Human Thyroid Function Research Articles

Serum levels of perchlorate and chlorate in pregnant women from south China and the related health risk with thyroid function

Perchlorate and chlorate are recognized as ubiquitously inorganic pollutants inenvrionment owing to their high solubility in water and resistance to degradation. Previous studies have confirmed the potential adverse effects of perchlorate and chlorate on human thyroid function, along with implications for fetal growth and development. The fetus grows and develops pregnant women's womb and absorbs nutrients from her body. However, there is still limited information on prenatal exposure to perchlorate and chlorate and the related health risks, especially in China. In this study, a total of 430 serum specimens obtained from pregnant females residing in Southern China were analyzed to ascertain the levels of perchlorate and chlorate, and explore the relationship between perchlorate and chlorate and thyroid function by linear regression, WQS, and QGC. The measured serum levels of perchlorate and chlorate were comparatively elevated, demonstrating median values of 0.693 μg/L and 1.36 μg/L, respectively. The estimated exposure dose of perchlorate in 19.7% of pregnant women exceeded the USEPA reference dose, indicating potential health risks. Although no significant association was found between serum perchlorate and thyroid hormone levels, the exposure to perchlorate for pregnant women in Southern China is cause for concern given their sensitivity to chemicals during pregnancy and the relatively high internal exposure levels.

The role of estrogen receptors (ERs)-Notch pathway in thyroid toxicity induced by Di-2-ethylhexyl phthalate (DEHP) exposure: Population data and in vitro studies

BackgroundThis study aimed to assess the exposure level and risk of Di-2-ethylhexyl Phthalate (DEHP) among adults in Jilin Province, China, clarify the impact of DEHP on human thyroid function, and to explore the role of estrogen receptors (ERs)-Notch signaling pathway in the effect of DEHP metabolites on thyroid hormones based on population data and in vitro experiments. Methods312 adults participated in this study. Urinary DEHP metabolites were determined by high performance liquid chromatography coupled to a tandem mass spectrometer (HPLC-MS/MS). Two pharmacokinetic models were used to evaluate the estimated daily intake (EDI) and hazard quotient (HQ) of the adults. Multiple linear regression and mediating effect models were used to evaluate the target associations. In cell experiments, thyroid follicular epithelial (Nthy-ori3–1) cells were exposed to mono (2-ethylhexyl) phthalate (MEHP) for testing. The inhibitions of ERα and Notch pathway were conducted by siRNA and Notch pathway inhibitor DAPT. ResultsThe detection rate of five DEHP metabolites was 97.1∼100.0%. The HQ value of 0.3% of adults was higher than 1. The levels of urinary DEHP metabolites were significantly correlated with thyrotropin (TSH), thyrotropin-releasing hormone (TRH), total triiodothyronine (TT3), total thyroxine (TT4), free triiodothyronine (FT3) and free thyroxine (FT4) and gene (estrogen receptor α (ERα), Notch1, Dll4) levels. The ERα-Notch pathway played a mediating role in the association between DEHP metabolite levels and FT4. The cell results showed, the levels of FT3 and FT4 in cell supernatant decreased after MEHP exposure, and the downward trend was reversed after ERα and notch pathways were inhibited, notch pathway genes also decreased after ERα inhibition. ConclusionAdults in the Jilin Province of China were widely exposed to DEHP. ERs-Notch pathway played an important role in the effect of DEHP metabolites on thyroid hormones.

