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Plasma branched chain amino acids are lower in short-term profound hypothyroidism and increase in response to thyroid hormone supplementation.
van der Boom, T, Gruppen, EG, Lefrandt, JD, Connelly, MA, Links, TP, Dullaart, RPF
Scandinavian journal of clinical and laboratory investigation. 2020;(7):562-566
Abstract
Branched chain amino acids (BCAA) are implicated in the pathogenesis of cardiometabolic diseases conceivably by affecting insulin resistance and mitochondrial dysfunction. Circulating BCAA levels may predict (subclinical) atherosclerosis, diabetes and hypertension development but the factors involved in BCAA regulation are incompletely understood. Given the key role of thyroid hormones on many metabolic processes including protein metabolism, we aimed to determine effects of thyroid dysfunction on circulating BCAA. Effects of short-term profound hypothyroidism on plasma BCAA were determined in 17 patients who had undergone total thyroidectomy for differentiated thyroid carcinoma. Patients were studied during hypothyroidism, i.e. after thyroidectomy, and after thyroid hormone supplementation. Plasma BCAA (sum of valine, leucine and isoleucine) and alanine were measured by nuclear magnetic resonance spectroscopy. During hypothyroidism (median thyroid-stimulating hormone 81 (IQR 67-120.5) mU/L), plasma BCAA were lower (255 (IQR 222-289) µmol/L) compared to a euthyroid reference population (n = 5579; 377 µmol/L (2.5th to 97.5th percentile 258-548), p < 0.001). After 20 weeks of thyroid hormone supplementation (thyroid-stimulating hormone 0.03 (IQR 0.01-0.14 mU/L) plasma BCAA had increased (328 (IQR 272-392) µmol/L, p = .001), but plasma alanine concentrations were unaltered (p = .50). Changes in body weight in response to thyroid hormone supplementation were correlated with changes in plasma BCAA (r = 0.721 p = .001, but not with changes in cholesterol or glucose (p > .80). In conclusion, plasma BCAA concentrations are lower during short-term profound hypothyroidism in humans, and increase in response to thyroid hormone supplementation. Changes in BCAA and in body weight after reversal of the hypothyroid state appear to be interrelated.
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Cold Exposure Distinctively Modulates Parathyroid and Thyroid Hormones in Cold-Acclimatized and Non-Acclimatized Humans.
Kovaničová, Z, Kurdiová, T, Baláž, M, Štefanička, P, Varga, L, Kulterer, OC, Betz, MJ, Haug, AR, Burger, IA, Kiefer, FW, et al
Endocrinology. 2020;(7)
Abstract
Cold-induced activation of thermogenesis modulates energy metabolism, but the role of humoral mediators is not completely understood. We aimed to investigate the role of parathyroid and thyroid hormones in acute and adaptive response to cold in humans. Examinations were performed before/after 15 minutes of ice-water swimming (n = 15) or 120 to 150 minutes of cold-induced nonshivering thermogenesis (NST) applied to cold-acclimatized (n = 6) or non-acclimatized (n = 11) individuals. Deep-neck brown adipose tissue (BAT) was collected from non-acclimatized patients undergoing elective neck surgery (n = 36). Seasonal variations in metabolic/hormonal parameters of ice-water swimmers were evaluated. We found that in ice-water swimmers, PTH and TSH increased and free T3, T4 decreased after a 15-minute winter swim, whereas NST-inducing cold exposure failed to regulate PTH and free T4 and lowered TSH and free T3. Ice-water swimming-induced increase in PTH correlated negatively with systemic calcium and positively with phosphorus. In non-acclimatized men, NST-inducing cold decreased PTH and TSH. Positive correlation between systemic levels of PTH and whole-body metabolic preference for lipids as well as BAT volume was found across the 2 populations. Moreover, NST-cooling protocol-induced changes in metabolic preference for lipids correlated positively with changes in PTH. Finally, variability in circulating PTH correlated positively with UCP1/UCP1, PPARGC1A, and DIO2 in BAT from neck surgery patients. Our data suggest that regulation of PTH and thyroid hormones during cold exposure in humans varies by cold acclimatization level and/or cold stimulus intensity. Possible role of PTH in NST is indicated by its positive relationships with whole-body metabolic preference for lipids, BAT volume, and UCP1 content.
