The thyroid status was investigated in 26 pregnant African women at term delivery in an iodine-deficient region (Jengere) of Nigeria, West Africa including the measurement of serum T4, T3, TSH, thyroxine binding capacity, TBG, free thyroxine index (FT4I) and the results were matched with those obtained in a corresponding group of 46 women at delivery in Jos, the non-iodine-deficient region which was used as a control. Corresponding cord-blood samples were obtained from all the neonates of the two groups. Twenty-three urinary samples in the former and 14 in the latter group were analysed for iodide levels to ascertain the degree of iodine deficiency. The results demonstrate that compared to the values seen in the Jos group the maternal serum T4, T3 and FT4I levels were significantly reduced in the iodine-deficient group, while TSH, TBG and thyroxine binding capacity were elevated. Cord serum samples showed a corresponding fall in T4 and FT4I levels in the group from the iodine-deficient region, while the T3 levels were significantly elevated with a concurrent significant rise in TSH and TBG levels. Significant correlations were found between the maternal and cord serum T4, TSH, TBG, thyroxine binding capacity and FT4I levels, but not T3. From these findings we suggest that fetal T3 plays an important defensive role against the danger of long-standing environmental iodine deficiency.
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Amirav Gordon and Theodore Coutsoftides
The binding properties of mouse serum for L-3'5'3,5 tetraiodothyronine (T4) and L-3'3,5, triiodothyronine (T3) were investigated by agar gel electrophoresis in several buffer systems at pH 7.4 and pH 8.6. Mouse serum binds T4 and T3 in the albumin and the α-globulin regions; these were designated as mouse thyroxine binding albumin (TBA) and mouse thyroxine binding globulin (TBG). The fractional distribution of T4 varied with the buffer, the pH and the molarity of the system. Mouse TBG contained two binders, the first with a binding capacity of 14.0 × 10−7 m and the second with a binding capacity of 54.3 × 10−7 m. The effect of various inhibitors on thyroxine binding by mouse TBG suggests that mouse TBG behaves in some respects like human TBG and in other respects like human thyroxine-binding pre-albumin (TBPA).
Johannes Pfeilschifter and Reinhard Ziegler
Based on findings that thyroxine may have a beneficial effect on the recurrence of Graves' hyperthyroidism, we prospectively studied the effects of a TSH suppressive treatment with thyroxine on the course of Graves' disease in fifty patients with recent onset of hyperthyroidism. After the normalization of serum tri-iodothyronine (T3) and thyroxine (T4) concentrations, one group of patients was randomly assigned to a combined treatment with carbimazole and a TSH suppressive dose of T4 for 12 months, followed by another 12 months of TSH suppressive therapy alone. The other group of patients also received carbimazole for one year, but T4 was only added as indicated to normalize elevated TSH serum concentrations, and patients received no therapy during the second year. By the end of the second year, a relapse of hyperthyroidism had occurred in 43% of the patients with and in 45% of the patients without suppressive T4 treatment. In those patients without a relapse of hyperthyroidism, initial thyroid size significantly (P = 0·01) decreased with time in both treatment groups. However, patients on suppressive T4 treatment tended to have a greater reduction in thyroid volume than patients with normal TSH serum concentrations (P = 005). In conclusion, we were unable to detect a preventive effect of exogenous TSH suppression on the recurrence of hyperthyroidism. However, our data suggest that TSH suppressive treatment may have a beneficial effect on thyroid enlargement in Graves' disease.