A-060 Thyroid Laboratory Database Assessment Shows that Total Triiodothyronine Significantly Decreases with Age

Abstract Introduction The effects of aging on human thyroid function are well studied in relationship to thyroid stimulating hormone (TSH) and free tiroxine (FT4); TSH increases, while FT4 decreases with age. Although animal studies show that total triiodotironine (TT3) is lower in aged male rats, these changes are still not clear enough in humans. The National Academy of Clinical Biochemistry (NACB) suggests that TT3 levels would be lower in subjects over 60 years (y.), but the number of elderly assessed was too small for a robust statistical analysis. In search on PubMed, crosschecking the terms elderly/age/aging, with triiodothyronine/T3/total T3, there are a few studies available using current assays with a significant number of patients. Therefore, the demonstration of how the TT3 performs with age is still an opened question. Objective The aim of this study was to observe if TT3 changes significantly with age. Methods We, retrospectively, analyzed blood samples requesting serum TT3 of unique patients, who had TSH measured on the same day; and thyroid peroxidase antibodies (TPOAb), thyroglobulin antibodies (TGAb), anti TSH receptor antibodies (TRAb) or TSH receptor-stimulating immunoglobulin (TSI) at any time since patient admission. Subjects were adults ≥20 y., admitted to a private reference clinical laboratory in Brazil, from January 01, 2014 to December 31, 2022, using anonymized data. Serum TT3 was measured in Cobas Roche, by electrochemiluminescence assay, reference interval 70–210 ng/dL. Exclusion criteria were (and/or): tests performed in hospitals, use of drugs that could interfere on TT3 or TSH, TSH ≤ 0.1 mIU/L or ≥10.0 mIU/L, and any positive antibody at any time. The level of statistical significance was P < 0.05. Results Initially, 959 297 records from the database were surveyed. After applying the exclusion criteria, 141 819 subjects were eligible: mean age = 45 y.; median = 42 y., 62% female (F). Statistically significant differences - P < 0.05 for all comparisons between groups - were found by age and gender in TT3 mean values (in ng/dL). Regarding age: from 20 to 59 y. = 120 ± 26.6; 60 to 79 y. = 109 ± 20.7; and 80 y. and over = 97.2 ± 20.0. By gender: F = 120 ± 28.9; male = 114 ± 20.4. It was also observed that, in elderly, while TT3 decreases, TSH increases (results not shown). Comparing TT3 means by age groups, it is 9% lower in subjects aged 60–79 y. and 19% lower in those aged 80 y. and older, compared to younger (20–59 y.) subjects. Conclusion TT3 results is influenced by several factors, including age, gender and laboratory assay. As far as we know, searching in PubMed, this is the largest collection of data on the relationship between TT3 and age. The data obtained showed a statistically significant decrease in TT3 in elderly, and mainly in very elderly, and higher levels in women than in men. This finding draws call attention to the fact that these parameters should taken into account when evaluating TT3 levels.

Evaluation of Thyroid and Lipid Profile of Hiv Patients Seen in a Faith-Based Health Facility in Anambra State, Nigeria

Background: Human Immunodeficiency Virus (HIV) and thyroid function have been described. Prevalence pattern and atherogenic status significantly differ from HIV-negative control in several studies. Unfortunately, few studies have determined the prevalence of thyroid function and lipids among Nigerians living with HIV. Objective: This study is to evaluate thyroid hormones and lipid profiles in HIV-positive subjects attending a faith-based health facility in Anambra State Nigeria. Materials and methods: The serum concentration of Thyroid Stimulating Hormone (TSH), free Triiodothyronine (fT3), triiodothyronine (T3), free Thyroxine (fT4), Thyroxine (T4), Total Cholesterol [TC], Triglyceride [TG], High-Density Lipoprotein [HDL], Low-Density Lipoprotein [LDL] and Very Low-Density Lipoprotein [VLDL] was determined in 95 HIV positive subjects which include 48 patients who were on HAART- group 1 and 47 not on HAART- group 2; and compared to 30 HIV negative controls – group 3. Results: The level of TSH and fT3 was significantly (p < 0.05) higher in group 1 participants than in group 2 and the group 3 participants. The level of T4 was significantly higher in group 2 than in group 1 and group 3 participants. The level of T3 was significantly lower in Control participants in comparison to both HAART and non-HAART participants. The prevalence of fT4 dysfunction across the groups was significantly different from each other. The total mean of Cholesterol (163.5 ± 22.7), Triglyceride (163.5 ± 22.7), and Very Low-Density Lipoprotein (14.2 ± 2.4) of the HIV-positive participants were significantly (p < 0.05) lower than that of the HIV negative participants. Conclusion: The results obtained from this study indicate that serum levels of thyroid hormones may be used as baseline periodic markers during antiretroviral therapy and many people living with HIV may benefit from supplementation if appropriate.