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Update on Thyroid Hormone Levels and Thyroid Dysfunction in the Korean Population Based on Data from the Korea National Health and Nutrition Examination Survey VI (2013 to 2015).
Chung, JH
Endocrinology and metabolism (Seoul, Korea). 2020;(1):7-13
Abstract
In 2017, the first Korean nationwide data on serum thyroid stimulating hormone (TSH) levels, serum free thyroxine (fT₄) levels, and urinary iodine concentration (UIC) were published based on a population of 7,061 Koreans who participated in the Korea National Health and Nutrition Examination Survey VI. The mean TSH level was 2.16 mIU/L, with a reference interval of 0.59 to 7.03 mIU/L (men 2.09 mIU/L, women 2.24 mIU/L, P<0.001). A U-shaped association was found between serum TSH levels and age. The mean fT₄ level was 1.25 ng/dL, and its reference interval was 0.92 to 1.60 ng/dL (men 1.29 ng/dL, women 1.20 ng/dL, P<0.0001). Serum fT₄ levels decreased with age (P for trend <0.0001). Serum thyroid peroxidase antibody (TPOAb) was detected in 7.30% of participants (men 4.33%, women 10.62%). TPOAb titers tended to increase with age, and were higher in women than in men. The median UIC was 294 μg/L, and UIC showed a U-shaped relationship with age. According to the World Health Organization recommendations, only 23% of participants were in the adequate range of iodine intake, while 65% were in the above requirements or excessive, and 12% in insufficient. The prevalence of overt hyperthyroidism and hypothyroidism in Koreans was 0.34% to 0.54% and 0.73% to 1.43%, respectively.
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Do maternal urinary iodine concentration or thyroid hormones within the normal range during pregnancy affect growth parameters at birth? A systematic review and meta-analysis.
Nazeri, P, Shab-Bidar, S, Pearce, EN, Shariat, M
Nutrition reviews. 2020;(9):747-763
Abstract
CONTEXT Iodine, an essential constituent of thyroid hormones, is required for proper growth and development. OBJECTIVE To investigate whether growth parameters at birth are associated with maternal urinary iodine concentration (UIC) or normal ranges of thyroid hormones during pregnancy. DATA SOURCES Using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines, electronic databases (namely, MEDLINE, Web of Science, the Cochrane Library, Scopus, and Google Scholar) were searched between January 1988 and November 2018 to identify relevant articles. DATA EXTRACTION Data from the studies included were independently extracted by 2 investigators using standardized forms developed for this review. DATA ANALYSIS The pooled mean birth weight, length, and head circumference values, and 95% confidence intervals were estimated in newborns born to women with UIC < 150 and UIC ≥150 μg/L during pregnancy. Possible linear or nonlinear associations between maternal UIC and the aforementioned anthropometric measures were evaluated. A narrative synthesis of the data was performed for thyroid hormones with levels within the normal range. RESULTS Of the 123 studies identified, 11 were eligible for inclusion in the meta-analysis. The pooled mean birth weight, length, and head circumference in newborns whose mothers had UIC < 150 μg/L vs UIC ≥150 μg/L were 2898 g vs 2900 g (P = 0.970), 49.6 cm vs 49.4 cm (P = 0.880), and 34.0 cm vs 34.1 cm (P = 0.933), respectively. Dose-response meta-analyses revealed no significant linear or nonlinear associations between maternal UIC during pregnancy and anthropometric measures at birth. Among the different thyroid function parameters evaluated, high-normal values of maternal free thyroxine and thyrotropin during pregnancy were inversely associated with neonatal birth weight. CONCLUSION This systematic review showed that birth weight may be affected by even mild variations in the normal concentrations of maternal thyroid hormones. However, in the current meta-analysis, birth anthropometric measures were not associated with maternal UIC during pregnancy.