European Journal of Endocrinology 136 81–86
Shi-Wen Kuo, Wen-Sheng Huang, Chan-An Hu, Wen-Kuei Liao, Tsi-Chiang Fung, and Sing-Yung Wu
Kuo SW, Huang W-S, Hu C-A, Liao W-K, Fung T-C, Wu S-Y. Effect of thyroxine administration on serum thyrotropin receptor antibody and thyroglobulin levels in patients with Graves' hyperthyroidism during antithyroid drug therapy. Eur J Endocrinol 1994;131:125–30. ISSN 0804–4643
Graves' hyperthyroidism is due primarily to overproduction of antibodies to thyrotropin receptors (TR-ab), which stimulate the thyroid gland and cause hyperthyroidism. Antibody production during antithyroid drug therapy is an important determinant of the course of the disease. We therefore observed the changes of serum TR-ab, thyroglobulin (Tg) and thyroid hormone levels in response to administration of l-thyroxine (T4) in Graves' hyperthyroid patients during antithyroid drug therapy. Serum levels of TR-ab, Tg and other thyroid hormones were measured by radioimmunoassay (RIA) during either methimazole treatment alone or in combination with thyroxine in 60 Graves' hyperthyroid patients. The patients initially were treated with 30 mg of methimozole daily for 3 months, which was then reduced to 15 mg daily for the following 3 months. All patients were euthyroid 6 months after the start of antithyroid therapy and the TR-ab level decreased from 61 ± 11% (±sd) to 28 ± 7% (p < 0.01). Patients then were divided into three groups: group A (N = 25), whose TR-ab level was 10% or more (the cut-off value for positivity), received 0.1 mg of T4 and 10 mg of methimazole daily for 6 months; group B (N = 15), whose TR-ab level also was 10% or more and was age- and thyroid function-matched with group A, received only 10 mg of methimazole daily for 6 months; group C (N = 20), with a TR-ab level of less than 10%, received 10 mg of methimazole alone daily for 6 months. In the T4-treated group (group A), the mean serum T4 level increased from 66 ± 21 to 117 ± 30 nmol/l (p < 0.05) and the TR-ab and Tg concentrations decreased from 38 ± 11 to 10 ± 5% (p < 0.01) and 135 ± 25 to 45 ± 12 μg/l (p < 0.01), respectively, after 6 months of combination therapy. In the non-T4-treated groups (groups B and C), the mean serum T4, TR-ab and Tg levels did not change significantly (p > 0.05). Serum TR-ab levels at the end of the combination therapy (group A) were significantly lower than with methimazole alone (27 ± 11%, p < 0.05). Serum TR-ab levels correlated positively with the serum Tg concentrations and ultrasonogram-measured thyroid volume in untreated (r = 0.281, p < 0.05 and r = 0.485, p < 0.001, respectively) and treated (r = 0.288, p < 0.05 and r = 0.480, p < 0.001, respectively) Graves' hyperthyroid patients after the first 6 months of methimazole therapy. A positive correlation was found between thyroid volume and serum Tg concentration before (r = 0.31, p < 0.01) and after (r = 0.450, p < 0.001) the first 6 months of methimazole therapy. However, the serum levels of thyrotropin were not correlated with those of TR-ab and Tg (p > 0.05) after methimazole therapy. In summary, the present study demonstrated a greater fall in serum TR-ab and Tg levels in patients with Graves' disease treated with combined methimazole and T4 than with methimazole alone.
Sing-Yung Wu, Station 151, Department of Nuclear Medicine and Medical Services, VA Medical Center, Long Beach, CA 90822, USA
W. Hung, R. W. Chandler, M. A. Kyle, and R. M. Blizzard
Thyroid hormone synthesis in rabbits with experimentally induced thyroiditis is compared with hormone synthesis in normal rabbits and in immunized rabbits receiving thyroid stimulating hormone. The immunized rabbits showed decreased thyroidal accumulation rates for 131I. T. S. H. administration produced an increase in the accumulation rate of immunized animals, but this increase was smaller than that obtained in normal rabbits stimulated with T. S. H. None of the rabbits' thyroids discharged iodide with the administration of potassium thiocyanate.
Twenty-four and 48 hours after 131I was administered, chromatography was performed on digested extracts of the thyroid glands. In the digested extracts of thyroids removed from normal rabbits the mono:diiodotyrosine ratio was greater than 1.0 whereas the extracts of thyroids removed from immunized rabbits and normal rabbits stimulated with T. S. H. consistently had a ratio of less than 1.0.
Thyroxine was not always present in the thyroids of normal rabbits but was consistently found in the thyroids of the immunized and T. S. H. treated animals. These findings suggest that the remaining thyroid cells in the glands of immunized rabbits are operating under increased T. S. H. stimulation.
