Thyroid Hormone Research Articles

Effects of thyroid status on HbA1c

Introduction: Altered erythrocyte turnover may not adequately reflect the glycemic status in the glycated hemoglobin (HbA1c) levels. Hypothyroidism is one such condition that might cause reduced erythropoiesis and falsely high HbA1c values. The aim of the study is to evaluate the effect of thyroid hormone on HbA1c levels on non-diabetic hypothyroid individuals and also to evaluate HbA1c levels in hypothyroid individuals with diabetes and to compare them with normal healthy subjects. Methods: This prospective study was conducted on 210 individuals, of whom 70 were assigned to group I- hypothyroid individuals, 70 to group II- hypothyroid individuals with diabetes, and 70 to group III—Normal individuals. Following data regarding laboratory investigations were collected which included fasting blood sugar (FBS), postprandial blood sugar (PPBS), HbA1c, free triiodothyronine (fT3), free thyroxine (fT4), and thyroid stimulating hormone (TSH). Data analysis was performed using SPSS version 16.0. Results: The median level of HbA1c was significantly higher in hypothyroid than in normal individuals (5.6 [5.5-5.7] % vs 5.2 [5-5.3] %, P≤0.001). The median level of TSH was significantly higher in hypothyroid than in normal individuals (11.13 [6.9-22.9] μIU/mL vs 2.15 (1.33-1.60) μIU/mL). The serum level of HbA1c was significantly positively correlated with TSH in hypothyroid individuals (r=0.281, P≤0.01). Conclusion: There is a positive correlation between HbA1c and TSH, and a negative correlation between HbA1c and fT4 levels. Serum HbA1c levels were significantly higher in hypothyroid individuals than the normal individuals. Therefore, our study suggests that we should proceed with caution while interpreting HbA1c levels in individuals with hypothyroidism.

Neurological and psycho-emotional manifestations of hyperthyroidism during pregnancy

Background. Hyperthyroidism is a state of thyroid hormone excess, which increases the metabolic rate and causes symptoms including anxiety and tremor. Graves’ disease is the most common etiology in developed countries. Excessive levels of thyroid hormones can impact mood, energy levels, and overall well-being. It is crucial to differentiate between symptoms related to thyroid function and clinical depression. The purpose of the study was to investigate the neurological and psycho-emotional manifestations of hyperthyroidism during pregnancy. Materials and methods. An examination of 50 pregnant women with subclinical and overt hyperthyroidism and 20 healthy women (control group) in the second trimester of pregnancy using the method of standardized multivariate personality study was carried out. Results. Based on the results of the study, it can be argued that pregnant women with thyrotoxicosis have changes in the psycho-emotional sphere: psychological maladaptation to the disease, an increase in the level of anxiety with hypochondriac tendencies, neuroticism, a decrease in intellectual performance and activity, a pronounced feeling of depression, anxiety, low mood. The identified criteria allow us to attribute these changes to the personality pattern or to the manifestations of a pathological neurotic state in conditions of mal­adaptation. The specific condition and behavior of pregnant women with thyrotoxicosis requires timely diagnosis and appropriate correction, which will contribute to the normalization and improvement of the psychological state, prevent the development of chronic stress and the occurrence of perinatal complications. Conclusions. Pregnant women with thyrotoxicosis have changes in the psycho-emotional sphere: psychological maladaptation to the disease, an increase in the level of anxiety with hypochondriac tendencies, neuroticism, a decrease in intellectual performance and activity, a pronounced feeling of depression and anxiety.

Thyroid hormones and prognosis in adults with status epilepticus: a retrospective study

ObjectivesThyroid hormone levels have been indicated to be associated with the functional outcome in critical illness. However, the studies on thyroid hormones and status epilepticus (SE) are rare. This study aimed to evaluate the predictive value of serum thyroid hormone levels on admission for unfavorable outcome in adult patients with SE.MethodsWe investigated and validated the predictive value of serum thyroid hormone levels on admission for the prognosis of adult SE patients. We extracted the clinical information and outcomes of patients. Modified Rankin scale (mRS) scores were applied to assess the patients’ functional outcome, and mortality at 30 days after SE onset was identified. Serum levels of thyroid hormones including free thyroxin (FT4), free triiodothyronine (FT3) and thyroid-stimulating hormone (TSH) were detected on admission.ResultsWe first analyzed the discovery cohort of 87 patients with SE. We found that 35.6% (31/87) of the patients had a poor outcome at discharge, and 18.4% (16/87) of the patients died during hospital stay and at 30-day follow up. The serum FT3 levels in the non-survivors group were significantly lower than those in the survivors group. Low T3 syndrome occurred in 29.9% (26/87) of SE cases and patients with low T3 syndrome were more likely to have unfavorable outcomes. Furthermore, we observed similar results in the external cohort, which validated our findings.ConclusionsSerum FT3 levels measured on admission are independently associated with 30-day mortality in SE patients. Additionally, low T3 syndrome may be a promising candidate for predicting SE prognosis.

