number of differing approaches have been adopted in an attempt to develop an animal model of GD. Methods in which synthetic peptides or fragments of the receptor produced in bacteria or insect cells have been injected into animals together with immunological adjuvants have had only limited success in inducing some of the signs and symptoms of GD. Genetic immunisation resulted in thyroiditis in the majority, but TSAB formation in only a minority, of treated inbred mice. Transfer of receptor in vitro primed T cells to syngeneic naive recipients, with priming either using a bacterial fusion protein or genetic immunisation, induced destructive thyroiditis in non-obese diabetic (NOD) mice but lymphocytic thyroiditis in BALBc mice. Furthermore, the orbits of 17/22 of the BALBc animals, but not the NOD animals, with thyroiditis had orbital changes similar to those seen in thyroid eye disease. TSAB and elevated thyroxine levels were induced in AKR/N mice injected with fibroblasts expressing the full length human TSHR and murine major histocompatibility complex (MHC) class II homologous to the recipient mice. No thyroiditis was induced but preliminary results from a different group using the same protocol suggest that receptor autoantibodies and thyroid dysfunction could be transferred using T cells primed in vitro with the receptor and MHC-II expressing cells. The majority of the studies described above have studied inbred mouse strains. In a novel departure, the NMR outbred strain has been treated by genetic immunisation with very promising results, including the induction of increased thyroxine levels in 4/30 female mice, accompanied by TSAB in addition to thyroiditis, and with signs of hyperactivity and orbital pathology. This review discusses the various protocols together with the information regarding the pathogenesis of GD which each has contributed, and concludes with an evaluation of how close we are to mimicking this polygenic, multifactorial disease.

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R. L. Himsworth and A. E. Kark


A patient with suppurative thyroiditis due to infection with Escherichia coli is described. Serial studies of thyroid function were performed. Before the abscess was drained there was no uptake of radio-iodine by the thyroid and there was some spillage of iodinated compounds from the gland. Post-operatively circulating thyroid hormone concentrations declined but were restored at four weeks. Thyroid uptake of radio-iodine was re-established two weeks after operation but there was little secretion of thyroxine at this time. Four weeks after operation the uptake of radio-iodine was greater than normal and thyroxine was being secreted. These changes in thyroid function were not associated with any significant rise in the plasma thyrotrophin concentration.

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Klaus Kølendorf, Kaj Siersbæk-Nielsen, Jens Mølholm Hansen, and Thorkild Friis


A new in vitro thyroid function test, "Effective Thyroxine Ratio" (ETR®) has been tested in 170 patients, and the ETR values in patients with normal and abnormal thyroid function have been compared to the concentration of absolute free thyroxine and free thyroxine index in serum. Among 42 hyperthyroid patients tested with ETR, 13 had values within normal range (30.9 per cent). Three of 18 hypothyroid patients had normal values (16.8 per cent). Eighty-nine per cent of 27 pregnant women and all of 17 patients treated with genuine oestrogens had ETR values within normal range. A high positive correlation was found between values of ETR, absolute free thyroxine in serum (r = 0.62) and free thyroxine index (r = 0.83).

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K. Siersbæk-Nielsen, J. Mølholm Hansen, and E. Hippe


Elevated thyroxine-binding globulin capacity in serum (TBG) was found in five members of a family. Two males and three females in three generations had elevated TBG, protein-bound iodine and serum thyroxine but decreased dialysable thyroxine. The patients were clinically euthyroid and calculations of free thyroxine in serum and 131I uptake in the thyroid gland showed normal values. These results support the assumption that TBG is genetically controlled. The mode of transmission was consistent with dominant inheritance but it is not possible to determine whether it is x-linked or autosomal.