Perchlorate and thyroid function

ContextThe COVID-19 pandemic continues to exert an immense burden on global health services. Moreover, up to 63% of patients experience persistent symptoms, including fatigue, after acute illness. Endocrine systems are vulnerable to the effects of COVID-19 as many glands express the ACE2 receptor, used by the SARS-CoV-2 virion for cellular access. However, the effects of COVID-19 on adrenal and thyroid gland function after acute COVID-19 remain unknown.ObjectiveOur objectives were to evaluate adrenal and thyroid gland function in COVID-19 survivors.MethodsA prospective, observational study was undertaken at the Clinical Research Facility, Imperial College NHS Healthcare Trust, including 70 patients ≥18 years of age, at least 3 months after diagnosis of COVID-19. Participants attended a research study visit (8:00-9:30 am), during which a short Synacthen test (250 µg IV bolus) and thyroid function assessments were performed.ResultsAll patients had a peak cortisol ≥450 nmol/L after Synacthen, consistent with adequate adrenal reserve. Basal and peak serum cortisol did not differ according to disease severity or history of dexamethasone treatment during COVID-19. There was no difference in baseline or peak cortisol after Synacthen or in thyroid function tests, or thyroid status, in patients with fatigue (n = 44) compared to those without (n = 26).ConclusionAdrenal and thyroid function ≥3 months after presentation with COVID-19 was preserved. While a significant proportion of patients experienced persistent fatigue, their symptoms were not accounted for by alterations in adrenal or thyroid function. These findings have important implications for the clinical care of patients after COVID-19.

For a long time it has been known that both hypo- and hyperthyroidism are associated with an increased risk of morbidity and mortality. In recent years, it has also become clear that minor variations in thyroid function, including subclinical dysfunction and variation in thyroid function within the reference range, can have important effects on clinical endpoints, such as bone mineral density, depression, metabolic syndrome, and cardiovascular mortality. Serum thyroid parameters show substantial interindividual variability, whereas the intraindividual variability lies within a narrow range. This suggests that every individual has a unique hypothalamus-pituitary-thyroid axis setpoint that is mainly determined by genetic factors, and this heritability has been estimated to be 40-60%. Various mutations in thyroid hormone pathway genes have been identified in persons with thyroid dysfunction or altered thyroid function tests. Because these causes are rare, many candidate gene and linkage studies have been performed over the years to identify more common variants (polymorphisms) associated with thyroid (dys)function, but only a limited number of consistent associations have been found. However, in the past 5 years, advances in genetic research have led to the identification of a large number of new candidate genes. In this review, we provide an overview of the current knowledge about the polygenic basis of thyroid (dys)function. This includes new candidate genes identified by genome-wide approaches, what insights these genes provide into the genetic basis of thyroid (dys)function, and which new techniques will help to further decipher the genetic basis of thyroid (dys)function in the near future.

Thyroid volume and thyroid function may vary in obese and nonobese women. It is not known whether weight loss could affect thyroid volume and function in obese subjects. The study population consisted of 98 premenopausal euthyroid obese [body mass index (BMI) = 30 kg/m2] women (mean age 40.5 +/- 11.4 years) and 31 nonobese (BMI < 25 kg/m2) women (mean age 38.6 +/- 12.9 years). Weight, height, BMI, waist circumference, body fat percentage and fat weight of all subjects were measured. Thyroid function and thyroid ultrasonography were performed at baseline and after 6 months of obesity treatment. Subgroup analysis was done according to weight loss. Thyroid volume (P = 0.021) and TSH concentration (P = 0.047) were higher; free T3 (P < 0.001) and free T4 concentrations (P = 0.045) were lower in obese women; however, all were still in the normal range. There was a positive correlation between thyroid volume and body weight (r = 0.319, P = 0.002), BMI (r = 0.504, P < 0.001), body fat percentage (r = 0.375, P = 0.001), body fat weight (r = 0.309, P = 0.01) and waist circumference (r = 0.386, P = 0.004). There was a positive correlation between TSH concentration and body weight (r = 0.227, P = 0.042) and body fat weight (r = 0.268, P = 0.038). After 6 months of obesity treatment, thyroid volume (P = 0.008) and TSH concentration (P = 0.006) decreased only in obese women who lost > 10% body weight. There was a positive correlation between the changes of thyroid volume and the change of body weight (r = 0.341, P = 0.009) and the change of body fat weight (r = 0.406, P = 0.013). Our study suggests that thyroid volume and function may vary in obese women in association with body weight and fat mass; > 10% weight loss may affect thyroid volume and function, which however, is clinically insignificant.