Genetically predicted selenium concentrations and thyroid function: A two-sample Mendelian randomization study.

The impact of selenium (Se) on human thyroid function remains unclear, with inconsistent results from recent epidemiological studies. Moreover, the observed associations are prone to bias due to potential confounding and reverse causation. Mendelian randomization (MR) analysis facilitates the large minimization of biases produced by environmental and lifestyle influences, providing unconfounded estimates of causal effects using instrumental variables. We aim to examine the association between Se concentrations and human thyroid function using a two-sample MR analysis. Genetic instruments for Se concentrations, including toenail and blood (TAB) and blood Se concentrations, were identified from a genome-wide association study (GWAS) of blood Se (n = 5477) and toenail Se levels (n = 4162). GWAS summary statistics on thyroid phenotypes were downloaded from the ThyroidOmics consortium, including thyroid-stimulating hormone (TSH) (n = 54,288), free thyroxin (FT4) (n = 49,269), hypo (n = 53,423), and hyperthyroidism (n = 51,823). The MR study was conducted using the inverse-variance weighted (IVW) method, supplemented with the weighted median and the mode-based method. Genetically determined TAB Se was negatively associated with FT4 (β = -.067; 95% confidence interval [CI] = -0.106, -0.028; p = 0.001) using the IVW analyses, as well in the additional analyses using the weighted median and weighted-mode methods. No evidence in heterogeneity, pleiotropyor outlier single-nucleotide polymorphisms was detected (all p > 0.05). Suggestive casual association between increased genetically determined TAB Se concentrations and decreased hypothyroidism risk was found by the IVW method (odds ratio [OR] = 0.847; 95% CI = 0.728, 0.985; p = 0.031). The causal effect of TAB Se on FT4 was observed in women (β = -.076; 95% CI = -0.129, -0.024; p = 0.004). However, the influence of genetically determined higher Se concentrations on TSH levels and hyperthyroidism revealed insignificance in the primary and sensitivity analyses. The present MR study indicated that high Se concentration enable the decreasing of FT4 levels, and the effects of Se concentrations on FT4 remain sex-specific.

Characterization of Novel Human Immortalized Thyroid Follicular Epithelial Cell Lines.

Investigation of normal human thyroid function using in vitro culture systems is dependent on cells that recapitulate physiology of differentiated thyrocytes. Primary thyrocytes retain features of the native organ but have limited lifespan in culture. Immortalized thyrocytes offer an alternative if challenges maintaining phenotypic stability can be overcome to retain functional features of primary cells. CI-SCREEN immortalization technology was applied to normal human thyroid tissue to generate four cell line variants. The lines were characterized for transgene integration, biomarker expression, genomic stability, and proliferation rates. Thyroid Stimulating Hormone (TSH)-dependent morphology, thyroglobulin production, thyroxine hormone synthesis, and viability were assessed using conventional 2D monolayer and 3D microtissue culture formats in huThyrEC or h7H medium. Despite differential transgene profiles, the lines had similar biomarker expression patterns and proliferation rates. In 2D culture there was no thyroxine synthesis or changes in viability, but TSH-dependent thyroglobulin production was more significant for several lines in h7H than huThyrEC medium. Comparatively, in 3D microtissues, TSH-dependent thyroglobulin induction was greater for cell lines in h7H medium. Synthesis of thyroxine in one cell line was higher than background with TSH exposure, but not significantly different than control. Immortalization of primary human thyrocytes yielded transgenic lines of epithelial origin. When evaluated in 2D or 3D culture formats, h7H medium supported thyroglobulin production to a greater magnitude than huThyrEC medium. One cell line cultured in 3D microtissue format marginally recapitulated T4 synthesis under continuous TSH exposure. Select human thyroid cell lines exhibited morphological and functional features of primary thyrocytes and are a novel resource for in vitro disease modeling and toxicity testing that will enable reproducible culture models more representative of normal human thyroid function.