The experimental thyroiditis of immunized rabbits was similar to Hashimoto's thyroiditis in respect to histological alteration and the presence of anti-thyroid antibodies. 131I accumulation rates, response to potassium thiocyanate, and chromatography studies revealed no correlation between the two groups.
Geraldo A. Medeiros-Neto, Meyer Knobel, Marcello D. Bronstein, José Simonetti, Fadlo Fraige Filho, and Emilio Mattar
A 19 year old man had congenital hypothyroidism and severely retarded development. His thyroid gland was not enlarged and laboratory findings included low serum concentration of T4 (2.8 μg/100 ml) and T3 (16 ng/100 ml) with a high level of TSH (52 μU/ml) that rose to 192 μU/ml after TRH. 131I uptake by the thyroid was normal (41.5 % at 24 h) and did not show a normal increase after exogenous TSH administration (49.5 % at 24 h). The perchlorate discharge test was negative and no antibodies against thyroid antigens were found. Studies on the biopsy specimen revealed low iodide trapping by the thyroid slices and no formation of cyclic AMP after TSH was added to the medium. The endogenous TSH of the patient was biologically active increasing cyclic adenosine monophosphate c-AMP concentration in normal thyroid slices. No thyroglobulin was found in the thyroid tissue either by immunological or ultracentrifugational methods. An increased proportion of iodoalbumin was present in the serum. We postulate that the fundamental defect in this gland is an impaired generation of c-AMP by the defective thyroid cell and deficiency of thyroglobulin formation resulting in inadequate thyroxine and triiodothyronine synthesis.
The inhibition of thyroidal hormone synthesis by propylthiouracil (PTU) was studied in intact, hypophysectomized and thyroxine-treated rats. Animals were fed a low iodine diet for 7 days before hypophysectomy or before thyroxine injection was started and continued on this diet for one more week up to autopsy. Graded doses of PTU were administered once daily for the last 2 days before autopsy. Radioiodine was given intraperitoneally immediately after the last dose of PTU and thyroids were removed 24 hours later.
In intact animals fed a low iodine diet for 2 weeks, the formation of T3 + T4 was the most easily, the formation of DIT next and the formation of MIT the least easily inhibited by PTU. In contrast, the formation of MIT and DIT in hypophysectomized and in thyroxine-treated animals given graded doses of PTU was apparently inhibited to an equal extent. No iodothyronines were formed in the hypophysectomized rats and very little was formed in the thyroxine-treated rats which did not receive PTU. Approximately 10 times as much PTU was required to depress MIT and DIT formation to an equivalent extent in the thyroxine-treated as in the hypophysectomized animals.
J. Sinadinović, M. Krainčanić, G. Kostić, and M. Jovanović
The effects of short- and long-term (from 3 days to 28 weeks) administration of excess thyroxine in the form of the iodinated casein "Protamone" (0.2%) to rats on the content of soluble thyroid iodoproteins and on biosynthesis and polymerization of thyroid proteins in vitro were investigated. The concentration of soluble iodoproteins significantly increased (40–80%) up to 2 weeks of treatment, and after that remained at the same level. 27S iodoprotein markedly increased during thyroxine treatment. The content of DNA in the gland and the thyroid weight were a little lower in the treated rats than in the control.
The incorporation rate of [14C]leucine into soluble and microsome-bound proteins in vitro was markedly reduced in the treated animals (30–80 % of control). Thyroxine pre-treatment of rats induced retarded synthesis of thyroglobulin and its subunits in vitro. The inhibition of the synthesis of thyroid proteins in vitro and the incrrease in the soluble iodopritein content in the gland in vivo was not correlated with the duration of thyroxine treatment.
The immobilization of pre-formed thyroglobulin in the follicle lumen for a long time period is probably an important factor in the enlarged conversion of thyroglobulin into 27S iodoprotein.