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Pro-Arrhythmic Signaling of Thyroid Hormones and Its Relevance in Subclinical Hyperthyroidism.
Tribulova, N, Kurahara, LH, Hlivak, P, Hirano, K, Szeiffova Bacova, B
International journal of molecular sciences. 2020;(8)
Abstract
A perennial task is to prevent the occurrence and/or recurrence of most frequent or life-threatening cardiac arrhythmias such as atrial fibrillation (AF) and ventricular fibrillation (VF). VF may be lethal in cases without an implantable cardioverter defibrillator or with failure of this device. Incidences of AF, even the asymptomatic ones, jeopardize the patient's life due to its complication, notably the high risk of embolic stroke. Therefore, there has been a growing interest in subclinical AF screening and searching for novel electrophysiological and molecular markers. Considering the worldwide increase in cases of thyroid dysfunction and diseases, including thyroid carcinoma, we aimed to explore the implication of thyroid hormones in pro-arrhythmic signaling in the pathophysiological setting. The present review provides updated information about the impact of altered thyroid status on both the occurrence and recurrence of cardiac arrhythmias, predominantly AF. Moreover, it emphasizes the importance of both thyroid status monitoring and AF screening in the general population, as well as in patients with thyroid dysfunction and malignancies. Real-world data on early AF identification in relation to thyroid function are scarce. Even though symptomatic AF is rare in patients with thyroid malignancies, who are under thyroid suppressive therapy, clinicians should be aware of potential interaction with asymptomatic AF. It may prevent adverse consequences and improve the quality of life. This issue may be challenging for an updated registry of AF in clinical practice. Thyroid hormones should be considered a biomarker for cardiac arrhythmias screening and their tailored management because of their multifaceted cellular actions.
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The association between prenatal exposure to organochlorine compounds and neonatal thyroid hormone levels: a systematic review.
Gheidarloo, M, Kelishadi, R, Hovsepian, S, Keikha, M, Hashemipour, M
Journal of pediatric endocrinology & metabolism : JPEM. 2020;(1):21-33
Abstract
In this systematic review, the association between prenatal exposure to organochlorine pesticides (OCPs) and neonatal thyroid hormone levels was studied. A systematic search of scientific literature was performed from the PubMed, SCOPUS and ISI web of science electronic bibliographic databases. The search strategy for the review was [(organochlorine OR "organochlorine pesticides" OR "organochlorine pollutants" OR "organochlorine pollutant") AND ("thyroid hormone" OR triiodothyronine OR Thyroxine OR "fetal thyroid function" OR "thyroid function" OR "Thyroid Stimulating Hormone" AND "prenatal" AND "maternal exposure")] in English sources. In this review, 305 papers (PubMed: 30; Scopus: 29; ISI: 246) were identified through an electronic database search. Twenty-seven articles were assessed for eligibility, from which 16 qualified articles were selected for the final evaluation. The most common OCP metabolites which were evaluated in order were hexachlorobenzene (HCB) (13 studies), pp-dichlorodiphenyldichloroethylene (pp-DDE) (13 studies), hexachlorocyclohexane (HCH) (10 studies) and dichlorodiphenyltrichlorethane (DDT) (eight studies). A review of the documents related to the association of prenatal exposure of OCPs with fetal or neonatal thyroid function tests provides us with heterogeneous data in this field. Factors such as differences in the studied populations and their area, ethnic and genetic background, time and rate of exposure, possible interaction of other thyroid-disrupting environmental factors and dietary intake of micronutrients such as iodine and/or selenium are considered the main limitations for making an accurate conclusion. For some OCPs including DDT, DDE, HCH and HCB, there are supporting evidences, and it is suggested that their exposure could potentially alter the fetal thyroid function and consequently impair the neurodevelopment process of the infants.