Neurodevelopment delay as the initial presentation of thyroid hormone resistance syndrome

Thyroid hormone (TH) resistance syndrome is a genetic disorder usually caused by a defect in TH receptors. Moreover, transport and intracellular metabolism alterations have also been described. This case report presents a child with Allan–Herndon–Dudley syndrome characterized by a mutation on the X-linked monocarboxylate transporter 8 gene, a condition that affects the transport of THs across the cell membrane, leading to hypothyroidism in the central nervous system and hyperthyroidism in peripheral tissues, causing severe neurodevelopmental delay manifesting as generalized hypotonia from birth. The utility of monitoring thyroid functions, genetic testing, and triiodothyroacetic acid in the management is highlighted.

Association between thyroid hormones and cognitive functioning in euthyroid elderly adults: a cross-sectional preliminary study from the NHANES 2011–2012 survey

ObjectiveChanges in serum thyroid hormone levels may affect cognitive functioning in euthyroid individuals. This study used representative data from the National Health and Nutrition Examination Survey (NHANES) to comprehensively examine the association of thyroid hormones with different tests of cognitive functioning among US elderly people aged ≥60 years.MethodsThis study was a cross-sectional preliminary study with a total of 734 participants from the NHANES 2011-2012 survey. Thyroid function was measured using competitive binding immune-enzymatic assays, while cognitive functioning was measured using a series of assessments, including the Consortium to Establish a Registry for Alzheimer’s Disease-Word Learning (CERAD W-L), Animal Fluency Test, and Digit Symbol Substitution Test (DSST). Weighted multiple linear regression models and binary logistic regression analyses were used to examine the association between thyroid hormone levels and cognitive functioning. All statistical analyses were performed using SPSS version 20.0, and R software.ResultsWeighted multivariable linear regression showed that FT3 was negatively associated with the Animal Fluency Test and DSST (β=-0.113, 95% CI: -3.279, -0.803, P=0.001; β=-0.062, 95% CI: -6.565, -0.470, P=0.024, respectively) after adjustment for potential covariates. subgroup analysis stratified by sex revealed a negative association between FT3 levels and the Animal Fluency Test in men (β=-0.163, 95% CI: -4.643, -1.153, P=0.001). For female participants, FT3 was negatively associated with not only the Animal Fluency Test but also DSST (β=-0.099, 95% CI: -3.543, -0.093, P=0.039; β=-0.093, 95% CI: -10.288, -1.326, P=0.011). Binary logistic regression showed that the significantly increased adjusted odds ratios (aORs) (95% CI) between the risk of impaired cognitive functioning and FT3 across Q3 and Q4 compared with Q1 were 2.025 (1.092, 3.753) and 2.365 (1.261, 4.433), respectively, for DSST in overall participants. Furthermore, there were significant differences between participants with and without impaired cognitive functioning for serum FT3 levels in overall participants based on DSST score (P=0.020).ConclusionsThere was a significant inverse relationship between FT3 levels within the normal range and cognitive functioning after adjusting for potential covariates. Future longitudinal cohort studies should be conducted to determine the causal relationship between thyroid hormone levels and cognitive functioning.

Analysis of risk factors for autoimmune thyroid disease based on blood indicators and urinary iodine concentrations

ObjectiveThe aim of this study was to elucidate the relationships between thyroid hormones, lifestyle factors, biochemical markers, and autoimmune thyroid disease (AITD), thereby identifying the factors influencing the development of these diseases.MethodsThe study encompassed 517 patients with AITD and 549 patients with non-autoimmune thyroid disease. Demographic and clinical data were collected, and various laboratory indicators, including urinary iodine and thyroid hormones, were measured and compared between the groups. Lasso regression was employed to select the independent variables, while logistic regression analysis determined the factors associated with the development of AITD.ResultsThe prevalence of drinking alcohol history, median urinary iodine, and TSH concentrations proved significantly greater in the AITD group compared to the control group, while FT3 levels demonstrated lower values within the AITD group (p<0.05). Furthermore, there was a significant difference in the distribution of iodine nutrition status between the two groups (p<0.05). Both univariate and multivariate logistic regression analyses revealed significant associations among excessive iodine intake, drinking alcohol history, TSH, FT3, and the development of AITD.ConclusionsExcessive iodine intake and drinking alcohol history are implicated in an augmented risk of developing AITD. The prevention of AITD may necessitate the regular monitoring of TSH and FT3 concentrations.