The thyroid gland regulates most of the physiological processes. Environmental factors, including climate change, pollution, nutritional changes, and exposure to chemicals, have been recognized to impact thyroid function and health. Thyroid disorders and cancer have increased in the last decade, the latter increasing by 1.1% annually, suggesting that environmental contaminants must play a role. This narrative review explores current knowledge on the relationships among environmental factors and thyroid gland anatomy and function, reporting recent data, mechanisms, and gaps through which environmental factors act. Global warming changes thyroid function, and living in both iodine-poor areas and volcanic regions can represent a threat to thyroid function and can favor cancers because of low iodine intake and exposure to heavy metals and radon. Areas with high nitrate and nitrite concentrations in water and soil also negatively affect thyroid function. Air pollution, particularly particulate matter in outdoor air, can worsen thyroid function and can be carcinogenic. Environmental exposure to endocrine-disrupting chemicals can alter thyroid function in many ways, as some chemicals can mimic and/or disrupt thyroid hormone synthesis, release, and action on target tissues, such as bisphenols, phthalates, perchlorate, and per- and poly-fluoroalkyl substances. When discussing diet and nutrition, there is recent evidence of microbiome-associated changes, and an elevated consumption of animal fat would be associated with an increased production of thyroid autoantibodies. There is some evidence of negative effects of microplastics. Finally, infectious diseases can significantly affect thyroid function; recently, lessons have been learned from the SARS-CoV-2 pandemic. Understanding how environmental factors and contaminants influence thyroid function is crucial for developing preventive strategies and policies to guarantee appropriate development and healthy metabolism in the new generations and for preventing thyroid disease and cancer in adults and the elderly. However, there are many gaps in understanding that warrant further research.

The relative associations of polycystic ovarian syndrome (PCOS) and metabolic syndrome (MS) with the risk for thyroid disease (thyroid function, volume, nodularity and autoimmunity) are unknown.We compared thyroid features and function in patients with PCOS and control subjects by the presence of MS. We recruited 84 women with PCOS and 81 age-matched healthy controls. PCOS was defined according to the Rotterdam criteria. Thyroid ultrasound and function tests were performed in all. Although thyroid disease was more prevalent in women with PCOS, ovarian disease was not significantly associated with the risk for thyroid disease. Thyroid volume did not differ between women with PCOS and control subjects (13.7±8.6 vs 12.4±4.4 ml, respectively; p=0.2); however, it differed significantly between subjects with and without MS (regardless of PCOS status): 19.1±14.8 vs 12.4±4.9 ml, respectively; p=0.001). Antithyroglobulin and antithyroid peroxidase antibody levels also were significantly higher in subjects with MS, but not in participants with PCOS vs control subjects. Overall, TSH level correlated significantly with body mass index (BMI), weight, waist circumference, diastolic blood pressure, and levels of LDL cholesterol, triglycerides, and HDL cholesterol. Thyroid volume correlated significantly with age, weight, BMI, waist circumference, systolic blood pressure, 120-min postprandial glucose and HDL level. PCOS alone was not associated with thyroid disease in our population. However, MS and some of its components appear to be related to thyroid volume, function, and antithyroid antibody levels.