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Trimester-specific reference ranges for thyroid hormones in pregnant women.
Zhang, D, Cai, K, Wang, G, Xu, S, Mao, X, Zheng, A, Liu, C, Fan, K
Medicine. 2019;(4):e14245
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Abstract
The aim of this study was to determine the trimester-specific reference range of thyroid function in Nanjing.A total of 805 pregnant women in the 1st, 2nd, and 3rd trimesters were recruited in the prospective, observational study during their routine antenatal clinic visit and 282 nonpregnant subjects served as controls. A questionnaire was completed by the subjects to record their personal health history, family history of thyroid disease, and consumption of estrogen or antithyroid drugs. Thyroid palpation was performed to exclude the thyroid goiter. Thyroid function and urine iodine were measured by chemiluminescence and arsenic cerium analysis.The trimester-specific reference ranges in Nanjing were as follows: thyroid-stimulating hormone (TSH) 0.02 to 3.78 mIU/L, free thyroxine (FT4) 13.93 to 26.49 pmol/L, total thyroxine (TT4) 103.39 to 319.43 nmol/L in the 1st trimester. TSH 0.47 to 3.89 mIU/L, FT4 12.33 to 19.33 pmol/L, TT4 92.28 to 234.88 nmol/L in the 2nd trimester. TSH 0.55 to 4.91 mIU/L, FT4 11.38 to 19.21 pmol/L, TT4 83.54 to 258.12 nmol/L in the 3rd trimester. According to the TSH reference range recommended by American Thyroid Association (ATA), the prevalence of subclinical hypothyroidism, subclinical hyperthyroidism, hyperthyroidism, hypothyroxinemia, and thyroid peroxidase antibody-positive were 12.42%, 0.50%, 0.99%, 1.61%, and 11.80%, respectively, prevalence according to the trimester-specific reference range were 1.99%, 0.25%, 1.61%, 0.37%, and 1.61%, respectively, which showed elevated hypothyroxinemia incidence and declined incidence of subclinical hypothyroidism and hyperthyroidism.Trimester-specific reference range varied from that of ATA's recommendation, influencing the diagnosis, and treatment of pregnant thyroid disorders. To detect and control these disorders properly, setting up trimester-specific reference is clinically essential.
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The possible global hazard of cell phone radiation on thyroid cells and hormones: a systematic review of evidences.
Asl, JF, Larijani, B, Zakerkish, M, Rahim, F, Shirbandi, K, Akbari, R
Environmental science and pollution research international. 2019;(18):18017-18031
Abstract
The aim of this review was to investigate the effects of possible harmful waves from either cell phone use or being within the range of the cell phone from 450 to 3800 MHz on the thyroid cells and hormones. Eight electronic datasets were systematically searched using MeSH terms, including "cell phone," "mobile phone," "GSM," "radio frequency," "smartphone," "triiodothyronine," "thyroxin," "thyroid-stimulating hormone," "T3," "T4," "TSH," and "morphological" and all possible combinations, to identify relevant studies published up to Dec 2018. We also manually searched the reference lists of potentially selected studies to identify further relevant publications. About 161 relevant studies were initially found. After screening titles and abstracts, 139 studies were excluded, and finally 22 studies (comprising 7182 cases) were included in the qualitative synthesis. Of the 22 included studies, 11 studies reported changes in T3 and T4 levels (six reported a decrease in T3 levels and one reported increase in it); moreover, five found decreased T4 levels and two studies an increased level. In other 10 studies, TSH alteration was reported. Of these, two studies reported a decrease in TSH level and one reported an increase in the hormone levels, while in the remaining studies non-significant changes were reported. Finally, seven studies examined histological changes in the thyroid gland follicles and showed that the volume of these cells was reduced. Based on the evidence discussed above, the reduction in diameter of thyroid follicles is potentially linked with cell phone radiation. Exposure may negatively influence the iodine uptake in the thyroid gland or increases temperature effect on the thyroid gland. However, further research are needed in order to show that the level of TSH and thyroid hormone suppression by microwave.