Myocardial Posttranscriptional Landscape in Peripartum Cardiomyopathy

BACKGROUND: Pregnancy imposes significant cardiovascular adaptations, including progressive increases in plasma volume and cardiac output. For most women, this physiological adaptation resolves at the end of pregnancy, but some women develop pathological dilatation and ultimately heart failure late in pregnancy or in the postpartum period, manifesting as peripartum cardiomyopathy (PPCM). Despite the mortality risk of this form of heart failure, the molecular mechanisms underlying PPCM have not been extensively examined in human hearts. METHODs: Protein and metabolite profiles from left ventricular tissue of end-stage PPCM patients (N=6–7) were compared with dilated cardiomyopathy (DCM; N=5–6) and nonfailing donors (N=7–18) using unbiased quantitative mass spectrometry. All samples were derived from the Sydney Heart Bank. Data are available via ProteomeXchange with identifier PXD055986. Differential protein expression and metabolite abundance and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed. RESULTS: Proteomic analysis identified 2 proteins, SBSPON (somatomedin B and thrombospondin type 1 domain-containing protein precursor) and TNS3 (tensin 3), that were uniquely downregulated in PPCM. SBSPON, an extracellular matrix protein, and TNS3, involved in actin remodeling and cell signaling, may contribute to impaired tissue remodeling and fibrosis in PPCM. Metabolomic analysis revealed elevated levels of homogentisate and deoxycholate and reduced levels of lactate and alanine in PPCM, indicating disrupted metabolic pathways and glucose utilization. Both PPCM and DCM shared pathways related to inflammation, immune responses, and signal transduction. However, thyroid hormone signaling was notably reduced in PPCM, affecting contractility and calcium handling through altered expression of PLN (phospholamban) and Sarcoendoplasmic Reticulum Calcium ATPase (SERCA). Enhanced endoplasmic reticulum stress and altered endocytosis pathways in PPCM suggested additional mechanisms of energy metabolism disruption. CONCLUSIONS: The present study reveals unique posttranslational molecular features of the PPCM myocardium, which mediates cellular and metabolic remodeling, and holds promise as potential targets for therapeutic intervention.

Relationship of serum iron and thyroid hormone in obesity and after laparoscopic sleeve gastrectomy

BackgroundIron is an essential element for thyroid function. However, no study focuses on the association between iron and thyroid in individuals with obesity. Our research aimed to investigate the iron status in relation to baseline thyroid hormone levels and after laparoscopic sleeve gastrectomy (LSG).MethodsA total of 216 subjects with obesity were enrolled and divided into low and high iron groups depending on the median value. The association between iron and thyroid hormone was analyzed and compared before and after LSG at the 6-month follow-up in patients who underwent LSG.Results1) In all, Total Triiodothyronine (TT3) was significantly higher in high iron than low iron group (P = 0.008). TT3 and thyroid stimulating hormone (TSH) were significantly higher in high iron than low iron group (1.92 ± 0.61 vs. 1.69 ± 0.28 nmol/l, P = 0.029; 2.93 ± 1.66 vs. 1.88 ± 1.03 mU/l, P = 0.002) in females while not in males (all P > 0.05). 2) Iron was significantly positively associated with free triiodothyronine (FT3), free thyroxine (FT4), TT3 and TSH (all P < 0.05). Adjusted for body mass index (BMI), total cholesterol (TCH), high-density lipoprotein cholesterol (HDL-C), fasting insulin (FINS) and homeostatic model assessment of insulin resistance (HOMA-IR), FT3, FT4 and TSH were still significantly associated with iron (all P < 0.05). 3). Regression analysis showed that iron was significantly associated with FT4 (β = 0.338, P = 0.038). 3) LSG led to decreased FT3, FT3, TT3, total thyroxine (TT4) and TSH at 6 months follow-up (all P < 0.05). Changed FT4 was significantly associated with changed iron (r = 0.520, P = 0.009). Subjects with iron decreased had more significant decreased TT4 than subjects without iron decreased (P = 0.021).ConclusionSerum iron overload is significantly associated with impaired thyroid function in subjects with obesity. LSG led to improved thyroid function which is associated with a change in iron.Trial RegistrationNCT04548232 registration date is on October 9, 2022, registered in https://register.clinicaltrials.gov/.

