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Abstract: Thyroid transcription factor-1 (TTF-1) is a key regulator of thyroid development and function. In order to identify the genes whose expression depends on TTF-1 transcriptional activity within the thyrocyte we analyzed the consequence of the functional inactivation of this factor in PCCl3 cells. The expression of a fusion protein composed of the DNA binding domain of TTF-1 and of the strong repressive domain of the engrailed protein resulted in a dramatic loss of epithelial cell morphology and in proliferation arrest. These changes were reversed when the inhibition of endogenous TTF-1 was relieved. No change was observed when a similar fusion protein containing point mutations abolishing DNA binding activity was produced in the cells. Besides the expected down-regulation of expression of the main genes linked to the differentiated thyroid function, we observed a decreased expression of the transcription factors Hhex, Pax 8 and TTF-2 and of E-cadherin. By contrast, both ThOX-1 and DUOXA-1 genes were up-regulated, as well as the ones encoding vimentin and several proteins involved in cell cycle arrest. Our data thus extend the known roles of TTF-1 in thyroid development and in the expression of differentiated function in the adult organ to the control of epithelial morphology and of cell division in mature thyrocytes. [Copyright &y& Elsevier]

Female F344 rats were exposed to 4,4′-methylenebis(N,N′-dimethyl)aniline (MDA) by dietary feed at concentrations of 0, 50, 200, 375, 500, or 750 ppm for 5 d, 2 wk, 4 wk, and 13 wk duration. Endpoints evaluated included clinical observations, body weights, thyroid weights, serum thyroid hormones, blood MDA, gross pathology, and thyroid histopathology. There were no MDA exposure-related clinical signs of toxicity. Mean body weight decreased 5% compared to control in the 750 ppm group during study wk 6 through 13. Serum TSH increased and serum T4 and T3 levels decreased with increasing feed concentrations of MDA and time of exposure. Thyroid weight increases were both concentration- and exposure time-dependent and statistically significant at ≥375 ppm. Incidence and severity of decreased colloid, follicular cell hypertrophy and follicular cell hyperplasia were also related to MDA concentration and exposure time. A no-observed-adverse-effect level (NOAEL) of 200 ppm was selected based on the statistically significant increase in incidence of follicular cell hyperplasia at concentrations ≥375 ppm. [ABSTRACT FROM AUTHOR]

Abstract: Iodine is required for the production of thyroid hormones. Normal thyroid function during pregnancy is important for both the mother and developing fetus. This review discusses the changes in thyroid physiology that occur during pregnancy, the significance of thyroid function tests and thyroid antibody titers assessed during pregnancy, and the potential obstetric complications associated with maternal hypothyroidism. [Copyright &y& Elsevier]

Incidences and morphological features of thyroid proliferative lesions induced by carcinogens in Wistar Hannover GALAS rats (GALAS rats) showing normal growth with or without thyroid dysplasia were examined. All thyroid tissue samples were obtained from our recently conducted study using male GALAS rats treated with 5 carcinogens according to the medium-term multiorgan carcinogenicity bioassay protocol (called DMBDD treatment). In the DMBDD-treated rats, thyroid dysplasia was found in 9 out of 114 rats. Follicular cell adenomas were found in 5 out of 9 rats with thyroid dysplasia and in 7 out of 105 rats without thyroid dysplasia. The incidence of adenoma was significantly increased in rats with thyroid dysplasia (55.6%) compared with that in rats without thyroid dysplasia (6.7%). Adenomas in rats with thyroid dysplasia were observed as single or multiple nodules, well demarcated and composed of variously sized vacuolated cells or unvacuolated cells. These histopathological features and staining profiles of luminal colloid for PAS and thyroglobulin, together with PCNA-positive cells, were fundamentally similar to those of rats without thyroid dysplasia. On the other hand, the luminal colloid in adenomas of rats with thyroid dysplasia had a tendency to be poorly stained for T4 compared with that of rats without thyroid dysplasia. From these findings, it appears that dysplastic thyroids of rats showing normal growth are more sensitive to carcinogens than normal thyroids. In addition, the morphological features of carcinogen-induced thyroid proliferative lesions in GALAS rats with thyroid dysplasia were fundamentally similar to those of rats without thyroid dysplasia, except for the vacuoles and T4 staining profile. (DOI: 10.1293/tox.25.11; J Toxicol Pathol 2012; 25: 11-17) [ABSTRACT FROM AUTHOR]

Abstract: Iodine is a critical element involved in thyroid hormone synthesis. Its efflux into the follicular lumen is thought to occur, in part, through pendrin at the apical membrane of thyrocytes. This study attempted to investigate whether iodide administration affects SLC26A4 mRNA expression in rat thyroid and in PCCl3 cells. Rats and cells were treated or not with NaI from 30min up to 48h. One group was concomitantly treated with sodium perchlorate. SLC26A4 mRNA expression was also investigated in PCCl3 cells treated with actinomycin D prior to NaI treatment. Iodide administration significantly increased SLC26A4 mRNA content in both models. The simultaneous administration of NaI and perchlorate, as well as the treatment of PCCl3 cells with actinomycin D prevented this effect, indicating that intracellular iodide is essential for this event, which appears to be triggered by transcriptional mechanisms. These data show that intracellular iodide rapidly upregulates SLC26A4 mRNA expression. [Copyright &y& Elsevier]

Aim. The primary objective of the study was to assess the iodine nutritional status, and its effect on thyroid function, of pregnant women in a private obstetrical practice in Sydney. Methods. It was a cross-sectional study undertaken between November 2007 and March 2009. Blood samples were taken from 367 women at their first antenatal visit between 7 and 11 weeks gestation for measurement of thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels and spot urine samples for urinary iodine excretion were taken at the same time as blood collection. Results. The median urinary iodine concentration (UIC) for all women was 81μg/l (interquartile range 41-169μg/l). 71.9% of the women exhibited a UIC of <150μg/l. 26% of the women had a UIC < 50μg/l, and 12% had a UIC <20μg/l. The only detectable influences on UIC were daily milk intake and pregnancy supplements. There was no statistically significant association between UIC and thyroid function and no evidence for an effect of iodine intake on thyroid function. Conclusions. There is a high prevalence of mild to moderate iodine deficiency in women in Western Sydney but no evidence for a significant adverse effect on thyroid function. The 6.5% prevalence of subclinical hypothyroidism is unlikely to be due to iodine deficiency. [ABSTRACT FROM AUTHOR]

The relation between thyroid function and depression has long been recognized. Patients with thyroid disorders are more prone to develop depressive symptoms and conversely depression may be accompanied by various subtle thyroid abnormalities. Traditionally, the most commonly documented abnormalities are elevated T4 levels, low T3, elevated rT3, a blunted TSH response to TRH, positive antithyroid antibodies, and elevated CSF TRH concentrations. In addition, thyroid hormone supplements appear to accelerate and enhance the clinical response to antidepressant drugs. However, themechanisms underlying the interaction between thyroid function and depression remain to be further clarified. Recently, advances in biochemical, genetic, and neuroimaging fields have provided new insights into the thyroid-depression relationship. [ABSTRACT FROM AUTHOR]