The thyroid gland exerts a major control on the physiology of the whole body, and it raises fundamental questions about molecular physiological processes. Moreover, an increased proliferation of thyroid cells is associated with several pathologies, and several mechanisms may be involved. Thyroid disorders are very common, affecting millions of people. These include hypothyroidism, hyperthyroidism, thyroid nodules, thyroid cancer, and so forth, but they are also associated with other nonthyroid disorders. This special issue is devoted to illustrate the particular richness of current investigations in the field of thyroid function and growth regulation under normal and abnormal conditions. Although thyroid gland function is mainly under the control of pituitary TSH in normal conditions, other factors may also play a role in this process. Thyroid disease is more common in women than in men. Tania Weber Furlanetto and Ana Paula Santin reviewed the direct effects of estrogens on thyroid function and growth regulation in the paper titled “Role of estrogen in thyroid function and growth regulation.” Thyroid cancer is the most common endocrine malignancy, and its incidence has significantly risen in the last decades in the world. The knowledge how thyroid cancer develops is expanding rapidly. The sequential acquisition of mutations which arise as a consequence of damage to the genome is required in order to transform a normal cell into a malignant one. The understanding of the process of thyroid carcinogenesis at the molecular level will improve not only the diagnostic but also the treatment of this pathology. Ioannis Legakis and Konstantinos Syrigos describe the molecular events associated with the progression and dedifferentiation of thyroid carcinoma in the paper titled “Recent advances in molecular diagnosis of thyroid cancer.” Thyroid-specific transcription factors regulate thyroid-specific gene expression and organogenesis. Their possible role in thyroid cancer as well as in the maintenance and/or activity of stem cells is discussed by Shioko Kimura in the paper titled “Thyroid-specific transcription factors and their roles in thyroid cancer.” MicroRNAs (miRNAs) are short ribonucleic acid molecules (around 22 nucleotides) found in eukaryotic cells. miRNAs are posttranscriptional regulators that bind to complementary sequences on messenger RNA transcripts inducing the translational repression or messenger RNA degradation. Several miRNAs have been found to have links with some types of cancer. Francesca Marini, Ettore Luzi, and Maria Luisa Brandi reviewed the role of miRNAs in thyroid cancer development in the paper titled “MicroRNA role in thyroid cancer development.” Growth factors play a role in thyroid proliferation and function, while EGF acts as a mitogen for thyroid cells inhibiting also thyroid differentiation. TGF-β is a potent inhibitor of thyroid cell growth. However, in some transformed thyroid cells this inhibition is lost. The role of TGF-β and EGF on thyroid carcinogenesis and the crosstalk between these growth factors are discussed by Gabriella Mincione Maria Carmela Di Marcantonio, Chiara Tarantelli, Sonia D'Inzeo, Arianna Nicolussi, Francesco Nardi, Caterina Francesca Donini, and Anna Coppa in the paper titled “EGF and TGF-β1 effects on thyroid function.” Grave's disease and Hashimoto's thyroiditis are the two main types of autoimmune thyroid disease. Occasionally they are also associated with other autoimmune diseases. Emina Kasumagic-Halilovic, Asja Prohic, Begler Begovic, and Nermina Ovcina-Kurtovic bring additional support to the existence of a significant association between vitiligo and thyroid autoimmunity in the paper titled “Association between vitiligo and thyroid autoimmunity.” Although some authors have found an association between an abnormal thyroid condition and bipolar disorder, little is known about the implication of the hypothalamo-pituitary-thyroid in neuropsychological deficits. Subho Chakrabarti review the last findings on this topic including genetic and neuroimaging investigations (Thyroid Functions and Bipolar Affective Disorder). Guillermo Juvenal Daniel Christophe Pierre Roger Mario Pisarev

