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J. R. Tata

ABSTRACT

The activity of the enzyme thyroxine dehalogenase and the nature of products of deiodination of thyroid hormones were studied in skeletal muscle of normal and thyroidectomized rats. The capacity to deiodinate thyroxine was also measured after administration of L-thyroxine, D-thyroxine, 2,4-dinitrophenol and in animals maintained on diets of different iodine contents. A 2 to 3-fold depression in the level of thyroxine dehalogenase occurred 3 months after thyroidectomy which was reversed by the administration of L-thyroxine. Injection of L-thyroxine also stimulated thyroxine dehalogenase activity in normal rats; the increase in enzyme activity was not merely a response to administration of substrate since D-thyroxine, although an almost equally good substrate, failed to alter enzyme activity. The enzyme increased in parallel with the oxygen consumption of the animals treated with L-thyroxine. This relationship does not seem to be a non-specific manifestation of increased cellular metabolic activity because 2,4-dinitrophenol administration failed to cause a similar effect. 3,5,3′-triiodothyronine was not a major product of deiodination of thyroxine; the function of thyroxine dehalogenase therefore does not appear to be that of the conversion of thyroxine to its »active« form. Thyroxine dehalogenase is not uniquely involved in the recovery of iodine from the spent thyroid hormone since its activity was independent of the level of dietary iodine. It is therefore concluded that enzymic deiodination of thyroid hormones by skeletal muscle is linked in some way to their calorigenic action, although the exact nature of this relationship remains unknown.

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G. Madeddu, M. Langer, C. Costanza, A. R. Casu, M. L. Arras, and S. Campus

Abstract.

Measurement of serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), thyroxine-binding-globulin (TGB), antithyroglobulin antibodies (anti-hTg), thyroid 131I uptake and scanning was performed on 12 patients during the early phase of subacute thyroiditis. Serum thyrotropin (TSH) was measured during baseline conditions and following administration of synthetic thyrotropin-releasing-hormone (TRH). The stimulation with exogenous TSH was performed on 7 subjects. 131I uptake was depressed in all patients including those with solitary nodules. Free and total hormone concentrations were elevated in the three cases with diffuse gland involvement, whereas an increase of T3 alone was present in 3 patients with unilobar involvement. In the latter group and in the 2 patients with a nodular form T4, FT3 and FT4 levels were within normal limits. Interruption of the pituitary-thyroid feed-back mechanism with absence of thyrotropin response to TRH occurred in 11 patients, independent of whether thyroid hormone concentrations were elevated or normal. In one patient only with unilateral involvement, TSH responsiveness to TRH was normal while 131I uptake was not raised by exogenous TSH, indicating diffuse cellular damage. The normal values of FT3 and FT4 found in patients with normal T3 and T4 levels seem to exclude the possibility that the free hormones are responsible for the interrupted feed-back which represents the main cause of suppressed iodine uptake. However, it is possible that the pituitary-thyroid axis is responding to transient or light increases of free and total T3 and T4 still within their 'normal range'.

Free access

P Biassoni, G Ravera, J Bertocchi, F Schenone, and P Bourdoux

OBJECTIVE: In contrast with the endemic goiter reported in several African countries, the nomadic Bororos of the Central African Republic have an unexpectedly low prevalence of goiter. This study was conducted to elucidate this puzzling observation. DESIGN: Thyroid function and iodine and thiocyanate intakes were evaluated in Bororos and inhabitants of the same area and compared with an Italian population. RESULTS: Urinary iodine concentrations indicated moderate iodine deficiency in the rural people and the Bororos. In the latter, no individual with clinical hypothyroidism was observed. Compared with the reference population, the Bororos had slightly lower thyroxine (T4) and free thyroxine (FT4), slightly increased tri-iodothyronine (T3) and T3/T4 ratio, slightly higher TSH, normal serum thyroglobulin, a prevalence of goiter of 17.1% and a higher urinary thiocyanate. The rural people showed striking differences: lower T4 and FT4, increased T3/T4 ratio, markedly increased TSH and thyroglobulin, a prevalence of goiter of 76.9% and a high urinary thiocyanate, indicating frequent consumption of cassava. A dietary survey indicated that the Bororos ingest large amounts of milk and related products but infrequently eat cassava. CONCLUSION: A minute difference in iodine deficiency between two populations induces totally different patterns of goiter and thyroid function. The reason for such a contrast probably involves differences in diet.

