sodium-perchlorate and Goiter

Topics: Carrier Proteins; Deafness; Goiter; Humans; Hypothyroidism; Membrane Transport Proteins; Mutation; Perchlorates; Sodium Compounds; Sulfate Transporters; Syndrome; Thyroid Hormones

Topics: Aged; Aging; Contrast Media; Goiter; Humans; Iodine; Perchlorates; Sodium Compounds; Thyrotoxicosis; Thyrotropin

Although thyroid-stimulating hormone (TSH) is known to be a major regulator of thyroid hormone biosynthesis and thyroid growth, insulin-like growth factor 1 (IGF-1) is required for mediating thyrocyte growth in concert with TSH in vitro. We generated mice with thyrocyte-selective ablation of IGF-1 receptor (TIGF1RKO) to explore the role of IGF-1 receptor signaling on thyroid function and growth. In 5-wk-old TIGF1RKO mice, serum thyroxine (T4) concentrations were decreased by 30% in concert with a 43% down-regulation of the monocarboxylate transporter 8 (MCT8), which is involved in T4 secretion. Despite a 3.5-fold increase in circulating concentrations of TSH, thyroid architecture and size were normal. Furthermore, thyrocyte area was increased by 40% in WT thyroids after 10 d TSH injection, but this effect was absent in TSH-injected TIGF1RKO mice. WT mice treated with methimazole and sodium perchlorate for 2 or 6 wk exhibited pronounced goiter development (2.0 and 5.4-fold, respectively), but in TIGF1RKO mice, goiter development was completely abrogated. These data reveal an essential role for IGF-1 receptor signaling in the regulation of thyroid function and TSH-stimulated goitrogenesis.

Topics: Animals; Antithyroid Agents; Down-Regulation; Goiter; Membrane Transport Proteins; Methimazole; Mice; Mice, Knockout; Monocarboxylic Acid Transporters; Perchlorates; Receptor, IGF Type 1; Sodium Compounds; Symporters; Thyroid Gland; Thyrotropin; Thyroxine

Thirty eight children suffering from congenital primary permanent hypothyroidism were studied to determine the diagnostic impact of 123I scintigraphy in comparison to laboratory findings and ultrasonography.. In all patients 123I scintigraphy was performed after intravenous administration of 3.7 MBq 123I. If accumulation of the radiotracer in thyroid tissue occurred a perchlorate discharge test was performed subsequently.. Scintigraphy revealed athyrosis in 7 children. In 9 children a lingual thyroid was observed. Deficiency in iodine organification was diagnosed by a significant discharge of 123I in 15 patients. In four of these children the diagnosis of Pendred's syndrome could be established. Ectopic thyroid tissue could be demonstrated only by scintigraphy where clinical examination and sonography failed in the diagnosis in all cases. Hypoplasia of the thyroid gland as it was diagnosed in 2 cases by ultrasonography appeared to be unlikely because a normal 123I uptake was seen in these patients. In 2 patients with scintigraphic proven athyrosis an orthotopic gland had been falsely considered by ultrasound. In 44% of our patients the final diagnosis could only be established if 123I scintigraphy and perchlorate discharge test were performed.. This findings suggest that scintigraphy is indispensible in the correct diagnostic work up of congenital hypothyroidism.

Topics: Child; Child, Preschool; Congenital Hypothyroidism; Diagnosis, Differential; Female; Goiter; Hearing Loss, Sensorineural; Humans; Hypothyroidism; Iodine Radioisotopes; Male; Perchlorates; Radionuclide Imaging; Sodium Compounds; Syndrome; Thyroid Gland; Ultrasonography

Free radical damage and fibrosis caused by selenium deficiency are thought to be involved in the pathogenesis of myxoedematous cretinism. So far, no pathway explains the link between selenium deficiency and tissue fibrosis. Pharmacological doses of iodine induce necrosis in iodine-deficient thyroids. Necrosis is much increased if the glands are also selenium-deficient, which then evolve to fibrosis. This rat model was reproduced to explore the role of selenium deficiency in defective tissue repair. At first, proliferation indexes of epithelial cells and fibroblasts were comparable between selenium-deficient and control groups. Then, in selenium-deficient thyroids the inflammatory reaction was more marked being mainly composed of macrophages. The proliferation index of the epithelial cells decreased, while that of the fibroblasts increased. These thyroids evolved to fibrosis. TGF-beta immunostaining was prominent in the macrophages of selenium-deficient rats. Anti TGF-beta antibodies restored the proliferation indexes, and blocked the evolution to fibrosis. In selenium deficiency, an active fibrotic process occurs in the thyroid, in which the inflammatory reaction and an excess of TGF-beta play a key role.

Topics: Animals; Cell Division; Epithelial Cells; Female; Fibroblasts; Fibrosis; Goiter; Inflammation; Macrophages; Perchlorates; Rats; Rats, Wistar; Selenium; Sodium Compounds; Sodium Iodide; Thyroid Gland; Transforming Growth Factor beta

Topics: Child; Child, Preschool; Deafness; Female; Goiter; Humans; Iodides; Male; Perchlorates; Sodium Compounds; Syndrome