Thyroid Function Abnormalities in COVID-19 Patients.

PurposeThe novel coronavirus COVID-19, has caused a worldwide pandemic, impairing several human organs and systems. Whether COVID-19 affects human thyroid function remains unknown.MethodsEighty-four hospitalized COVID-19 patients in the First Affiliated Hospital, Zhejiang University School of Medicine (Hangzhou, China) were retrospectively enrolled in this study, among which 22 cases had complete records of thyroid hormones. In addition, 91 other patients with pneumonia and 807 healthy subjects were included as controls.ResultsWe found that levels of total triiodothyronine (TT3) and thyroid stimulating hormone (TSH) were lower in COVID-19 patients than healthy group (p < 0.001). Besides, TSH level in COVID-19 patients was obviously lower than non-COVID-19 patients (p < 0.001). Within the group of COVID-19, 61.9% (52/84) patients presented with thyroid function abnormalities and the proportion of thyroid dysfunction was higher in severe cases than mild/moderate cases (74.6 vs. 23.8%, p < 0.001). Patients with thyroid dysfunction tended to have longer viral nucleic acid cleaning time (14.1 ± 9.4 vs. 10.6 ± 8.3 days, p = 0.088). To note, thyroid dysfunction was also associated with decreased lymphocytes (p < 0.001) and increased CRP (p = 0.002). The correlation between TT3 and TSH level seemed to be positive rather than negative in the early stage, and gradually turned to be negatively related over time.ConclusionThyroid function abnormalities are common in COVID-19 patients, especially in severe cases. This might be partially explained by nonthyroidal illness syndrome.

Reinterpreting Patterns of Variation in Human Thyroid Function: An Evolutionary Perspective

Two hundred million people worldwide experience some form of thyroid disorder, with women being especially at risk. However, why human thyroid function varies between populations, individuals and across the lifespan has attracted little research to date. This limits our ability to evaluate the conditions under which patterns of variation in thyroid function are best understood as 'normal' or 'pathological'. In this review, we aim to spark interest in research aimed at understanding the causes of variation in thyroid phenotypes. We start by assessing the biomedical literature on thyroid imbalance to discuss the validity of existing reference intervals for diagnosis and treatment across individuals and populations. We then propose an evolutionary ecological framework for understanding the phylogenetic, genetic, ecological, developmental and physiological causes of normal variation in thyroid function. We build on this approach to suggest testable predictions for how environmental challenges interact with individual circumstances to influence the onset of thyroid disorders. We propose that dietary changes, ecological disruptions of co-evolutionary processes during pregnancy and with pathogens, emerging infections and exacerbated stress responses can contribute to explaining the onset of thyroid diseases. For patients to receive the best personalised care, research into the causes of thyroid variation at multiple levels is needed.

Interference on Iodine Uptake and Human Thyroid Function by Perchlorate-Contaminated Water and Food.

Background: Perchlorate-induced natrium-iodide symporter (NIS) interference is a well-recognized thyroid disrupting mechanism. It is unclear, however, whether a chronic low-dose exposure to perchlorate delivered by food and drinks may cause thyroid dysfunction in the long term. Thus, the aim of this review was to overview and summarize literature results in order to clarify this issue. Methods: Authors searched PubMed/MEDLINE, Scopus, Web of Science, institutional websites and Google until April 2020 for relevant information about the fundamental mechanism of the thyroid NIS interference induced by orally consumed perchlorate compounds and its clinical consequences. Results: Food and drinking water should be considered relevant sources of perchlorate. Despite some controversies, cross-sectional studies demonstrated that perchlorate exposure affects thyroid hormone synthesis in infants, adolescents and adults, particularly in the case of underlying thyroid diseases and iodine insufficiency. An exaggerated exposure to perchlorate during pregnancy leads to a worse neurocognitive and behavioral development outcome in infants, regardless of maternal thyroid hormone levels. Discussion and conclusion: The effects of a chronic low-dose perchlorate exposure on thyroid homeostasis remain still unclear, leading to concerns especially for highly sensitive patients. Specific studies are needed to clarify this issue, aiming to better define strategies of detection and prevention.