Background: Celiac disease (CD) is closely associated with other autoimmune endocrine disorders, particularly autoimmune thyroid disease. The aim of this study was to find the frequency of celiac disease in patients with hypothyroidism in Guilan province, north of Iran. Methods. A total of 454 consecutive patients with hypothyroidism underwent celiac serological tests antiGliadin antibodies (AGA), antitissue transglutaminase antibodies (IgA-tTG) and antiendomysial antibodies (EMA-IgA). Small intestinal biopsy was performed when any of celiac serological tests was positive. Results. Eleven (2.4%) patients were positive for celiac serology, and two patients with documented villous atrophy were diagnosed with classic CD (0.4%; 95%). Two patients with classic CD had Hashimoto's thyroiditis (HT) (0.6%; 95%). Six (54.5%) of 11 were suffering from overt hypothyroidism and 45.5% from subclinical hypothyroidism. Six (54.5%) had HT, and 45.5% had nonautoimmune hypothyroidism. Conclusions. In this study, prevalence of CD was lower than other studies. Most of the patients with CD were suffering from HT, but there was no significant statistical relation between CD and HT. [ABSTRACT FROM AUTHOR]

This paper provides the reader with an overview of our current knowledge of hypothalamic-pituitary-thyroid feedback from a cybernetic standpoint. Over the past decades we have gained a plethora of information from biochemical, clinical, and epidemiological investigation, especially on the role of TSH and other thyrotropic agonists as critical components of this complex relationship. Integrating these data into a systems perspective delivers new insights into static and dynamic behaviour of thyroid homeostasis. Explicit usage of this information with mathematical methods promises to deliver a better understanding of thyrotropic feedback control and new options for personalised diagnosis of thyroid dysfunction and targeted therapy, also by permitting a new perspective on the conundrum of the TSH reference range. [ABSTRACT FROM AUTHOR]

Graves' disease is a most common cause of hyperthyroidism. It is an autoimmune disease, and autoimmune process induces an inflammatory reaction, and reactive oxygen species (ROSs) are among its products. When balance between oxidants and antioxidants is disturbed, in favour of the oxidants it is termed "oxidative stress" (OS). Increased OS characterizes Graves' disease. It seems that the level of OS is increased in subjects with Graves' ophthalmopathy compared to the other subjects with Graves' disease. Among the other factors, OS is involved in proliferation of orbital fibroblasts. Polymorphism of the 8-oxoG DNA Nglycosylase 1 (hOGG1) involved in repair of the oxidative damaged DNA increases in the risk for developing Grave's disease. Treatment with glucocorticoids reduces levels of OS markers. A recent large clinical trial evaluated effect of selenium on mild Graves' ophthalmopathy. Selenium treatment was associated with an improved quality of life and less eye involvement and slowed the progression of Graves' orbitopathy, compared to placebo. [ABSTRACT FROM AUTHOR]

Two TRAbs: TSBAb and TSAb. TSBAb causes hypothyroidism. TSAb causes Graves' hyperthyroidism. TSBAb and TSAb block TSH-binding to cells as TRAb, measured as TSH-binding inhibitory immunoglobulin (TBII). We reevaluate TSBAb and TSAb. We studied TSBAb, TSAb, and TBII over 10 years in 34 TSBAb-positives with hypothyroidism and in 98 TSAb-positives with hyperthyroidism. Half of the 34 TSBAb-positives with hypothyroidism continued to have persistently positive TSBAb, continued to have hypothyroidism, and did not recover from hypothyroidism. Ten of the 98 TSAb-positives with hyperthyroidism continued to have positive TSAb and continued to have hyperthyroidism. TSBAb had disappeared in 15 of the 34 TSBAb-positives with hypothyroidism. With the disappearance of TSBAb, recovery from hypothyroidism was noted in 13 (87%) of the 15 patients. TSAb had disappeared in 73 of the 98 TSAb-positives with hyperthyroidism. With the disappearance of TSAb, remissions of hyperthyroidism were noted in 60 (82%) of the 73. Two of the 34 TSBAb-positives with hypothyroidism developed TSAbpositive Graves' hyperthyroidism. Two of the 98 TSAb-positive Graves' patients with hyperthyroidism developed TSBAb-positive hypothyroidism. TSBAb and TSAb are TRAbs. TSBAb-hypothyroidism and TSAb-hyperthyroidism may be two aspects of one disease (TRAb disease). Two forms of autoimmune thyroiditis: atrophic and goitrous. We followed 34 TSBAb-positive patients with hypothyroidism (24 atrophic and 10 goitrous) over 10 years. All of the 10 TSBAb-positive goitrous patients recovered from hypothyroidism and 19 (79%) of the 24 TSBAb-positive atrophic patients continued to have hypothyroidism. [ABSTRACT FROM AUTHOR]

Thyroid carcinoma showing squamous differentiation throughout the entire lesion is diagnosed as squamous cell carcinoma of the thyroid (SCCT) in the WHO classification. This entity is a rare disease and shows a dire prognosis; however, squamous differentiation ismore frequently detected in only a portion of papillary thyroid carcinoma. In this paper, we present our experience of 10 patients (8 primary lesions and 2 with recurrence in the lymph nodes) with papillary thyroid carcinoma having an SCC component (PTC-SCC). Only 3 of 8 primary lesions (38%) and none of the 2 recurrent nodes were preoperatively diagnosed as or suspected of having SCC components. All 10 patients underwent locally curative surgery. To date, 3 patients have died of carcinoma, and 2 had distant metastasis at diagnosis or had an undifferentiated carcinoma component. The other 7 are currently alive 5 to 43 months after diagnosis. Systemic adjuvant therapy after the detection of recurrence was effective for 2 patients. It is possible that some PTC-SCC patients without distant metastasis who undergo locally curative surgery can survive for a prolonged period and adjuvant therapies can be effective for local and distant recurrences. [ABSTRACT FROM AUTHOR]

18F-fluorodeoxyglucose positron emission tomography (FDG-PET) plays an increasingly important role in the prognostication, diagnosis, andmanagement of thyroid carcinoma. For patients diagnosed with primary or persistent/recurrent thyroid carcinoma, a finding of FDG-PET positivity implies a more aggressive tumor biology and a distinct mutational profile, both of which carry prognostic significance. Therefore, FDG-PET positivity may be a useful potential risk factor for preoperative risk stratification in primary thyroid carcinoma. This information may help in the planning of subsequent treatment strategy such as the extent of thyroidectomy, prophylactic central neck dissection, and radioiodine ablation. FDG-PET scan has also been found to be a useful adjunct in characterizing indeterminate thyroid nodules on fine needle aspiration cytology. However, larger-sized prospective studies are required to validate this finding. FDG-PET or FDG-PET/CT scan has become the imaging of choice in patients with a negative whole-body radioiodine scan, but with an abnormally raised thyroglobulin level after total thyroidectomy and radioiodine ablation. [ABSTRACT FROM AUTHOR]