Background: Elevated levels of antithyroperoxidase antibodies (TPOAbs) have been associated with progression of subclinical thyroid dysfunction, extrathyroidal diseases, and decrease in functional status. However, TPOAb as determinant of future thyroid dysfunction and other clinical outcomes has not been studied well for adults aged 85 years and over. This study aimed to assess associations of TPOAb levels with thyroid function, survival, physical function, disability in activities of daily living (ADL), cognitive function, and depressive symptoms in the oldest old. Methods: Data from a population-based cohort study (Leiden 85-plus Study) of residents of Leiden, the Netherlands, aged 85 and older were used. Baseline serum TPOAb levels were available for 488 participants (82% of the total cohort). We considered levels ≥35 IU/mL as elevated. Thyroid function (thyrotropin [TSH] and free thyroxine) was assessed at age 85 (baseline), 87, and 88 years. Survival, physical function, disability in ADL, cognitive function, and depressive symptoms were assessed from age 85 through 90 years. Results: At baseline, 64 of the 85-year old participants (13.1%) had elevated TPOAb levels. They were more often female, had higher TSH levels, and a higher prevalence of overt or subclinical hypothyroidism than participants with normal TPOAb levels. Over time, elevated TPOAb levels were independently associated with a lower mortality risk (hazard ratio 0.72, [95% confidence interval 0.53-0.99]), but were not associated with changes in thyroid function, nor with physical function, disability in ADL, cognitive function, or depressive symptoms. Conclusions: In community-dwelling oldest old, elevated TPOAb levels are cross-sectionally associated with higher TSH levels. Over time, elevated TPOAb levels are associated with a survival benefit but are not associated with changes in thyroid function, functional status, or depressive symptoms in old age. The added clinical value of TPOAb tests in oldest old persons with thyroid dysfunction is limited.

Aging causes morphological and functional changes in the thyroid gland. Free radicals play a key role in the pathology of normal aging. Vimentin and cytokeratin are cytoskeletal intermediate filaments that are often used as indirect indices of tissue injury. The aim of the study was to clarify the age-related alterations in the structure and function of the thyroid gland. The relationship between oxidative/antioxidative stress markers and cytoskeletal intermediate filaments (vimentin and cytokeratin) and oxidative/antioxidative stress markers as well as vascular endothelial growth factor (VEGF) during aging were elucidated. Finally, the role of Nigella sativa (NS) oil in ameliorating age-related alterations of the structure and function of the thyroid gland was studied. Thirty Sprague-Dawley albino rats were divided into five groups: young adult control, young adult NS-treated, late adult control, late adult NS-treated, and senile. The age of young adult, late adult, and senile rats was nearly 7, 18 and 22 months, respectively. NS oil was added to food pellets and was administered at a daily dose of 0.1 g/kg body weight for one month. The thyroid gland was dissected and fixed immediately in 10% formalin saline. The assessment of thyroid structure was based on hematoxylin and eosin, and Masson's trichrome stainings, and histomorphometric analysis of the deparaffinized sections. Localization and distribution of vimentin and cytokeratin filaments was assessed by immunohistochemistry. Measurements of VEGF gene expression by qPCR and oxidative/antioxidative markers (malondialdehyde and glutathione content, superoxide dismutase activity) in thyroid gland homogenates were performed. Serum concentration of thyroid hormones (T3, T4) and TSH were assessed by radioimmunoassay. Follicles in the late adult control group were dilated and disrupted. Follicular cells showed cytoplasmic vacuolation. Follicles in the thyroids of senile rats were of irregular shape, often with cellular exfoliations. Many follicles were dilated and lined with flattened cells. A notable amelioration of these morphological alterations was observed in late adult NS-treated rats. Decrease in serum T3 and T4 levels and increase in TSH levels were observed in the late adult control and senile groups. A clear shift of the oxidative/antioxidative markers (MDA/ /GSH, SOD) was observed in the late adult control and senile groups in favor of oxidants. Administration of NS to late adult rats resulted in normalization of these parameters. Increased area of collagen fibers, immunoreactivity of vimentin and cytokeratin filaments and VEGF gene expression were observed in the thyroids of late adult and senile rat groups as compared to young animals. The mean number of follicular cells decreased in the late adult control and senile groups. Administration of NS to the late adult rats returned these parameters to the level of the young adult rats. Aging-related alterations in both structure and function of the rat thyroid gland that are associated with increased indices of oxidative stress might be abrogated by administration of antioxidative agents present in Nigella sativa oil.