Urinary Concentrations of Phthalate Metabolite Mixtures in Relation to Serum Biomarkers of Thyroid Function and Autoimmunity among Women from a Fertility Center.

Background:Although previous epidemiological studies have explored associations of phthalate metabolites with thyroid function, no studies to date have assessed associations of mixtures with thyroid function and autoimmunity among potentially susceptible subgroups such as subfertile women.Objective:We aimed to explore associations of mixtures of urinary phthalate metabolites with serum markers of thyroid function and autoimmunity.Methods:This cross-sectional study included 558 women attending a fertility center who provided one spot urine and one blood sample at enrollment (2005–2015). We quantified urinary concentrations of eight phthalate metabolites using mass spectrometry, and biomarkers of thyroid function [thyroid-stimulating hormone (TSH), free and total thyroxine (, ) and triiodothyronine (, ), and autoimmunity [thyroid peroxidase and thyroglobulin antibodies (TPOAb and TgAb, respectively)] in serum using electrochemiluminescence assays. We applied principal component analysis (PCA) and Bayesian kernel machine regression (BKMR) to identify the main patterns of urinary phthalate metabolites. We used linear mixed models to assess the association between PCA-derived factor scores in quintiles and serum thyroid function and autoimmunity, adjusting for age, body mass index (BMI), specific gravity (SG), and, for the PCA, other factor scores.Results:We observed two factors using PCA, one representing the di(2-ethylhexyl) (DEHP) and another non-DEHP metabolites. Compared to women in the lowest quintile of the DEHP factor scores, women in the highest quintile had significantly lower serum concentrations of , , , and [absolute difference: ; 95% confidence interval (CI): , ; ; absolute difference: ; 95% CI: , ; ; absolute difference: ; 95% CI: 0.54, ; ; and absolute difference: ; 95% CI: , ; , respectively]. Using BKMR, we observed that mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) was the primary contributor to these negative associations. DEHP and non-DEHP factor scores were not associated with serum TSH, TgAb, or TPOAb.Conclusions:Mixtures of urinary DEHP metabolites were inversely associated with serum biomarkers of thyroid function but not with autoimmunity, which were within normal ranges for healthy adult women. https://doi.org/10.1289/EHP6740

SUN-575 Anabolic Steroids Induced Hyperthyroidism

Anabolic steroid injections widely used by athletes during strength training period, all studies were done in this field showed transient effect of androgenic anabolic steroids on thyroid which were mainly causing hypothyroidism, However hyperthyroidism cases were never reported up to our knowledge. We present a 25-year-old Emarati male previously healthy, who is referred to endocrine service for hyperthyroidism management. He presented with thyrotoxicosis manifestations. Medical history revealed that he was using anabolic steroids, testosterone, and gonadotropin injection which were prescribed in private gym by trainer. Anabolic steroids were taken twice for few months over 2years prior to his current presentation with hyperthyroidism. Autoimmune profile was negative for thyroid disorder. Radioiodine uptake scan was normal initially then after a year showed diffuse uptake. No evidence of clear cause of his hyperthyroidism. He remained in thyrotoxic state for more than a year post stopping the anabolic steroids. He was treated with radioactive iodine ablation (RAI) according to his preference. Develop post-RAI thyroiditis treated with beta blockers and analgesia. Symptoms completely resolved after 6 weeks and thyroid function returned to normal. The patient has remained asymptomatic on continued follow up care. This case points to the effect of anabolic steroids on thyroid function. Hence all published studies showed that it could cause hypothyroidism not hyperthyroidism. few Literatures are showing that anabolic steroid’s prominent effect on human thyroid function is reduction of TBG with consequent reduction of Total T3 and T4. In rats, anabolic steroids also act in the peripheral metabolism of thyroid hormones and seem to exert an important proliferative effect on thyroid cells. By this effect we believe that, anabolic steroid might cause hyperthyroidism in our patient. To our knowledge, this is the first case report addressing anabolic steroids causing permanent hyperthyroidism. Our patient proved that the effect of anabolic steroid was not transient as he remained in thyrotoxic state for more than a year after stopping steroids and uptake scan showed diffuse high uptake which goes with thyroid cells proliferation hypothesis.