Abstract: The pituitary gland is made of clusters of cells producing specific hormones that control growth (growth hormones, GH), thyroid function (TH), adrenal function (ACTH), gonadal function (FSH and LH). In addition, the neurons that join the posterior pituitary (neurohypophysis) secrete vasopressin - the antidiuretic hormone involved in maintaining water balance. The negative feedback loop is the basic mechanism to control the regulation of all endocrine glands. Hypothalamic peptides - releasing hormones (e.g. TRH, CRH) reach the hypophysis via the portal venous system and induce the secretion of specific stimulating hormones (e.g. TSH, ACTH) that drive the end-target endocrine cells to secrete hormones (e.g. thyroid hormones - T3 and T4 or adrenal hormones - cortisol, DHEAS). The plasma levels of these circulating hormones inhibit the pituitary (short feedback) or the hypothalamus (long feedback) and limit the further release of releasing- and stimulating- hormones. The effects of circulating hormones on different tissues are mediated via specific receptors on the cell membrane (e.g. vasopressin receptors), in the cytoplasm (steroid receptor for cortisol) or in the nucleus (e.g. thyroid hormone receptors). Understanding the physiological effects of peripheral hormones helps understanding the mechanisms by which clinical signs and symptoms developed in diseases characterised by excessive hormone secretion (e.g. thyrotoxicosis, Cushing syndrome, phaeochromocytomas) or lack of hormone secretion (e.g. diabetes insipidus). [Copyright &y& Elsevier]

Tea is a rich source of polyphenolic flavonoids including catechins, which are thought to contribute to the health benefits of it. Flavonoids have been reported to have antithyroid and goitrogenic effect. The purpose of this study was to evaluate whether high doses of green and black tea have a harmful effect on thyroid physiology. Un-fractionated green and black tea extracts were administered orally to male rats for 30 days at doses of 1.25 g%, 2.5 g% and 5.0 g%. The results showed that green tea extract at 2.5 g% and 5.0 g% doses and black tea extract only at 5.0 g% dose have the potential to alter the thyroid gland physiology and architecture, that is, enlargement of thyroid gland as well as hypertrophy and/or hyperplasia of the thyroid follicles and inhibition of the activity of thyroid peroxidase and 5′-deiodinase I with elevated thyroidal Na+, K+-ATPase activity along with significant decrease in serum T3 and T4, and a parallel increase in serum thyroid stimulating hormone (TSH). This study concludes that goitrogenic/antithyroidal potential of un-fractionated green tea extract is much more than black tea extract because of the differences in catechin contents in the tea extracts. [ABSTRACT FROM PUBLISHER]

Thyroid diseases are prevalent among endocrine disorders, and careful evaluation of patients' symptoms is a very important part in their diagnosis. Developing new pedagogical strategies, such as problembased learning (PBL), is extremely important to stimulate and encourage medical and biomedical students to learn thyroid physiology and identify the signs and symptoms of thyroid dysfunction. The present study aimed to create a new pedagogical approach to build deep knowledge about hypo-/hyperthyroidism by proposing a hands-on activity based on a detective case, using alternative materials in place of laboratory animals. After receiving a description of a criminal story involving changes in thyroid hormone economy, students collected data from clues, such as body weight, mesenteric vascularization, visceral fat, heart and thyroid size, heart rate, and thyroid-stimulating hormone serum concentration to solve the case. Nevertheless, there was one missing clue for each panel of data. Four different materials were proposed to perform the same practical lesson. Animals, pictures, small stuffed toy rats, and illustrations were all effective to promote learning, and the detective case context was considered by students as inviting and stimulating. The activity can be easily performed independently of the institution's purchasing power. The practical lesson stimulated the scientific method of data collection and organization, discussion, and review of thyroid hormone actions to solve the case. Hence, this activity provides a new strategy and alternative materials to teach without animal euthanization. [ABSTRACT FROM AUTHOR]

Foot-and-mouth disease (FMD) is a highly contagious and economically important viral disease with high morbidity and reduced productivity of affected animals. We studied the heat intolerance (HI) (panting) syndrome and the effect of FMD virus (FMDV) infection on thyroid gland function in Indian cattle ( Bos indicus). Experimental infection with FMDV Asia 1 resulted in a mild form of disease with superficial lesions. Heat intolerance syndrome and its signs were not observed among the recovered animals. Subtle changes in the serum level of thyroid hormones, triiodothyronine (T) and thyroxine (T) were observed. However, there were no distinct histological changes in the thyroid gland, and FMDV antigens were not detected in the thyroid tissues. Our results thus suggest that the absence of panting syndrome in FMD-affected Bos indicus cattle may be associated with intact thyroid gland function. [ABSTRACT FROM AUTHOR]

With a binary response Y, the dose-response model under consideration is logistic in flavor with pr(Y=1 | D) = R (1+R)-1, R = λ0 + EAR D, where λ0 is the baseline incidence rate and EAR is the excess absolute risk per gray. The calculated thyroid dose of a person i is expressed as Dimes = fiQimes/Mimes. Here, Qimes is the measured content of radioiodine in the thyroid gland of person i at time tmes, Mimes is the estimate of the thyroid mass, and fi is the normalizing multiplier. The Qi and Mi are measured with multiplicative errors ViQ and ViM, so that Qimes = QitrViQ (this is classical measurement error model) and Mitr = MimesViM (this is Berkson measurement error model). Here, Qitr is the true content of radioactivity in the thyroid gland, and Mitr is the true value of the thyroid mass. The error in fi is much smaller than the errors in (Qimes, Mimes) and ignored in the analysis. By means of Parametric Full Maximum Likelihood and Regression Calibration (under the assumption that the data set of true doses has lognormal distribution), Nonparametric Full Maximum Likelihood, Nonparametric Regression Calibration, and by properly tuned SIMEX method we study the influence of measurement errors in thyroid dose on the estimates of λ0 and EAR. The simulation study is presented based on a real sample from the epidemiological studies. The doses were reconstructed in the framework of the Ukrainian-American project on the investigation of Post-Chernobyl thyroid cancers in Ukraine, and the underlying subpolulation was artificially enlarged in order to increase the statistical power. The true risk parameters were given by the values to earlier epidemiological studies, and then the binary response was simulated according to the dose-response model. [ABSTRACT FROM AUTHOR]

Objectives: This study was designed to answer the question: Does the contact of the human organism with the Earth via a copper conductor affect physiologic processes? Subjects and experiments: Five (5) experiments are presented: experiment 1-effect of earthing on calcium-phosphate homeostasis and serum concentrations of iron ( N = 84 participants); experiment 2-effect of earthing on serum concentrations of electrolytes ( N = 28); experiment 3-effect of earthing on thyroid function ( N = 12); experiment 4-effect of earthing on glucose concentration ( N = 12); experiment 5-effect of earthing on immune response to vaccine ( N = 32). Subjects were divided into two groups. One (1) group of people was earthed, while the second group remained without contact with the Earth. Blood and urine samples were examined. Results: Earthing of an electrically insulated human organism during night rest causes lowering of serum concentrations of iron, ionized calcium, inorganic phosphorus, and reduction of renal excretion of calcium and phosphorus. Earthing during night rest decreases free tri-iodothyronine and increases free thyroxine and thyroid-stimulating hormone. The continuous earthing of the human body decreases blood glucose in patients with diabetes. Earthing decreases sodium, potassium, magnesium, iron, total protein, and albumin concentrations while the levels of transferrin, ferritin, and globulins α1, α2, β, and γ increase. These results are statistically significant. Conclusions: Earthing the human body influences human physiologic processes. This influence is observed during night relaxation and during physical activity. Effect of the earthing on calcium-phosphate homeostasis is the opposite of that which occurs in states of weightlessness. It also increases the activity of catabolic processes. It may be the primary factor regulating endocrine and nervous systems. [ABSTRACT FROM AUTHOR]