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M Rotondi, G Mazziotti, F Sorvillo, M Piscopo, M Cioffi, G Amato, and C Carella

OBJECTIVE: To compare the effects of pregnancy on the serum free thyroxine (FT4) levels in two cohorts of primary hypothyroid women treated with different levothyroxine (L-T4) doses before gestation. DESIGN AND METHOD: Twenty-five women with compensated hypothyroidism of different aetiology (thyroidectomized and Hashimoto's thyroiditis) were enrolled in this prospective study. The women were receiving substitutive doses of L-T4 and were anticipating pregnancy. They were assigned to two groups: 14 patients (group I) were switched to partially suppressive treatment while 11 patients (group II) continued the same therapeutic regimen. RESULTS: Pre-conceptional thyroid function evaluation demonstrated significantly higher FT4 and lower TSH in group I (P<0.001, for both hormones) and comparable free 3,5,3'-triiodothyronine (FT3) levels. The first post-conception thyroid function evaluation occurred at a median time of 6 (5-8) and 7 (5-9) weeks of gestation, for groups I and II respectively (P<0.05); all women in group I showed adequate serum FT4 levels while three patients in group II showed low-normal FT4 levels and one case was below normal levels. Statistical analysis demonstrated significantly higher frequencies (0% vs 36.4%; P<0.05) of low-normal FT4 levels in patients receiving substitutive doses of L-T4. None of the Hashimoto's-affected patients showed low or low-normal serum FT4 levels regardless of their therapeutic regimen. CONCLUSION: Our results suggest that in hypothyroid women anticipating pregnancy (with serum TSH in the lower quartile of normal range), the pre-conception adjustment of L-T4 doses may result in adequate maternal thyroid function up to the first post-conception evaluation. The procedure seems safe and inexpensive; it may be a worthwhile treatment, at least in thyroidectomized women, in view of the well-known potential effects of even marginal maternal thyroid hypofunction on the subsequent IQ of the progeny.

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Giorgio Radetti, Claudio Paganini, Roberto Crepaz, Walter Pittscheider, and Lino Gentili

Radetti G, Paganini C, Crepaz R, Pittscheider W, Gentili L. Cardiovascular effects of long-term l-thyroxine therapy for Hashimoto's thyroiditis in children and adolescents. Eur J Endocrinol 1995;132:688–92. ISSN 0804–4643

Morphology and function of the left ventricle were evaluated by echo and Doppler examination in 16 females affected by Hashimoto's thyroiditis. aged 13.3 (4.5) years (range 7.9–24.6). They were on l-thyroxine (l-T4) treatment for a period of 2.8 (2.8) years (range 0.8–7.6) with a mean daily dose of 77 (18) μg/m2. Left ventricular mass, systolic and diastolic function, cardiac output and systemic vascular resistance did not differ from a control group matched for age, sex and body size. A further analysis of the patients according to thyrotrophin serum levels (less or more than 0.1 mU/l) gave similar results. Moreover, no relationship was found between echocardiographic findings and age, l-T4 daily doses, duration of treatment and serum level of thyroid hormones. We can therefore conclude that chronic l-T4 treatment for Hashimoto's thyroiditis at the given doses did not affect cardiac function and morphology in children and adolescents; however, a longer follow-up is needed before confirming the safety of this therapy in the long term.

Giorgio Radetti, Department of Paediatrics, Regional Hospital of Bolzano, via L Boehler no. 5, 39100 Bolzano, Italy

Free access

Nitash Zwaveling-Soonawala, M Emma Witteveen, Jan Pieter Marchal, Femke C C Klouwer, Nadine A Ikelaar, Anne M J B Smets, Rick R van Rijn, Erik Endert, Eric Fliers, and A S Paul van Trotsenburg

Objective

The hypothalamus–pituitary–thyroid (HPT) axis set point develops during the fetal period and first two years of life. We hypothesized that thyroxine treatment during these first two years, in the context of a randomized controlled trial (RCT) in children with Down syndrome, may have influenced the HPT axis set point and may also have influenced the development of Down syndrome-associated autoimmune thyroiditis.