Occupational exposure to pesticides and thyroid function in Brazilian soybean farmers

IntroductionAgriculture production has been supported especially by the use of pesticides for crop protection and pest control. Although the agricultural production has been increased by pesticides use, these substances also reach non-target organisms and may become a risk to the health of farmers. Several epidemiological studies in human have investigated the association between exposure to pesticides and altered serum levels of thyroid hormones, reporting both positive and negative results. Overall, the impact of pesticides on human thyroid function is still limited. ObjectiveThe aim of this study was to access serum levels of free thyroxin (FT4), total triiodothyronine (TT3), thyroid-stimulating hormone (TSH), and butyrylcholinesterase (BChE) in soybean farmers in southern Brazil. MethodsThe exposed group was composed by 46 rural workers and 27 subjects not exposed to pesticides composed the control group. All subjects had blood samples collected by venipuncture in order to analyze the serum levels of FT4, TT3, TSH and BChE. ResultsThe results showed a significant decreasing in TSH and increasing in TT3 and FT4 in rural workers, compared to control group. BChE levels were lower in exposed group than in control group. The results suggest that farmers are exposed to mixtures of pesticides with endocrine disruptor properties.

Maternal smoking and high BMI disrupt thyroid gland development

BackgroundMaternal lifestyle factors, including smoking and increased body weight, increase risks of adult diseases such as metabolic syndrome and infertility. The fetal thyroid gland is essential for the control of fetal metabolic rate, cardiac output, and brain development. Altered fetal thyroid function may contribute to increased disease onset later in life. Here, we investigated the impact of maternal smoking and high maternal weight on human fetal thyroid function during the second trimester.MethodsThyroid glands and plasma were collected from fetuses electively terminated in the second trimester (normally progressing pregnancies). Plasma total triiodothyronine (T3) and total thyroxine (T4) were measured by solid-phase extraction-liquid chromatography-tandem mass spectrometry. Fetal plasma thyroid-stimulating hormone (TSH) levels were measured using a multiplex assay for human pituitary hormones. Histology and immunolocalization of thyroid developmental markers were examined in thyroid sections. Transcript levels of developmental, functional, apoptotic, and detoxification markers were measured by real-time PCR. Statistical analyses were performed using multivariate linear regression models with fetal age, sex, and maternal smoking or maternal body mass index (BMI) as covariates.ResultsMaternal smoking was associated with significant changes in fetal plasma T4 and TSH levels during the second trimester. Smoke-exposed thyroids had reduced thyroid GATA6 and NKX2-1 transcript levels and altered developmental trajectories for ESR2 and AHR transcript levels. Maternal BMI > 25 was associated with increased fetal thyroid weight, increased plasma TSH levels, and abnormal thyroid histology in female fetuses. Normal developmental changes in AHR and ESR1 transcript expression were also abolished in fetal thyroids from mothers with BMI > 25.ConclusionsFor the first time, we show that maternal smoking and high maternal BMI are associated with disturbed fetal thyroid gland development and endocrine function in a sex-specific manner during the second trimester. These findings suggest that predisposition to post-natal disease is mediated, in part, by altered fetal thyroid gland development.