The natural history of thyroid function in adults with Down syndrome is relatively unknown with limited long-term follow-up data. This study investigated annual thyroid function tests in 200 adults with Down syndrome over a 15-year period. For healthy adults with Down syndrome there is a gradual increase in thyroxine and possible gradual decline in thyroid-stimulating hormone with age. The 15-year incidence for definite hypothyroidism remains low and subclinical hypothyroidism is not a precursor for the onset of definite hypothyroidism. The incidence of thyroid dysfunction is markedly less than would be expected from prevalence studies. Subclinical hypothyroidism is not necessarily a precursor to definite hypothyroidism. Prevalence studies have overstated the association between thyroid dysfunction and Down syndrome. Routine screening for adults with Down syndrome who are euthyroid can be reduced to every 5 years rather than the 1-2 years, as is the present policy. [ABSTRACT FROM AUTHOR]

In this case-control study of euthyroid first-cycle IVF patients ≥38 years old with singleton baby, miscarriage, biochemical pregnancy, and no pregnancy outcomes from 2005–2008, we assayed frozen serum for autoimmune thyroid disease (AITD) and thyroid function at cycle start, trigger, and 4 and 5 weeks’ gestation. AITD prevalence in older infertile women was similar across clinical outcomes, and although AITD was associated with a higher baseline TSH, TSH remained within acceptable ranges, suggesting that T4 supplementation may not affect maternal outcomes in older euthyroid AITD patients through 5 weeks gestation. [Copyright &y& Elsevier]

Introduction. It has been reported that low normal circulating thyrotropin (TSH) levels correlate with lower bone mineral density (BMD) in the Korean postmenopausal female. The goal of this study is to evaluate this relationship in different sex and age groups in a Chinese population. Materials and methods. A total of 2,957 subjects in Taiwan, 1,343 males and 1,614 females, aged from 45 to 64 years, were enrolled in this study. They were divided into four groups: group 1 was males aged between 45 and 50 years (young male, YM); group 2 was females aged between 45 and 50 years (young female, YF); group 3 was males older than 50 years (old male, OM); and group 4 was females older than 50 years (old female, OF). Plasma total thyroxine (T4) and TSH were measured. BMD was quantified at the wrist using dual energy X-ray absorptiometry. Results. YM had the highest BMD whereas OF had the lowest BMD. Among the four groups, no significant correlation between TSH level and BMD was found in the four groups, but a significant negative correlation existed between T4 and BMD in OF ( r = −0.089, p = 0.005) and YM ( r = −0.109, p = 0.018). Conclusion. Our study did not find significant correlations between TSH and BMD in both men and women with normal thyroid function in Taiwan. Weak negative correlations existed between T4 and BMD in postmenopausal women and young men. Further studies with measurement of FT4 and TSH and with a longitudinal design may shed light on this population difference. [ABSTRACT FROM AUTHOR]

Background. The present study is to look for a correlation between oxidative stress and thyroid function in patients with the nephrotic syndrome in the remission phase as well as in a persistent proteinuric state. Introduction. Nephrotic syndrome is a form of chronic kidney disease due to which blood loses protein through the urine. We wanted to know if there was an increased loss of thyroid hormones in urine affecting thyroid function. Methods. 60 patients with nephrotic syndrome and 20 healthy non-proteinuric individuals as control subjects were enrolled in the study. We measured their serum tri-iodothyronine, thyroxine and thyroid-stimulating hormone. Estimation of lipid peroxidation (LPx) catalase, superoxide dismutase (SOD), and Glutathione peroxidase (GPx) were carried out by standard methods. Results. TSH was elevated in the nephrotic patients compared to controls, while TT4 and TT3 were significantly lower in the patients than in controls. Lipid Peroxidation and GPx were significantly higher in the nephrotic syndrome patients than in the controls, while SOD and catalase were significantly lower than in patients than in the control subjects. Conclusion. Nephrotic patients can lose significant amounts of thyroid hormones along with protein in urine, which can affect thyroid status, but this is reversible on remission. [ABSTRACT FROM AUTHOR]

In order to minimize risks to human and environmental health, chemical safety assessment programs are being reinforced with toxicity tests more specifically designed for detecting endocrine disrupters. This includes the necessity to detect thyroid-disrupting chemicals, which may operate through a variety of modes of action, and have potential to impair neurological development in humans, with resulting deficits of individual and social potential. Mindful of these concerns, the consensus favors in vivo models for both hazard characterization (testing) and hazard identification (screening) steps, in order to minimize false negatives. Owing to its obligate dependence on thyroid hormones, it has been proposed that amphibian metamorphosis be used as a generalized vertebrate model for thyroid function in screening batteries for detection of thyroid disrupters. However, it seems unlikely that such an assay would ever fully replace in vivo mammalian assays currently being validated for human health risk assessment: in its current form the amphibian metamorphosis screening assay would not provide capacity for reliably detecting other modes of endocrine-disrupting activity. Conversely, several candidate mammalian screening assays appear to offer robust capacity to detect a variety of modes of endocrine-disrupting activity, including thyroid activity. To assess whether omission of an amphibian metamorphosis assay from an in vivo screening battery would generate false negatives, the response of amphibian and mammalian assays to a variety known thyroid disrupters, as reported in peer-reviewed literature or government agency reports, was critically reviewed. Of the chemicals investigated from the literature selected (41), more had been tested in mammalian studies with thyroid-relevant endpoints (32) than in amphibian assays with appropriate windows of exposure and developmental endpoints (27). One chemical (methoxychlor) was reported to exhibit thyroid activity in an appropriate amphibian assay in the absence of corresponding activity in a suitable mammalian assay, whereas none of the chemicals surveyed were reported as thyroid active in mammalian assays but reported as negative in an appropriate amphibian assay. Given the need for one or more in vivo mammalian assays for screening chemicals for detecting (anti-)estrogenic/(anti-)androgenic activity and effects on steroidogenesis, inclusion of an in vivo amphibian assay specifically to detect thyroid disrupters would likely be as an addition to these mammalian assays. As there is little convincing evidence that an amphibian screening assay would detect significant numbers of thyroid-active chemicals not picked up by mammalian assays, the routine use of an amphibian metamorphosis assay at screening level could introduce unnecessary and unjustified redundancy into chemical safety assessment programs, when there is pressure to reduce animal use in toxicity testing. [ABSTRACT FROM AUTHOR]

Background:Thymic hyperplasia is associated with Graves'' disease, particularly in young patients. The degree of thymic transformation is minimal in most but not all patients. In the latter group radiological measurements of thyroid size and their change with treatment have rarely been reported. We present two patients with Graves'' disease and relatively rapid resolution of thymic enlargement after successful treatment of their hyperthyroidism.Summary:Three patients with thyrotoxicosis secondary to Graves'' disease and marked thymic enlargement were seen at our institution during a 2-year period. On computed tomography (CT) studies their volumes were 67, 81, and 54 cm3. Thymic hyperplasia in the setting of Graves'' disease was the diagnosis of exclusion. Two of the patients returned for follow-up after successful treatment of thyrotoxicosis as requested. On repeat CT their thymic volumes had decreased by 72% and 78%, respectively. Two types of histological modifications of the thymus have been described in association with Graves'' disease, namely, thymic parenchyma hyperplasia and medullary lymphoid hyperplasia. The mechanisms underlying thymic transformation in patients with Graves'' hyperthyroidism are not completely elucidated, but autoimmune processes underlying Graves'' disease are presumed to play a role. The clinical course of our patients is consistent with earlier literature, indicating that thymic enlargement may occur in conjunction with Graves'' hyperthyroidism, and that it usually resolves as hyperthyroidism is treated, but there is little quantitative pre- and posttreatment of hyperthyroidism data.Conclusion:Although every patient must be individually considered, it appears that thymic hyperplasia can be diagnosed in most Graves'' hyperthyroid patients by considering the clinical context and appropriate radiologic studies such as CT. Raising awareness of the association of thymic hyperplasia in patients with Graves'' hyperthyroidism and its resolution with the reversibility of the hyperthyroid state should prevent unnecessary thymic evaluation and surgery with its attendant risks. [ABSTRACT FROM AUTHOR]