Trace elements, such as iodine and selenium (Se), are vital to human health and play an essential role in metabolism. They are also important to thyroid metabolism and function, and correlate with thyroid autoimmunity and tumors. Other minerals such as iron (Ir), lithium (Li), copper (Co), zinc (Zn), manganese (Mn), magnesium (Mg), cadmium (Cd), and molybdenum (Mo), may related to thyroid function and disease. Normal thyroid function depends on a variety of trace elements for thyroid hormone synthesis and metabolism. These trace elements interact with each other and are in a dynamic balance. However, this balance may be disturbed by the excess or deficiency of one or more elements, leading to abnormal thyroid function and the promotion of autoimmune thyroid diseases and thyroid tumors.The relationship between trace elements and thyroid disorders is still unclear, and further research is needed to clarify this issue and improve our understanding of how trace elements mediate thyroid function and metabolism. This paper systematically reviewed recently published literature on the relationship between various trace elements and thyroid function to provide a preliminary theoretical basis for future research.

ObjectiveTo investigate the correlations between thyroid function, renal function, and depression.MethodsClinical data of 67 patients with Major depressive disorder (MDD) and 36 healthy control subjects between 2018 and 2021 were collected to compare thyroid and renal function. Thyroid and renal functions of depressed patients were then correlated with the Hamilton Depression Rating Scale (HAMD) and the Hamilton Anxiety Rating Scale (HAMA).Spearman correlation analysis was used to find the correlation between renal function, thyroid function, and depression. A logistic regression was performed to find significant predictors of depression.ResultsTriiodothyronine protamine (T3), thyroxine (T4), free triiodothyronine protamine (FT3), uric acid, sodium, and anion gap were lower in the MDD group than in the control group (p < 0.05). Correlation analysis of thyroid function, renal function, and factor terms of HAMD in the MDD group suggested that diurnal variation, hopelessness, and depression level were positively correlated with thyrotropin (TSH) (p < 0.05). Cognitive disturbance, retardation, and depression level were negatively correlated with creatinine (p < 0.05). Diurnal variation was negatively correlated with sodium ion (p < 0.01); hopelessness and depression level were positively correlated with chloride ion (p < 0.05); diurnal variation, retardation, and depression level were negatively correlated with anion gap (p < 0.05). Diurnal variation (p < 0.01) and retardation (p < 0.05) were negatively correlated with osmolality. Cognitive disturbance and depression level were positively correlated with estimated glomerular filtration rate (eGFR) (p < 0.05). In the MDD group, correlation analysis of thyroid function, renal function, and HAMA factor terms suggested that the total HAMA score and anxiety level were positively correlated with chloride ion (p < 0.05); psychic anxiety, total HAMA score, and anxiety level were negatively correlated with anion gap (p < 0.05). Furthermore, a low level of anion gap was an independent risk factor for depression and anxiety levels (p < 0.05).ConclusionLow thyroid function and reduced waste metabolized by the kidneys in patients with MDD suggest a low intake and low metabolism in depressed patients. In addition, subtle fluctuations in the anion gap in depressed patients were strongly correlated with the degree of depression and anxiety.