Ensuring Iodine Adequacy in Pregnant and Lactating Vegan Women

As a component of thyroid hormones, iodine is essential for brain development in the fetus and in young children. Some evidence suggests that pregnant and lactating women who consume a vegan diet may be at risk for iodine deficiency. Iodine sources for vegans include supplements, iodized salt, and seaweed. However, because the iodine content of seaweed is variable, with some types providing amounts that may lead to excessive intake, recommendations for consumption of these foods during pregnancy and breastfeeding should be specific regarding types and amounts. Pregnant and lactating women who choose a vegan diet should include a supplement of potassium iodide in their diet and should follow advice about the types of seaweed to avoid or limit.

Recombinant Human Thyrotropin Plus Radioactive Iodine Among Patients With Thyroid Cancer

ImportanceRadioactive iodine (131I or RAI) therapy has long been the standard of care for most patients with differentiated thyroid cancer (DTC) after primary surgery. However, no multicenter prospective studies have identified the optimal administered activity and stimulation method for RAI therapy in patients with intermediate-risk DTC.ObjectiveTo compare the efficacy and safety of recombinant human thyrotropin (SNA001) with thyroid hormone withdrawal (THW) plus 3.7 GBq RAI in patients with intermediate-risk DTC.Design, Setting, and ParticipantsThis noninferiority, open-label, phase 3 randomized clinical trial was conducted at 19 sites in China from April 16, 2020, to September 9, 2021, with a follow-up period of 8 months. Patients aged 18 to 70 years with DTC who had undergone a total or near-total thyroidectomy and had no distant metastasis were enrolled in the trial. Statistical analysis followed the full analysis and per-protocol analysis sets and was performed between November 18, 2021, and April 18, 2022.InterventionPatients were randomly assigned 1:1 to receive SNA001, 0.9 mg, intramuscular injection daily for 2 days or to undergo thyroid hormone withdrawal for 3 to 6 weeks.Main Outcomes and MeasuresThe primary end point was the success rate after 6 to 8 months of RAI therapy. Success was defined as a negative diagnostic whole-body scan result and a stimulated thyroglobulin level less than 1.0 ng/mL.ResultsA total of 307 patients (192 females [62.5%]; median [range] age, 40 [19-69] years) were randomized: 154 to the SNA001 group and 153 to the THW group. Baseline characteristics were evenly matched between the 2 groups. Noninferiority in the success rate of RAI therapy between groups was met, with success rates of 43.8% in the SNA001 group and 47.1% in the THW group (risk difference, −3.3; 95% CI, −14.8 to 8.3 percentage points). Forty-six patients (29.9%) in the SNA001 group reported adverse events compared with 90 (58.8%) in the THW group during RAI therapy (P &amp;amp;lt; .001). No treatment-related adverse events leading to discontinuation and drug modification occurred in the SNA001 group.Conclusions and RelevanceThis randomized clinical trial showed that SNA001 was noninferior to THW plus 3.7 GBq RAI in patients with predominantly intermediate-risk DTC. SNA001 also demonstrated a favorable safety profile compared with THW and had a lower incidence of adverse events.Trial RegistrationChinese Clinical Trial Registry Identifier: ChiCTR2100046907

Thyroid hormones in female and male reproduction with special reference to dogs and cats