Background:Studies have shown that overt hypothyroidism is associated with a substantial risk of miscarriage. There is controversy as to whether subclinical hypothyroidism has the same effect and whether such effect is mediated by the presence of antithyroid antibodies. Our hypothesis is that maternal thyroid function in the first trimester is altered in pregnancies ending in miscarriage or fetal death.Methods:Thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine, anti-thyroperoxidase antibody, and anti-thyroglobulin antibody at 11–13 weeks of gestation were measured in 202 singleton pregnancies that subsequently resulted in miscarriage or fetal death, and the values were compared with the results of 4318 normal pregnancies.Results:In the fetal loss group, compared to the unaffected group, there was an increase in median TSH multiple of the normal median (1.133 vs. 1.007 MoM), decrease in median FT4 MoM (0.958 vs. 0.992 MoM), and increase in the incidence of TSH above the 97.5th centile (5.9% vs. 2.5%) and FT4 below the 2.5th centile (5.0% vs. 2.5%). Logistic regression analysis demonstrated that in the prediction of fetal loss there were significant contributions from FT4 MoM, maternal black ethnic origin, history of chronic hypertension, and use of ovulation drugs. The prevalence of antithyroid antibody positivity was not significantly different in the fetal loss group compared to that of normal pregnancies (15.3% vs. 16.8%).Conclusions:Impaired thyroid function may predispose to miscarriage and fetal death. [ABSTRACT FROM AUTHOR]

Abstract: Background: Iodide has direct effects on thyroid function. Several iodinated lipids are biosynthesized by the thyroid and they were postulated as intermediaries in the action of iodide. Among them 6 iodo-δ-lactone (IL-δ) has been identified and proposed to play a role in thyroid autoregulation. The aim of this study was to compare the effect of iodide and IL-δ on several thyroid parameters. Methods: Thyroid bovine follicles were incubated with the different compounds during three days. Results: KI and IL-δ inhibited iodide uptake, total protein and Tg synthesis but only KI had an effect on NIS and Tg mRNAs levels. Both compounds inhibited Na+/K+ ATPase and deoxy-glucose uptake. As PAX 8, FOXE 1 and TITF1 are involved in the regulation of thyroid specific genes their mRNA levels were measured. While iodide inhibited the expression of the first two, the expression of TITF1 was stimulated by iodide and IL-δ had no effect on these parameters. Conclusion: These findings indicate that IL-δ reproduces some but not all the effects of excess iodide. These observations apply for higher micromolar concentrations of iodide while no such effects could be demonstrated at nanomolar iodide concentrations. [Copyright &y& Elsevier]

The article discusses common causes of thyroid disease. The author reviews the anatomy and physiology of the thyroid gland and the possible causes of thyroid dysfunction which often lead to hyperthyroidism and hypothyroidism. Hyperthyroidism can be caused by several conditions including Graves disease and toxic adenoma while hypothyroidism can be caused by factors including thyroid irradiation and certain autoimmune disorders. Different treatment options for thyroid disease are described.

Adequate levels of iodine, a trace element variably distributed on the earth, are required for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). The iodide cycle consists of a series of transport, oxidation and coupling steps in thyroid follicular cells to produce thyroid hormone. The sodium/iodide symporter (NIS) transports iodide into the thyrocyte. Competitive inhibitors of NIS, such as perchlorate and thiocyanate, can decrease the entrance of iodide into the follicular cell. Pendrin is the primary protein that is responsible for iodide efflux out of the thyrocyte and into the follicular lumen. T4 is deiodinated in target tissues to produce the active form of thyroid hormone, T3, and other metabolites. Exposure to excessive iodine or chronic iodine deficiency may result in various clinical disorders. The Wolff-Chaikoff effect and Jöd-Basedow phenomenon describe mechanisms of thyroid autoregulation and dysregulation, respectively, during iodine excess. Population studies have determined that iodine deficiency exists in approximately 38% of the world's population, is the leading cause of preventable mental retardation, and is of particular concern to women and their infants. Finally, the unique role of iodine utilization in thyroid physiology has applications in many important clinical areas. INSETS: Box 1. Risk factors for iodine-induced hypothyroidism …;Key issues. [ABSTRACT FROM AUTHOR]

Background:Pregnancy influences thyroid function and may bring to light mild and latent disorders. Thyroid dysfunction has been related to obstetrical complications such as premature delivery, gestational hypertension, preeclampsia, and placental abruption. The aim of our study was to evaluate whether the occurrence and timing of pregnancy loss could be related to thyroid autoimmunity or subclinical hypothyroidism (SH) per se.Methods:Two hundred sixteen apparently healthy pregnant women with no previous history of thyroid disease and with diagnosis of early miscarriage (before the 12th week of gestation) were enrolled. Miscarriages were classified as very early pregnancy loss (EPL) or embryo loss (crown rump length ≤10 mm) and EPL or fetal loss (crown rump length > 10 mm). Women were subdivided into four groups: euthyroid (ET), SH, overt hypothyroidism, and thyroid autoimmunity group.Results:One hundred seventy-six women had a normal thyroid function (84.6%), 24 patients were found to have positive thyroid antibodies (11.5%), 8 women (3.8%) an SH, and 8 cases were excluded. Thyroid-stimulating hormone levels were found to be higher in the very early (1.4 ± 1.0 mU/L) than in the EPL group (1.1 ± 0.7 mU/L) (p= 0.04), and in patients affected by SH (3.9 ± 0.1 mU/L) compared to ET (1.0 ± 0.5 mU/L) (p< 0.001) and autoimmune women (1.0 ± 0.4 mU/L) (p< 0.001). Although the multivariate logistic regression analysis revealed that both autoimmunity and SH were independently correlated with the onset of very EPL, abortion was more precocious in the SH group (6.5 ± 0.9 weeks), followed by the autoimmune (8.2 ± 2.1 weeks) and ET groups (8.2 ± 1.6 weeks) (p= 0.02).Conclusions:Both thyroid diseases SH and autoimmune disorder are independently associated with very early embryo loss, but women suffering from SH have a lower gestational age at abortion. [ABSTRACT FROM AUTHOR]