A molecular view of the normal human thyroid structure and function reconstructed from its reference transcriptome map

BackgroundThe thyroid is the earliest endocrine structure to appear during human development, and thyroid hormones are necessary for proper organism development, in particular for the nervous system and heart, normal growth and skeletal maturation. To date a quantitative, validated transcriptional atlas of the whole normal human thyroid does not exist and the availability of a detailed expression map might be an excellent occasion to investigate the many features of the thyroid transcriptome.ResultsWe present a view at the molecular level of the normal human thyroid histology and physiology obtained by a systematic meta-analysis of all the available gene expression profiles for the whole organ. A quantitative transcriptome reference map was generated by using the TRAM (Transcriptome Mapper) software able to combine, normalize and integrate a total of 35 suitable datasets from different sources thus providing a typical reference expression value for each of the 27,275 known, mapped transcripts obtained. The experimental in vitro validation of data was performed by “Real-Time” reverse transcription polymerase chain reaction showing an excellent correlation coefficient (r = 0.93) with data obtained in silico.ConclusionsOur study provides a quantitative global reference portrait of gene expression in the normal human thyroid and highlights differential expression between normal human thyroid and a pool of non-thyroid tissues useful for modeling correlations between thyroidal gene expression and specific thyroid functions and diseases. The experimental in vitro validation supports the possible usefulness of the human thyroid transcriptome map as a reference for molecular studies of the physiology and pathology of this organ.

The heterogeneity of islet autoantibodies and the progression of islet failure in type 1 diabetic patients.

Type 1 diabetes mellitus is heterogeneous in many facets. The patients suffered from type 1 diabetes present several levels of islet function as well as variable number and type of islet-specific autoantibodies. This study was to investigate prevalence and heterogeneity of the islet autoantibodies and clinical phenotypes of type 1 diabetes mellitus; and also discussed the process of islet failure and its risk factors in Chinese type 1 diabetic patients. A total of 1,291 type 1 diabetic patients were enrolled in this study. Demographic information was collected. Laboratory tests including mixed-meal tolerance test, human leukocyte antigen alleles, hemoglobinA1c, lipids, thyroid function and islet autoantibodies were conducted. The frequency of islet-specific autoantibody in newly diagnosed T1DM patients (duration shorter than half year) was 73% in East China. According to binary logistic regressions, autoantibody positivity, longer duration and lower Body Mass Index were the risk factors of islet failure. As the disease developed, autoantibodies against glutamic acid decarboxylase declined as well as the other two autoantibodies against zinc transporter 8 and islet antigen 2. The decrease of autoantibodies was positively correlated with aggressive beta cell destruction. Autoantibodies can facilitate the identification of classic T1DM from other subtypes and predict the progression of islet failure. As there were obvious heterogeneity in autoantibodies and clinical manifestation in different phenotypes of the disease, we should take more factors into consideration when identifying type 1 diabetes mellitus.

Exposure to non-persistent pesticides and thyroid function: A systematic review of epidemiological evidence.

Numerous pesticides are recognized for their endocrine-disrupting properties. Non-persistent pesticides such as organophosphates, dithiocarbamates and pyrethroids may interfere with thyroid function as suggested by animal studies. However, the influence of chronic exposure to these compounds on thyroidal functions in humans remains to be determined. The present study aimed to review epidemiological evidence for an association between exposure to non-persistent pesticides and circulating levels of thyroid hormones (thyroxin [T4] and triiodothyronine [T3]) and thyroid-stimulating hormone (TSH). A systematic review was conducted using MEDLINE, SCOPUS and Virtual Health Library (BVS) databases. Articles were limited to original studies and reports published in English, Portuguese or Spanish. Nineteen epidemiological studies were identified, 17 of which were cross-sectional, 14 were of occupationally exposed workers and 11 used exposure biomarkers. Fungicides and organophosphates (OP) insecticides were the most studied pesticides. Although methodological heterogeneity between studies was noted, particularly regarding study design, exposure assessment, and control of confounding, most of them showed associations with changes in T3 and T4, and/or TSH levels, while results from a few of these are consistent with experimental data supporting the findings that non-persistent pesticide exposure exerts hypothyroid-like effects. However, reporting quality was moderate to poor in 50% of the studies, particularly regarding method of selection of participants and discussion of external validity. Overall, current knowledge regarding the impact of non-persistent pesticides on human thyroid function is still limited. Given the widespread use of pesticides, future research should assess effects of exposure to currently-used pesticides in cohort studies combining comprehensive questionnaire-based assessment and biomarkers. Investigators need to pay particular attention to exposure during critical windows of brain development and exposure in agricultural populations.