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Thyroid peroxidase as a dual active site enzyme: Focus on biosynthesis, hormonogenesis and thyroid disorders of autoimmunity and cancer.
Godlewska, M, Banga, PJ
Biochimie. 2019;:34-45
Abstract
Thyroid peroxidase (TPO) is the key enzyme involved in thyroid hormone synthesis. Autoantibodies to TPO (TPOAbs) are a hallmark of autoimmune thyroid disease (AITD). Here, we highlight recent progress over several years in understanding TPO biochemistry and function in various pathologies. TPO undergoes complex post-translational modifications as a dimer in endoplasmic reticulum during secretory pathway to apical membrane of thyrocytes. In silico modelling of TPO dimer has provided new information into the two enzyme active site regions and autoantigenic determinants. TPO and hydrogen peroxide generating DUOX and caveolin-1 form a complex known as thyroxisome to bring together in close proximity the components of hormone synthesis in apical membrane. Autoimmunity to TPO is characterised by autoantibodies and T cell reactivity in Hashimoto's disease and Graves' disease. TPOAbs are directed predominantly to two immunodominant determinants (IDR) termed IDR-A and IDR-B regions, with the latter antibodies more predominant in autoimmune disease. Strong genetic risk has been shown to be associated with TPOAbs for AITD development. A different antibody with unusual features of bispecificity for both TPO and thyroglobulin may play protective role in Hashimoto's disease. In the context of TPO biology in human cancer, thyroid tumor tissue and breast cancer differ in TPO expression and isoform composition. In thyroid cancer, TPO expression is decreased partly by the BRAF(V600E) mutation, with direct impact on significant hormone production. TPOAbs may play a protective role in breast cancer development. An understanding of TPO and its unique two enzymatic active sites and autoantigenic determinants continues to add new knowledge on the biochemistry and immunology of this enzyme.
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Low thyroid function is not associated with an accelerated deterioration in renal function.
Meuwese, CL, van Diepen, M, Cappola, AR, Sarnak, MJ, Shlipak, MG, Bauer, DC, Fried, LP, Iacoviello, M, Vaes, B, Degryse, J, et al
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 2019;(4):650-659
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Abstract
BACKGROUND Chronic kidney disease (CKD) is frequently accompanied by thyroid hormone dysfunction. It is currently unclear whether these alterations are the cause or consequence of CKD. This study aimed at studying the effect of thyroid hormone alterations on renal function in cross-sectional and longitudinal analyses in individuals from all adult age groups. METHODS Individual participant data (IPD) from 16 independent cohorts having measured thyroid stimulating hormone, free thyroxine levels and creatinine levels were included. Thyroid hormone status was defined using clinical cut-off values. Estimated glomerular filtration rates (eGFR) were calculated by means of the four-variable Modification of Diet in Renal Disease (MDRD) formula. For this IPD meta-analysis, eGFR at baseline and eGFR change during follow-up were computed by fitting linear regression models and linear mixed models in each cohort separately. Effect estimates were pooled using random effects models. RESULTS A total of 72 856 individuals from 16 different cohorts were included. At baseline, individuals with overt hypothyroidism (n = 704) and subclinical hypothyroidism (n = 3356) had a average (95% confidence interval) -4.07 (-6.37 to -1.78) and -2.40 (-3.78 to -1.02) mL/min/1.73 m2 lower eGFR as compared with euthyroid subjects (n = 66 542). In (subclinical) hyperthyroid subjects (n = 2254), average eGFR was 3.01 (1.50-4.52) mL/min/1.73 m2 higher. During 329 713 patient years of follow-up, eGFR did not decline more rapidly in individuals with low thyroid function compared with individuals with normal thyroid function. CONCLUSIONS Low thyroid function is not associated with a deterioration of renal function. The cross-sectional association may be explained by renal dysfunction causing thyroid hormone alterations.