Thyroid hormones have an important function in numerous physiological processes in humans and animals, including the regulation of metabolism, growth and development of individual and reproductive function. The thyroid hormones, triiodothyronine (T3) and thyroxine (T4), have a direct effect on the reproductive organs and an indirect effect in interaction with other hormones. Thyroid hormones influence the reproductive system by regulating metabolism and tissue development of the ovaries, uterus and placenta. Changes in the serum concentrations of T3 and T4 lead to disturbances in overall body function. Thyroid dysfunction, including hypothyroidism and hyperthyroidism, can lead to significant reproductive problems. The aim of this review was to describe the functions of thyroid hormones and the effects of hypothyroidism and hyperthyroidism on the animal reproductive system. Hypothyroidism is often caused by autoimmune diseases such as lymphocytic thyroiditis, and is associated with later puberty, reduced fertility and abnormalities in reproductive organ development. Hypothyroidism can lead to a prolonged interval, absent cycles, silent oestrus cycles, prolonged oestrus bleeding, and a lack of libido, with the occurrence of infertility, miscarriages, stillbirths and mummified foetuses. In males, hypothyroidism leads to a decrease in libido, semen quality, ejaculate volume, testicular atrophy, hypospermia and azoospermia. Hyperthyroidism, on the other hand, is usually the result of thyroid cancer, which produces excessive amounts of thyroid hormones. Increased concentrations of thyroid hormones lead to disturbances in the physiological balance of reproductive hormones, irregular oestrus cycles, anovulation and reduced fertility, as well as a decrease in the weight of the ovaries and the number of healthy follicles, with a simultaneous increase in the number of atretting follicles. The effects of hyperthyroidism on male fertility include disorders of spermatogenesis, changes in sex hormone levels and changes in sperm quality, such as hypospermia, oligozoospermia, asthenozoospermia and teratozoospermia. It is important to diagnose and treat thyroid disorders in time in order to prevent negative effects on fertility and reproduction in animals.

Breast cancer cells utilize T3 to trigger proliferation through cellular Ca2+ modulation

High levels of thyroid hormones are linked to increased risk and advanced stages of breast cancer. Our previous work demonstrated that the biologically active triiodothyronine (T3) facilitates mitochondrial ATP production by upregulating Ca2+ handling proteins, thereby boosting mitochondrial Ca2+ uptake and Krebs cycle activity. In this study, different cell types were utilized to investigate whether T3 activates a Ca2+-induced signaling pathway to boost cancer cell proliferation. Using live-cell imaging, biochemical assays, and molecular profiling, differences in intracellular signaling among MCF7 and MDA-MB-468 breast cancer cells, non-cancerous breast cells hTERT-HME1, and PC3 prostate carcinoma cells, previously found to be insensitive to thyroid hormones in terms of proliferation, were investigated. Our findings revealed that T3 upregulates 1,4,5-trisphosphate receptor 3 via thyroid hormone receptor α. This boosts mitochondrial Ca2+ uptake, reduction equivalent yield, and mitochondrial ATP production, supporting the viability and proliferation of breast cancer cells without affecting non-cancerous hTERT-HME1 or PC3 prostate carcinoma cells. Understanding the interplay between T3 signaling, organellar interaction, and breast cancer metabolism could lead to targeted therapies that exploit cancer cell vulnerabilities. Our findings highlight T3 as a crucial regulator of cancer metabolism, reinforcing its potential as a therapeutic target in breast cancer.Graphical

Gonadotropin releasing hormone - gonadotropes interactions revealed by pituitary single-cell transcriptomics in zebrafish.

Gonadotropin-releasing hormone (GnRH) governs reproduction by regulating pituitary gonadotropins. Unlike most vertebrates, gnrh-/- zebrafish are fertile. To elucidate the role of the hypophysiotropic-Gnrh3 and other mechanisms regulating pituitary gonadotropes, we profiled the gene expression of all individual pituitary cells of wild-type and gnrh3-/- adult female zebrafish. The single-cell RNA-Seq showed that Lh and Fsh gonadotropes express the two gonadotropin beta subunits with a ratio of 140:1 (lhb:fshb) and 4:1 (fshb:lhb), respectively. Lh gonadotropes predominantly express genes encoding receptors for Gnrh (gnrhr2), thyroid hormone, estrogen, and steroidogenic factor 1 (SF1). No Gnrh receptor transcript was enriched in Fsh gonadotropes. Instead, cholecystokinin receptor-b and galanin receptor-1b transcripts were enriched in these cells. The loss of Gnrh3 gene in gnrh3-/- zebrafish resulted in downregulation of fshb in Lh gonadotropes and upregulation of pituitary hormones like thyroid-stimulating hormone, growth hormone, prolactin and proopiomelanocortin-a. Likewise, targeted chemogenetic ablation of Gnrh3 neurons led to a decrease in the number of fshb+, lhb+ and fshb+/lhb+ cells. Our studies suggest that Gnrh3 directly acts on Lh gonadotropes through Gnrhr2, but the outcome of this interaction is still unknown. Gnrh3 also regulates fshb expression in both gonadotropes, most likely via a non-Gnrh receptor route. Altogether, while Lh secretion and synthesis are likely regulated in a Gnrh-independent manner, Gnrh3 seems to play a role in the cellular organization of the pituitary. Moreover, the co-expression of lhb and fshb in both gonadotropes provides a possible explanation as to why gnrh3-/- zebrafish are fertile.