Methods

We included 123 children with Down syndrome 8.7 years after the end of an RCT comparing thyroxine treatment vs placebo and performed thyroid function tests and thyroid ultrasound. We analyzed TSH and FT4 concentrations in the subgroup of 71 children who were currently not on thyroid medication and had no evidence of autoimmune thyroiditis.

Results

TSH concentrations did not differ, but FT4 was significantly higher in the thyroxine-treated group than that in the placebo group (14.1 vs 13.0 pmol/L; P = 0.02). There was an increase in anti-TPO positivity, from 1% at age 12 months to 6% at age 24 months and 25% at age 10.7 years with a greater percentage of children with anti-TPO positivity in the placebo group (32%) compared with the thyroxine-treated group (18.5%) (P = 0.12). Thyroid volume at age 10.7 years (mean: 3.4 mL; range: 0.5–7.5 mL) was significantly lower (P < 0.01) compared with reference values (5.5 mL; range: 3–9 mL) and was similar in the thyroxine and placebo group.

Conclusion

Thyroxine treatment during the first two years of life led to a mild increase in FT4 almost 9 years later on and may point to an interesting new mechanism influencing the maturing HPT axis set point. Furthermore, there was a trend toward less development of thyroid autoimmunity in the thyroxine treatment group, suggesting a protective effect of the early thyroxine treatment. Lastly, thyroid volume was low possibly reflecting Down-specific thyroid hypoplasia.

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B.-A. Lamberg, S. Rosengård, K. Liewendahl, P. Saarinen, and D. C. Evered

ABSTRACT

A male aged 21 was found to have elevated serum PBI on several occasions. Further studies revealed clinical euthyroidism with raised serum concentrations of T4, T3 and free T4 with normal hormone binding capacity of the thyroxine binding proteins and normal thyroid-pituitary relationships. The response to TRH was high normal or on one occasion exaggerated. The extrathyroidal thyroxine pool and the daily turnover of thyroxine were considerably above the upper limit of the normal. The subject had no goitre. These findings indicated partial peripheral resistance to thyroid hormones including the pituitary gland. There were no circulating antibodies to thyroglobulin, thyroid microsomes, T4 or T3. A study of the propositus' family revealed an autosomal dominant heredity of this abnormality. Similar findings were found in the brother, mother and the two uncles of the propositus. In these subjects the serum concentrations of T4, T3 and free T4 as well as that of rT3 were raised above the normal. The subjects studied were clinically euthyroid. Goitre was present only in the older members of the family. The response to TRH was usually high normal or at times exaggerated and the basal TSH level seemed to fluctuate during years of follow-up indicating a continuous adjustment of the thyroid function by means of TSH secretion. The mother and the older uncle had previously been treated because of hyperthyroidism. Only the mother had circulating thyroid antibodies and none of the family members had antibodies against T4 or T3. This hereditary condition seems to have a very mild clinical manifestation in this family.

Open access

Claire L Wood, Michael Cole, Malcolm Donaldson, David B Dunger, Ruth Wood, Niamh Morrison, John N S Matthews, Simon H S Pearce, Timothy D Cheetham, and the British Society for Paediatric Endocrinology and Diabetes (BSPED)

Objective

First-line treatment of thyrotoxicosis in young people is thionamide anti-thyroid drug (ATD) in a blocking dose with levothyroxine replacement (block and replace, BR) or in a smaller dose tailored to render the patient euthyroid (dose titration, DT). Our objective was to determine which regimen provides more stable biochemical control.

Design

A multi-centre phase III, open-label randomised trial comparing BR with DT in patients aged 2–17 years with newly diagnosed thyrotoxicosis at 15 UK centres.

Methods

Patients were randomised shortly after diagnosis and treated for 3 years. The primary outcome was the percentage of serum thyroid-stimulating hormone (TSH) levels in the reference range between 6 months and 3 years. Secondary outcomes included the proportion of Free thyroxine (FT4) levels in the reference range, adverse event frequency and 4 years outcome (remission/relapse).