In conclusion, the long-term suppression of endogenous TSH secretion by administration of thyroxine results in an accumulation of iodoproteins in the thyroid and a reduced rate of synthesis of iodoproteins; after 2 weeks a steady state is reached both with regard to iodoprotein accumulation and synthesis. Finally, the results obtained suggest that the thyroid-pituitary axis becomes adapted to chronic administration of excess thyroxine.
Marek Ruchala, Ewelina Szczepanek-Parulska, Ariadna Zybek, Jerzy Moczko, Agata Czarnywojtek, Grzegorz Kaminski, and Jerzy Sowinski
Reports on sonoelastography, which provide an objective estimation of tissue elasticity, are scarce in terms of thyroiditis. The aim of this study was to prospectively assess the applicability of sonoelastography in different types of thyroiditis.
The study assessed and compared the thyroid tissue stiffness in patients with acute thyroiditis (AT), subacute thyroiditis (SAT), and chronic autoimmune thyroiditis (CAT) with healthy control subjects (CS), followed up for 10 weeks.
The study group consisted of two patients with AT, 18 patients with SAT, 18 patients with CAT, and 40 CS matched for age and gender. Sonoelastography was performed at baseline, at a 4-week follow-up during treatment, and at 10 weeks following diagnosis and treatment initiation.
Thyroid tissue stiffness was higher in SAT at baseline (214.26±32.5 kPa) in comparison with values recorded at a 4-week follow-up (45.92±17.4 kPa) and at 10 weeks following diagnosis and treatment initiation (21.65±5.3 kPa, P<0.0001). Baseline thyroid stiffness in SAT was higher than that found in CAT (36.15±18.7 kPa, P<0.0001) and CS (16.18±5.4 kPa, P<0.0001). In the remission of SAT, thyroid stiffness was lower than that found in CAT (P=0.006), while it was higher than that in CS (P=0.0008). No difference was observed between thyroid stiffness in SAT at 4-week follow-up and in CAT. Patients with CAT presented higher thyroid stiffness than CS (P<0.0001), which was not influenced by l-thyroxine treatment. Thyroid stiffness in patients with AT was 216.6 and 241.9 kPa at baseline; after treatment, it decreased to 17.93 and 85.348 kPa respectively.
Sonoelastography may assist in the diagnosis and treatment monitoring of AT, SAT and CAT, as well as in the differentiation of the various types of thyroiditis.
Y. Rakover, O. Sadeh, E. Sobel, A. Shneyour, and Z. Kraiem
Transient neonatal hypothyroidism has been observed in three successive offspring of a mother with autoimmune thyroiditis. Thyroxine replacement therapy was initiated in a 23-year-old woman with overt clinical and laboratory findings of non-goitrous primary hypothyroidism. While on such treatment, she gave birth to three infants manifesting hypothyroidism immediately after birth. The neonates were treated with thyroxine replacement therapy which was discontinued in the three siblings at ages 2½ years, 3½ years, and 13 months. Continuous observation following cessation of therapy revealed clinical and biochemical euthyroidism in the children. Thyroid scanning during the neonatal period in the first child failed to identify functional thyroid tissue, suggesting thyroid agenesis, whereas thyroid scan performed on subsequent follow-up revealed a normal gland. Sequential serum measurements of autoantibodies directed towards the thyrotropin receptor were made in the mother and third child by a cAMP bioassay. High titres (five-six fold above normal) of blocking antibodies (tested by measuring the inhibition of TSH-stimulated cAMP production of cultured human thyroid cells by serum immunoglobulin preparations) were present in the mother and newborn 10 days after birth. The levels remained persistently high in the mother, whereas they declined and were undetectable in the child at four months. Thyroid-stimulating immunoglobulin was absent in both mother and child. The data are compatible with transient neonatal hypothyroidism caused by transplacental transfer of antibodies which block thyroid response to TSH. The half-life of the maternally-derived blocking antibody in the infant was estimated as 1-2 months. This is the first report on sequential serum measurements and estimate of half-life of the blocking antibodies performed by a cAMP bioassay (using thyroid cells of human origin). Unlike the radioreceptor assay employed so far in such cases, this assay can distinguish between stimulating and blocking TSH receptor antibodies.