Cigarette smoking has multiple effects on thyroid function. These include both pro(e.g. thyroidstimulating) and anti-thyroid actions and also actions that increase susceptibility to or exacerbation of the manifestations of Graves’ disease. In this issue of the Journal, Gasparoni et al. describe the effects of parental smoking on fetal thyroid secretion and also on thyroid function of some of the same infants at one year of age (1). Before considering the results of this new study, it seems appropriate to review briefly earlier work on the effects of smoking on the thyroid in adults. In normal adults, smoking has either no effect on thyroid function and size or a weak pro-thyroid effect. The abnormalities described include small goiters and small, thyrotropin-independent increases in thyroid function, most often small increases in serum triiodothyronine and thyroglobulin concentrations (see references 2 and 3 for reviews). These findings suggest that smoking in some way directly stimulates thyroid growth and function, but how it might do so is not known. Nicotine causes sympathetic activation, which can increase thyroid secretion. Alternatively, nicotine or some other component of tobacco smoke might have direct thyroid-stimulating actions. Despite the association with goiter and small increases in thyroid secretion, in several case-control studies smoking was not a risk factor for either non-toxic or toxic multinodular goiter, indicating that its overall contribution to these disorders must be small (4, 5). Most, if not all, of the subjects in these studies and in those to be described were women. Nevertheless, the conclusions are probably applicable to men. Among patients with subclinical hypothyroidism, those who smoke have higher serum thyrotropin concentrations, a higher serum ratio of tri-iodothyronine to free thyroxine, and higher serum cholesterol and lowdensity lipoprotein cholesterol concentrations than those who do not smoke (6). In contrast, among patients with overt hypothyroidism, smokers and nonsmokers have similar serum thyrotropin and thyroid hormone concentrations, but more symptoms, signs and biochemical and physiological changes of hypothyroidism (6). Thus smoking reduces thyroid secretion in patients with subclinical hypothyroidism and exacerbates the peripheral effects of thyroid deficiency in those patients and in patients with overt hypothyroidism. Notwithstanding these results, in the same case-control studies cited above smoking was not a risk factor for chronic autoimmune thyroiditis (4, 5), although it was associated with postpartum thyroiditis, a precursor of chronic autoimmune thyroiditis, in one study (7). At the other end of the spectrum, there is substantial evidence that smoking is a risk factor for Graves’ hyperthyroidism, and especially Graves’ ophthalmopathy (4, 5, 8, 9). In a case-control study done in The Netherlands, for example, the odds ratio for smoking among patients with Graves’ hyperthyroidism was 1.9. It was 7.7 among those with Graves’ hyperthyroidism and ophthalmopathy, and the ophthalmopathy was more severe in those who smoked (5). How might smoking contribute to the pathogenesis of Graves’ disease? It might alter the structure of the thyrotropin receptor, making it more immunogenic in a way that leads to the production of thyrotropin-receptor stimulating antibodies that react strongly with retro-orbital tissue. It might augment immunologic responsiveness to whatever factor initiates Graves’ disease or, on the other hand, it might impair restoration of tolerance to thyroid auto-antigens. Lastly, it might in some way sensitize retro-orbital tissue to the antibodies or other substances that cause ophthalmopathy. The results of the effects of parental smoking on thyroid function of fetuses or infants aged one year, as described by Gasparoni et al. (1), provide additional insight into the interrelationships between smoking and thyroid dysfunction. They found that infants whose mothers and fathers smoked had higher cord serum thyroglobulin and thiocyanate concentrations than infants whose parents did not smoke. The infants had no other evidence of thyrotropin-independent thyroid stimulation, such as increased serum thyroxine or triiodothyronine or decreased serum thyrotropin concentrations, as has been reported by others (10). Thyroid size was not determined, but in another study it was increased in infants born of mothers who smoked (11). Of note is their finding that cord serum thyroglobulin concentrations were increased in the infants whose fathers, but not mothers, smoked, indicating that the component(s) of tobacco smoke that stimulates thyroglobulin secretion can be transferred passively. Also of note is the finding that at age one year the infants whose fathers and mothers both smoked had higher serum thyroglobulin and thiocyanate concentrations than the infants whose parents did not smoke (the infants whose European Journal of Endocrinology (1998) 138 368–369 ISSN 0804-4643

The effect of recombinant human TSH (rhTSH) on thyroid function and ultrasonically determined thyroid volume was investigated in nine healthy euthyroid male volunteers. Each received either 0.9 mg rhTSH or isotonic saline in a randomized order, and thyroid volume and function were closely monitored during the following 28 d. No significant changes were observed after saline injection. After rhTSH stimulation, the median serum TSH increased from 2.03 mU/liter (range, 0.99-3.07 mU/liter) to more than 200 mU/liter (range, 78.9 to >200.0 mU/liter) after 4 h, with a subsequent rapid decline. Mean (+/-SEM) serum free T(4) and free T(3) peaked at 48 h with levels 204.7 +/- 26.1% and 226.9 +/- 31.4%, respectively, above baseline (P < 0.001). Twenty-four hours after rhTSH stimulation, mean (+/-SEM) thyroid volume was significantly increased by 23.3 +/- 5.8% (P = 0.003) and after 48 h by 35.5 +/- 18.4% (P = 0.02). On d 4 the mean thyroid enlargement had reverted to baseline values. One individual developed a 90-ml tender thyroid enlargement (initially 21 ml) 36 h after rhTSH administration, associated with a very high level of serum thyroglobulin. It is concluded that 0.9 mg rhTSH may result in a profound stimulation of not only thyroid function but also of thyroid size, appearing in the period 1-4 d after injection. Further dose-response studies are needed to clarify the potential hazards before routine use, for example in the context of (131)I therapy and goiter.