Exposure To Non-Persistent Pesticides And Thyroid Hormone Levels: A Systematic Review Of The Epidemiological Evidence

Introduction: Numerous pesticides are recognized for their endocrine-disrupting properties. Non-persistent pesticides such as organophosphates (OP), carbamate and pyrethroids may interfere with thyroid function, as suggested by animal studies. However, how chronic exposure to these compounds affects human health is unknown. The present study aimed to review the epidemiological evidence for the association between exposure to non-persistent pesticides and thyroid hormone (TH) levels. Methods: A systematic review was conducted using MEDLINE and Virtual Health Library databases. Articles were limited to original studies and reports published in English, Portuguese or Spanish. Case-reports and studies only addressing organochlorine pesticides were excluded. Results: Seventeen epidemiological studies were identified that investigated the association between exposure to non-persistent pesticides and TH levels. The full text of one of them was not available. Of the remaining studies, 14 were cross-sectional, 11 were of occupationally exposed workers and 11 used exposure biomarkers. OP and metabolites were the most studied pesticides. Overall, pesticide exposure was not associated with TH levels. However, alterations compatible with hypothyroidism, i.e. reduced triiodotironine (T3) or thyroxin (T4), and elevated thyroid-stimulating hormone (TSH) were observed in 7 and 5 studies, respectively, whereas a few reports found positive association with T4 and negative association with TSH. Methodological heterogeneity between studies was noted, particularly regarding sample size, type of pesticide, exposure assessment method and statistical analysis. Conclusions: Current knowledge about the impact of non-persistent pesticides on human thyroid function is limited. In addition, the varying methodological approaches hamper drawing conclusions about the evidence on the topic. This review highlights the need for research to explore this relationship in different exposure scenarios.

Thyroid gland: Human thyroid gland development and function--angiogenesis in the spotlight.

Thyroid gland: Human thyroid gland development and function--angiogenesis in the spotlight.

Human fetal thyroid function.

The early steps of thyroid development that lead to its function in the human fetus and subsequently the further maturation that allows the human fetus to secrete thyroxine (T4) in a significant amount are reviewed here. We underline the importance of the transfer of T4 from the pregnant woman to her fetus, which contributes at all stages of the pregnancy to fetal thyroid function and development. In the first trimester of pregnancy, the temporal and structural correlation of thyroid hormone synthesis with folliculogenesis supported the concept that structural and functional maturations are closely related. Human thyroid terminal differentiation follows a precisely timed gene expression program. The crucial role of the sodium/iodine symporter for the onset of thyroid function in the human fetus is shown. Fetal T4 is detected by the eleventh week of gestation and progressively increases throughout. The pattern of thyroid hormones and thyroid-stimulating hormone levels in the course of pregnancy is given from fetal blood sampling data, and the mechanisms governing this maturation in the human fetus are discussed. Finally an example of primary human fetal thyroid dysfunction, such as in Down syndrome, is given. The understanding of the physiology of the human fetal thyroid function is the basis for fetal medicine in the field of thyroidology.

Effect of excess fluoride ingestion on human thyroid function in Gaya region, Bihar, India

Fluoride (F) is mainly ingested through drinking water and food. In addition to producing dental and skeletal fluorosis, excess fluoride may affect the functioning of many organs including the thyroid gland. The present study investigated the thyroid function of subjects with dental fluorosis from F-endemic areas of Gaya region, Bihar, India and compared it with control individuals from Bodh Gaya. The mean F concentration in groundwater of F-endemic area was 2.82 ± 0.18 mg/L (range 0.62–7.2 mg/L), while that of control area was 0.49 ± 0.04 mg/L (range 0.21–0.76 mg/L). Abnormal levels of T3, T4, and TSH were found in the study subjects from both control and F-endemic areas.