Summary: Physiological changes during gestation and after delivery are associated with postpartum thyroid dysfunction, which is due to thyroid autoimmunity in some cases. Postpartum thyroid dysfunction, in turn, has been associated with postpartum depression (PPD). The aim of the present study was to evaluate whether thyroid function immediately after delivery can predict postpartum depression at 8 weeks and 32 weeks after delivery. This study examined 1053 postpartum Spanish women without a previous history of depression. We evaluated depressive symptoms at 48h, 8 weeks and 32 weeks postpartum and used a diagnostic interview to confirm major depression for all probable cases. Free thyroxin (fT4), thyroid-stimulating hormone (TSH), thyroid peroxidase antibodies (TPOAb) and C-reactive protein (CRP) were assayed at 48h postpartum. Binary and multivariate logistic regression analyses were performed to determine independent risk factors for PPD. Although 152 women (14.4%) had high TPOAb (>27IU/mL) and slightly elevated TSH concentrations with normal fT4, we did not find any association between thyroid function and PPD. This thyroid dysfunction was not associated with CRP concentrations that were outside of the normal range (>3mg/L). We conclude that thyroid function at 48h after delivery does not predict PPD susceptibility. [Copyright &y& Elsevier]

OBJECTIVE: The present study re-evaluates the inverse log TSH–free thyroxine (fT4) relationship, which has generally been assumed to characterize the thyroid pituitary hypothalamic feedback regulation in thyroid function. DESIGN AND METHODS: The correlation between fT4and TSH was analyzed in two data sets from differing time periods involving 3223 and 6605 patients referred for thyroid testing, representing the whole range of thyroid functions from hypothyroidism to hyperthyroidism. RESULTS: We found that the data do not support a linear log TSH–fT4relationship; instead, the correlation's gradient varies with thyroid function. As a consequence, an alternate model, based on the error function, was introduced. When directly comparing the models by means of curve fitting, using F-test and Akaike criteria, the alternate model results in a significantly better fit. The model was verified in the independent second set of data. Subgroup analysis of untreated patients added further proof to the non-linear model. CONCLUSIONS: We propose a refined non-linear model to describe the relationship between TSH and fT4. It implies that TSH response to a deviating fT4value may not be log-linear, but may be disproportionally related to the extent of the deviation from an optimum set point. A better understanding of the complex nature of the TSH–fT4relationship may further the development of more precise clinical models and aid in better defining subclinical states of thyroid dysfunction. Also, it may encourage other biological interrelations to be reconsidered in the wake of advanced measurement techniques and more powerful computerized statistical procedures. [ABSTRACT FROM AUTHOR]

Abstract: As part of a multi-endpoint systems approach to develop comprehensive methods for assessing endocrine stressors in vertebrates, differential protein profiling was used to investigate expression patterns in the brain of the amphibian model (Xenopus laevis) following in vivo exposure to a suite of T4 synthesis inhibitors. We specifically address the application of Two Dimensional Polyacrylamide Gel Electrophoresis (2D PAGE), Isobaric Tags for Relative and Absolute Quantitation (iTRAQ®) and LC–MS/MS to assess changes in relative protein expression levels. 2D PAGE and iTRAQ proved to be effective complementary techniques for distinguishing protein changes in the developing amphibian brain in response to T4 synthesis inhibition. This information served to evaluate the use of distinctive protein profiles as a potential mechanism to screen chemicals for endocrine activity in anurans. Regulatory pathways associated with proteins expressed as a result of chemical effect are reported. To our knowledge, this is also the first account of the anuran larvae brain proteome characterization using proteomic technologies. Correlation of protein changes to other cellular and organism-level responses will aid in the development of a more rapid and cost-effective, non-mammalian screening assay for thyroid axis-disrupting chemicals. [Copyright &y& Elsevier]

Abstract: In the literature, data obtained in signal transduction from various species thyroids and cells lines are often integrated in a common model. We investigate qualitatively and systematically, using the same protocol, the control by TSH of the two main functions of the thyrocytes, the synthesis and the secretion of thyroid hormones. In all species investigated, the TSH receptor activates both. In some species, including humans, rats and mice, the TSH receptor activates both the cAMP and phospholipase C-PIP2 cascades, in others (e.g. dog) it only stimulates the first. The cAMP pathway activates the limiting step in thyroid hormones synthesis, the generation of H2O2, in dog, rat and mice but not in human, pig, horse and beef. Thus although the physiological result of TSH action is the same in all species, the signaling pathways used are different. Other distinctions in signaling are observed such as the relative effects of one cascade on the other. [Copyright &y& Elsevier]

Abstract: Arecoline is a plant alkaloid of betel nut Areca catechu. Arecoline has immunosuppressive, hepatotoxic, mutagenic and teratogenic effects, and disturbs some endocrine organs in rats. The objective is to investigate the untoward effects of arecoline on the thyroid gland in mice. Intraperitoneal injection of arecoline (10mg/kg body weight only once) increased the serum T3 and T4 levels and decreased the serum TSH 20, 40 or 60min after the treatment, with maximum effect at 40min. Chronic arecoline treatment (10mg/kg body weight daily for 15 days) caused light microscopic and ultrastructural degenerations of thyro-follicular cells with depletion of T3 and T4 levels followed by the elevation of the TSH level. Atropine (arecoline antagonist) injection prevented the changes (hyperactivity) induced by acute (40min) arecline treatment. Arecoline initially stimulates thyroid activity, and eventually inhibits the activity; atropine prevents thyroid dysfunction induced by arecoline. Arecoline action is mediated probably via muscarinic cholinergic receptor—hypothalamic–pituitary–thyroid axis in mice. [Copyright &y& Elsevier]

Abstract: Endocrine disruptors are man-made chemicals that can disrupt the synthesis, circulating levels, and peripheral action of hormones. The disruption of sex hormones was subject of intensive research, but thyroid hormone synthesis and signaling are now also recognized as important targets of endocrine disruptors. The neurological development of mammals is largely dependent on normal thyroid hormone homeostasis, and it is likely to be particularly sensitive to disruption of the thyroid axis. Here, we survey the main thyroid-disrupting chemicals, such as polychlorinated biphenyls, perchlorates, and brominated flame-retardants, that are characteristic disruptors of thyroid hormone homeostasis, and look at their suspected relationships to impaired development of the human central nervous system. The review then focuses on disrupting mechanisms known to be directly or indirectly related to the transcriptional activity of the thyroid hormone receptors. [Copyright &y& Elsevier]

Abstract: Background: Postpartum mood disturbances are very common with postpartum blues being as high as 44.5% among Greek women. This study aimed to investigate whether thyroid function within the normal range affects the incidence of postpartum mood disturbances. Methods: In a cross-sectional study in the maternity ward of Aretaieion Hospital, 57 Greek women were evaluated for postpartum mood swings by the Maternity Blues Questionnaire and the Edinburgh Postnatal Depression Scale on the first and sixth week postpartum. Serum Free T4, Free T3 and TSH concentrations as well as thyroglobulin and thyroid peroxidase antibodies were measured on admission for delivery and daily until the fourth postpartum day. We examined the association between hormone and antibody levels, and scores in the two scales evaluating postpartum mood disturbances. Results: Prepartum serum FT3 and FT4 correlated negatively with blues scores in the first week postpartum (blues on day 4: with FT3, rho=−0.44, p ≤0.01; with FT4 rho=−0.36, p ≤0.01). Women with lower FT3 and FT4 levels belonged to the high scoring group (high scoring group: FT3=1.22 pg/ml, FT4=0.66 ng/dl; low scoring group: FT3=1.64 pg/ml, FT4=0.73 ng/dl). Serum FT3 showed a negative independent correlation with postpartum blues scores in the first postpartum days. No association was found between thyroid antibody levels and mood scores. Conclusion: Our findings indicate an association between the occurrence of postpartum mood disorders and antenatal thyroid function. Within normal limits, lower levels of serum FT3 and FT4 are associated with increased incidence of mood disturbances in the first postpartum week. [Copyright &y& Elsevier]