Thyroid dysfunction has been associated with kidney function decline, but mainly in cross-sectional studies. Therefore, we aimed to determine the association between thyroid and kidney function in a prospective population-based cohort study longitudinally. Prospective cohort study. Participants aged ≥45 years from the Rotterdam Study with thyroid and kidney function assessment were included. Kidney function and new onset chronic kidney disease (CKD) were defined using estimated glomerular filtration ate (eGFR), with CKD defined as eGFR <60 mL/min/1.73 m2 according to the CKD-EPI formula. We included 5103 participants (mean age of 63.6 years) with a mean follow-up of 8.1 years. Cross-sectionally, higher TSH levels were associated with lower eGFR (Beta (β): -1.75 mL/min; 95% confidence interval (CI): -2.17, -1.33), in multivariable models adjusting for several cardiovascular risk factors including smoking, hypertension and history of coronary heart disease among others. In contrast, longitudinally, higher TSH levels were associated with less annual eGFR decline (β: -0.06 mL/min; CI: -0.11, -0.01) and lower CKD incidence (odds ratio 0.85, CI; 0.75, 0.96). Compared with euthyroid participants, subclinical hyperthyroid individuals had an increased risk for CKD whereas hypothyroid individuals had a decreased risk (P for trend = 0.04). Hyperactive thyroid function is associated with increased risk of kidney function decline while hypothyroidism is associated with a decreased CKD risk. More insight is needed in the pathophysiological pathways connecting high thyroid function and kidney function decline.

Thyroid volume and thyroid function may vary to anthropometric measurements. It is not known whether anthropometric measurements could affect thyroid volume and function in adult subjects.The studied population consisted of 57 premenopausal euthyroid women (mean age 39.5±10.4 years) and 31 men (mean age 37.3±9.9 years). Weight, height, BMI, neck circumference, neck height and thyrosternal distance of all subjects were measured. Thyroid function and thyroid ultrasonography were performed.Thyroid volume (P=0.03) and TSH concentration (P=0.04) were higher; free T3 (P<0.001) and free T4 concentrations (P=0.045) were lower in obese subjects; however, all parameters were still in the normal range. There was a positive correlation between thyroid volume and body weight (r=0.309, P=0.004), thyrosternal distance (r=0.504, P<0.001) and neck circumference (r=0.327, P=0.003).Our study suggests that thyroid volume and function may vary to neck anthropometric measurements. But there must be performed more other studies which research the relationship between thyroid volume and neck anthropometry. We are convinced that our study will set light to the awareness of this deficiency.

Lithium is especially taken as a maintenance medication for Bipolar Disorder. In women with bipolar disorder, lithium is often effective during postpartum period, but breast-feeding for medicated mothers is controversial because of harmful effects for her child. At present, the biological mechanisms of lithium are not well-understood, affecting its usage and overall health implications. We developed a rat lithium and breast-feeding model at human therapeutic levels to study the effects of lithium exposure through breast-milk on pups' thyroid function. Novel laser analytical spectroscopy, along with traditional blood and immunohistochemical tests, were applied to further investigate the mechanisms behind the thyroid dysfunction. Maternal iodine supplementation was evaluated as a therapeutic method to address the pups' thyroid dysfunction. Pups exposed to lithium via breastmilk, even with the dam on a sub-therapeutic level, experienced weight gain, reduced blood thyroxine (T4 ), and elevated blood urea nitrogen, indicating effects on thyroid and kidney function. We show that lithium inhibited iodine uptake by thyroid follicles, initiating a mechanism that reduced iodination of tyrosine, thyroglobulin cleavage, and thyroid hormone production. Importantly, infant thyroid function can be significantly improved by administering supplementary iodine to the medicated dam's diet during breast-feeding. These results elucidate the mechanisms of lithium in thyroid function, provide valuable information on use postpartum, and suggest a clinically applicable remedy to side-effects. The results are particularly important for patients (and their infants) who respond well to lithium and need, or choose, to breast-feed.