Results

Eighty-two patients were randomised, with details on clinical course in 81 (62 Female); 40 were allocated to BR (41 DT). Three withdrew with one ineligible. The mean percentage of serum TSH within reference range was 60.2% in BR and 63.8% in DT patients; adjusted difference 4.3%, 95% CI (−7.8 to 16.4); P = 0.48. Proportions for FT4 were 79.2% in BR and 85.7% in DT patients; adjusted difference 6.8%, (−0.2 to 15.6); P = 0.13. Three patients developed neutropenia – all on BR. 6 BR and 10 DT patients were in remission at 4y.

Conclusion

This randomised trial has shown no evidence to suggest that BR, when managing the young patient with thyrotoxicosis, is associated with improved biochemical stability when compared to DT.

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Kimio Nakanishi, Yoshiyasu Taniguchi, and Yasuyuki Ohta

Abstract.

We measured soluble interleukin 2 receptor, a part of the Tac protein (p55), in peripheral blood to study the immunological condition of the T cell in autoimmune thyroid disease. In 26 patients with untreated Graves' disease and 7 hyperthyroid patients with Hashimoto's thyroiditis, the mean levels of soluble IL-2 receptor were both significantly higher than in normal controls (1497±649 (mean ± sd), 641±137 vs 221±63 103 U/l, p<0.001). There was good correlation between soluble IL-2 receptor levels and blood thyroxine levels (r=0.684, p<0.001) in patients with untreated Graves' disease, but no correlation of soluble IL-2 receptor with TSH-inhibitory immunoglobulins, TS-ab, thyroidal autoantibodies to thyroglobulin and thyroidal microsomal antigen was found. We thought that the level of soluble IL-2 receptor is not dependent only on immunological conditions, but also on thyroid hormone status. When T3 was administered to subjects in remission from Graves' disease and in normal controls, the soluble IL-2 receptor levels significantly increased. Moreover, the mean level of soluble IL-2 receptor in patients with toxic multinodular goitre was also significantly higher than in normal controls (411±148 vs 221±63 103U/l, p<0.05). We conclude that the soluble IL-2 receptor levels are higher in sera of subjects with elevated levels of thyroid hormone.

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S Corbetta, P Englaro, S Giambona, L Persani, WF Blum, and P Beck-Peccoz

Leptin is the protein product of the ob gene, secreted by adipocytes. It has been suggested that it may play an important role in regulating appetite and energy expenditure. The aim of this study was to evaluate a possible interaction of thyroid hormones with the leptin system. We studied 114 adult patients (65 females and 49 males): 36 were affected with primary hypothyroidism (PH), 38 with central hypothyroidism (CH) and 40 with thyrotoxicosis (TT). Patients with CH were studied both before and after 6 months of L-thyroxine replacement therapy. Body mass index (BMI; kg/m2), thyroid function and fasting serum leptin were assessed in all patients. Since BMI has been proved to be the major influencing variable of circulating leptin levels, data were expressed as standard deviation score (SDS) calculated from 393 male and 561 female controls matched for age and BMI. No difference in SDS was recorded between males and females whatever the levels of circulating thyroid hormones. In males, no significant difference was recorded among the SDSs of PH (-0.36 +/- 1.2), TT (-0.35 +/- 1.2) and CH (0.01 +/- 1.4) patients. Females with PH had an SDSs significantly lower than TT females (-0.77 +/- 1.0 vs -0.06 +/- 1.2; P < 0.02), while no significant differences between CH (-0.34 +/- 0.7) and TT females or between CH and PH females were observed. SDS in CH patients after 6 months of L-thyroxine therapy significantly varied only in females (0.25 +/- 1.4). In conclusion, circulating thyroid hormones do not appear to play any relevant role in leptin synthesis and secretion. However, as females with either overt hypo- or hyper-thyroidism or central hypothyroidism after L-thyroxine therapy show differences in their SDSs, a subtle interaction between sex steroids and thyroid status in modulating leptin secretion, at least in women, may occur.