Abstract: It is well documented that many coastal and estuarine environments adjacent to developed and industrialized urban centers, such as the San Francisco Bay Area, are significantly contaminated by anthropogenic chemicals. However, it is not well understood to what extent existing contaminants, many with continuing inflows into the environment, may impact exposed wildlife. This study provided an initial characterization of thyroid endocrine-related effects and their relationship to accumulated contaminants in two indigenous fish species sampled from different San Franicsco Bay Area study sites. Plasma concentrations of thyroxine (T4) were significantly reduced in fish sampled from highly impacted locations such as Oakland Inner Harbor and San Leandro Bay as compared with fish from other locations representing relatively lower human impact, including Bodega Bay, Redwood City and a remote site on Santa Catalina Island. Triiodothyronine (T3) levels also varied significantly by location, with differing T3/T4 ratios in fish from some locations suggestive of altered peripheral deiodinase activity. The changes in thyroid endocrine parameters were significantly correlated with hepatic concentrations of certain environmental contaminants. A large number of polychlorinated biphenyl (PCB) congeners, both co-planar (dioxin-like) and non-co-planar, exhibited significant inverse correlations with T4 levels in the fish, while in contrast, T3 and T3/T4 ratio were positively correlated with PCB exposures. The positive correlation between T3/T4 ratio and PCBs supports the hypothesis that environmental PCBs may alter T4 deiodination or turnover, actions of PCBs reported in laboratory experiments. Some relationships between chlorinated pesticides including DDT and chlordanes, but fewer relationships with PAHs, were also observed. Together, these findings indicate that the thyroid endocrine system is exhibiting alterations associated with different aquatic environments in the San Francisco Bay Area, which are significantly related to current-day exposures of the fish to contaminant chemicals such as PCBs. [Copyright &y& Elsevier]

Abstract: The ability of organophosphate pesticides to disturb thyroid gland function has been demonstrated by experimental studies on animal, but evidence of such effects on human remains scarce. The aim of this study was to assess the association between exposure to organophosphate compounds and serum levels of thyroid hormones in floriculture workers. A longitudinal study was conducted on 136 male subjects from the State of Mexico and Morelos, Mexico, occupationally exposed to organophosphate pesticides, during agricultural periods of high (rainy season) and low (dry season) levels of pesticide application. Using a structured questionnaire, a survey was carried out on sociodemographic characteristics, anthropometry, clinical history, alcohol and tobacco consumption, residential chemical exposure, and occupational history. Urine and blood samples were taken the day after pesticide application to determine urine dialkylphosphate (DAP) levels, serum levels of TSH, total T3, total T4, serum PON1 activity, and serum p,p′-DEE levels. The analysis of the association between DAP levels and thyroid hormonal profile was carried out using multivariate generalized estimating equation (GEE) models. Our results showed an increase in both TSH and T4 hormones in serum associated with a increase in total dimethylphosphate levels (ΣDMP) in urine (p-trend<0.001) and a decrease in total T3 serum levels with an increase of ΣDMP levels in the urine (p-trend=0.053). These results suggest that exposure to organophosphate pesticides may be responsible of increasing TSH and T4 serum hormone levels and decreasing T3 serum hormone levels, therefore supporting the hypothesis that organophosphate pesticides act as endocrine disruptors in humans. [Copyright &y& Elsevier]

This study investigated the recombinant human thyrotropin (rhTSH) stimulation test in healthy cats (group 1), cats with non-thyroidal illness (group 2) and cats with low serum total T4 (TT4) and azotaemia after 131I treatment (group 3). Serum TT4 responses and thyroidal pertechnetate uptake after administration of 25μg rhTSH IV were assessed. Baseline serum TT4 was significantly lower in group 3 compared with group 1, but not between other group pairs. Serum TT4 increased significantly in groups 1 and 2 but not in group 3 after rhTSH administration. Post-rhTSH serum TT4 concentrations differed significantly between groups 1 and 3 and groups 2 and 3, but not between groups 1 and 2. Thyroid/salivary gland uptake ratio (T/S uptake ratio) differed only significantly between groups 1 and 3. Stimulation with rhTSH is valuable to differentiate euthyroidism from iatrogenic hypothyroidism in cats. [Copyright &y& Elsevier]

Background:Estrogen promotes the growth of thyroid cells. Therefore, we analyzed the influence of estrogen and selective estrogen receptor modulators (SERMs) on the expression of vascular endothelial growth factor (VEGF) and nitric oxide synthase III (NOS III) in the thyroid gland of ovariectomized (Ovx) rats.Methods:Wistar rats were divided into five groups, and bilateral ovariectomies were performed, except on the Sham-operated controls (Sham). Rats were grouped as follows: Sham; Ovx; and Ovx rats treated with daily subcutaneous injections of estradiol benzoate 3.5 μg/kg, tamoxifen 2.5 mg/kg, or raloxifene 2.5 mg/kg for 50 consecutive days. Control animals received vehicle (propyleneglycol), and at the end of the treatment, rats were sacrificed. The thyroid glands were excised, weighed, and processed for analysis of the expression of VEGF or NOS III by immunohistochemistry. The mean vascular areas were evaluated by immunodetection of α-smooth muscle actin.Results:Thyroid weight and mean vascular area were lower in Ovx as compared with Sham, Ovx + estradiol benzoate, Ovx + Tam, or Ovx + Ral (p< 0.01). VEGF (p< 0.01) and NOS III expressions (p< 0.05) were significantly lower in the Ovx group, as compared with Sham, Ovx + estradiol benzoate, Ovx + Tam, and Ovx + Ral. Immunoreactivity for both VEGF and NOS III was mainly detected in the cytoplasm of the follicular epithelial cells.Conclusions:Our data suggest that estrogen and SERMs regulate the thyroid gland vascularization and that tamoxifen and raloxifene behave like estrogen does. Estrogen and SERMs upregulate VEGF and NOS III in such a way as to reverse the effects detected on the thyroid microvasculature of the Ovx rats. [ABSTRACT FROM AUTHOR]

Background. Ultrasound (US) is the most accurate tool in the diagnosis of thyroid nodules if performed by expert physician. Misdiagnosis due to extrathyroidal lesions mimicking thyroid nodules is reported in literature. We describe the first case of an esophageal fibrovascular polyp misdiagnosed as a thyroid nodule on US examination. Patient Findings. A 54-year-old woman presented to emergency department for headache and underwent carotid Doppler extended to neck ultrasound with incidental finding of a nodule in the posterior side of the left thyroid lobe. A following thyroid US performed by an endocrinologist allowed the characterization of the lesion as an esophageal pathology, considering the extrathyroidal position, the typical peripheral hyperechoic spots and hypoechoic rim, the connection to the esophagus, and the swallowing connected movement. The patient was addressed to further investigations and finally to anterior pharyngotomy with histological diagnosis of esophageal fibrovascular polyp. Summary. Differential diagnosis between thyroid nodules and other neck lesions is important to prevent an unnecessary fine needle aspiration biopsy and to treat the extrathyroidal pathology. In this case, an US performed by an expert endocrinologist allowed detecting an esophageal fibrovascular polyp requiring surgical removal. In conclusion, the possibility of an esophageal pathology, and even fibrovascular polyp, should be considered during US thyroid examination. [ABSTRACT FROM AUTHOR]

Background:Ectopic thyroid tissue can be found anywhere between the foramen cecum and the normal position of the thyroid gland, most commonly located in the anterior cervical area, the region of the thyroglossal duct. Although thyroid cancer has been described frequently in thyroglossal duct remnants, thyroid dysfunction related to this tissue is rare. We report a patient with recurrent Graves' disease arising in a thyroglossal duct remnant.Summary:A 40-year-old woman with a history of total thyroidectomy for Graves' disease, presented with a slowly enlarging midline neck mass in association with clinical signs of hyperthyroidism. Serum-free triiodothyronine (6.6 pg/mL) and serum-free thyroxine (2.2 ng/dL) were elevated (normal range, 2.3–4.2 pg/mL and 0.9–1.8 ng/dL, respectively), and thyroid-stimulating hormone was suppressed (<0.01 mIU/mL; normal range, 0.35–5.50 mIU/mL). Neck ultrasonography showed a solid mass, localized at the infrahyoid area; radionuclide scanning confirmed an increased uptake at the same level. A 4 cm solid mass was removed by the Sistrunk technique. Microscopic examination revealed marked follicular hyperplasia, with tall cells, small follicles, scant, and scalloped colloid, in association with patchy lymphocytic infiltrate consistent with Graves' disease.Conclusions:There appears to be no reason why thyroid cells within thyroglossal duct remnants should not be influenced by the thyroid-stimulating immunoglobulins of Graves' disease. Thyrotoxicosis resulting from this must be very rare, however, as were unable to find reports of patients with thyrotoxicosis due to Graves' disease in thyroglossal duct remnants. Although some thyroid tissue can be found within the thyroglossal duct in 1.6% to 40% of normal adults, the risk of thyroid dysfunction from this is far too low to justify new therapeutic approaches. [ABSTRACT FROM AUTHOR]

BACKGROUND: Adaptive alterations in maternal physiology cause changes in thyroid hormone levels throughout pregnancy, and precise biochemical evaluation is thus highly dependent on gestation-specific reference intervals and expected intra-individual variation. OBJECTIVE: The aim of the study was the assessment of the intra-individual variation as well as the longitudinal course of thyroid hormones during normal pregnancy and factors that influence the normal reference range for thyroid function. For this purpose, a longitudinal statistical model was applied. DESIGN: In a cohort of 132 pregnant women, serial blood samples were obtained and ultrasound scans were performed throughout pregnancy. METHODS: Serum levels of TSH, free and total thyroxine (T4), free and total triiodothyronine (T3) as well as autoantibodies against thyroid peroxidase and thyroglobulin were measured in 979 serum samples. RESULTS: Intra-individual variations of thyroid hormone concentrations were smaller than inter-individual variations (individuality index range: 0.38–0.71). Maternal height was positively associated with free T4(FT4) (b=0.003; P=0.031) and pre-pregnancy body mass index with T3and free T3(b=0.017; <0.001 and b=0.007; P<0.001). Smoking was positively associated with T4and FT4, but it was modulated by gestational age. Gestation-specific reference intervals for thyroid function variables from autoantibody-negative participants are presented. CONCLUSIONS: In accordance with the data from nonpregnant adults, intra-individual variations of thyroid hormones were smaller than inter-individual variations also during pregnancy. In the evaluation of thyroid function in pregnancy, the individual longitudinal course of thyroid hormones rather than absolute values should be considered. We present a longitudinal model for the prediction of maternal thyroid function tests in pregnant women. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Exercise training may cause changes in thyroid function. This thyroid response may be due to exercise-induced modulation of energy metabolism but also of the adipocytes endocrine function. In particular, the role of leptin and of circulating soluble leptin receptor (sOB-R) was unexplored. The aim of this study was to assess the relationships between thyroid function, whole body energy metabolism, and adipokines – mainly leptin and its receptor, sOB-R. METHODS: We measured serum TSH, free tri-iodothyronine (FT3), free thyroxine, leptin, and sOB-R and assessed energy homeostasis by means of indirect calorimetry, in 27 highly trained athletes and 27 sedentary, healthy men. RESULTS: TSH–FT3ratio was lower in athletes (P<0.03), either in sustained power or anaerobic power-sprint athletes (n=13) or marathon runners (n=14). Whole body respiratory quotient was lower in athletes. Fasting serum sOB-R was higher and leptin lower in athletes than controls. Also serum adiponectin, resistin, and retinol binding protein-4 concentrations were different in athletes than in controls. The ratio between leptin and sOB-R, the free leptin index (FLI), was lower in athletes than in controls (0.025±0.014 vs 0.085±0.049; P<0.001). In multivariate analysis, FLI retained independent association with TSH–FT3ratio. CONCLUSION: Male, elite athletes had lower TSH–FT3ratio and FLI than controls while FLI was independently associated with TSH–FT3ratio supporting the hypothesis that the level of biologically active leptin is involved in the adaptive response of thyroid function in professional athletes. [ABSTRACT FROM AUTHOR]

Abstract: Many studies have considered recent increases in ultraviolet B radiation (UVBR) and endocrine disrupting chemicals polluting the environment as possible contributing factors to the reduction in amphibian populations. It has been demonstrated that exposure of amphibians to estrogenic chemicals or UVBR can affect the timing of larval development and metamorphosis. However, amphibians in the wild are exposed to multiple environmental stressors simultaneously. Therefore, our study examines the effects of UVBR and the estrogenic chemical 4-tert-octylphenol (OP), alone and in combination, on the thyroid system of Rana pipiens tadpoles, which is the main regulator of amphibian metamorphosis. Results demonstrate that thyroid gland histomorphology measurements in Gosner stage 31 tadpoles continuously exposed to UVBR (0.21W/m2) were not different than those measured in animals from the control group. In a separate experiment, tadpoles exposed to environmentally relevant levels of UVBR (0.22W/m2) and/or OP (0.01nM or 10nM) exhibited significantly delayed development starting from Gosner stage 29, given that fewer tadpoles developed past stage 29 in these groups. In addition, significantly fewer UVBR-treated tadpoles developed past stage 34 and metamorphosed. Samples were collected from stages 29 and 34 tadpoles for gene expression analysis in tail tissue and measurements of T3 (triiodothyronine) whole body levels (minus tail). UVBR and/or OP exposure did not affect T3 levels in stages 29 and 34 tadpoles. However, a decrease in deiodinase type 2 (D2) or increase in deiodinase type 3 (D3) mRNA levels was observed in groups of tadpoles with slowed developmental rates at those developmental stages. Given that D2 activates and D3 inactivates thyroid hormones (TH), UVBR/OP mediated disruptions in development are likely caused by dysfunctions in the localized metabolism of THs through alterations in the expression of these enzymes in peripheral tissues. This is the first study to our knowledge reporting a potential thyroid-based mechanism of action for the developmental delays in amphibians exposed to UVBR and/or OP. [Copyright &y& Elsevier]