Diabetic Ketoacidosis as a Debut and Immune-Mediated Complication Caused by Pembrolizumab: Case Report

Background/Objectives: Diabetic ketoacidosis (DKA) is an acute and potentially life-threatening complication characterized by the accumulation of ketone bodies in the blood, primarily occurring in patients with type 1 diabetes and occasionally in those with type 2 diabetes under certain conditions. DKA presents with symptoms such as polyuria, polydipsia, polyphagia, and, in severe cases, mental status changes. Identifying the triggering factor is crucial to prevent complications and effectively manage this medical emergency. Methods: This report describes the case of a 58-year-old male patient with stage IIIb nodular melanoma, diagnosed in November 2022. Results: After receiving five cycles of pembrolizumab, the patient developed de novo DKA, presenting with blurred vision, asthenia, adynamia, polyuria, and polydipsia. He was admitted to the emergency department with a blood glucose level of 764 mg/dL, confirming hyperglycemia and metabolic acidosis. He was transferred to the intensive care unit for fluid resuscitation and insulin infusion. After adequate clinical evolution and meeting the criteria for DKA resolution, possible autoimmune endocrinopathies secondary to immunotherapy were considered. Due to this complication, the oncological treatment was changed. Finally, the patient was discharged with the need to continue insulin therapy and oral hypoglycemic agents, along with thyroid hormone supplementation. Conclusions: The novelty of this case lies in the presentation of DKA as an immune-mediated complication induced by pembrolizumab, highlighting the importance of closely monitoring patients receiving immune checkpoint inhibitors to detect and manage emerging autoimmune endocrinopathies. It is essential to adjust oncological treatment according to the patient’s response and promptly manage autoimmune endocrinopathies to improve clinical outcomes and the patient’s quality of life.

A 2024 inventory of test methods relevant to thyroid hormone system disruption for human health and environmental regulatory hazard assessment

Thyroid hormone system disruption (THSD) is a growing concern in chemical hazard assessment due to its impact on human and environmental health and the scarce methods available for assessing the THSD potential of chemicals. In particular, the general lack of validated in silico and in vitro methods for assessing THS activity is of high concern. This manuscript provides an inventory of test methods relevant to THSD. Building on the Organisation for Economic Co-operation and Development (OECD) Guidance Document 150 and recent international developments, we highlight progress in in silico and in vitro methods, as well as in vivo assays. The provided inventory categorizes available methods according to the levels of the OECD Conceptual Framework, with an assessment of the validation status of each method. At Level 1, 12 in silico models that have been statistically validated and are directly related to THSD have been identified. At Level 2, 67 in vitro methods have been listed including those assessed in key initiatives such as the European Union Network of Laboratories for the Validation of Alternative Methods (EU-NETVAL) validation study to identify potential thyroid disruptors. At Levels 3-5, THSD-sensitive endpoints are being included in existing fish-based OECD Test Guidelines to complement amphibian assays. In total, the inventory counts 108 entries comprising established methods (e.g., OECD Test Guidelines) as well as citable methods that are under further development and in some cases are ready for validation or in the initial stages of validation. This work aims to support the ongoing development of strategies for regulatory hazard assessment, such as integrated approaches to testing and assessment (IATAs), for endocrine disruptors, addressing critical gaps in the current testing landscape for THSD in both human and environmental health contexts.

Development of a molecularly imprinted poly‐pyrrole biosensor for rapid and accurate estimation of liothyronine: Toward point‐of‐care quality assessment

AbstractLiothyronine (T3) is a thyroid hormone, which is frequently administered alongside thyroxine in the treatment of hypothyroidism. However, several market withdrawals have been called for due to persistent quality issues with liothyronine tablets. Given its narrow therapeutic index, maintaining optimal liothyronine levels is imperative, highlighting the criticality of ensuring quality both during manufacturing and at the patient's bedside. In this study, we introduce a pioneering electroanalytical biosensor designed for liothyronine estimation using molecularly imprinted poly‐pyrrole (MIP‐Ppy). Notably, the sensor demonstrates linear response within the concentration range of 50–300 pg/mL (r2 = 0.986) with a remarkable limit of detection (LOD) of 80 pg/mL. Interference studies were performed to validate the sensor's robustness, displaying negligible response alterations. This method was used for the assay of liothyronine tablets and was compared with the traditional HPLC method. The MIP‐Ppy biosensor showed 90.7% recovery with a minimal relative standard deviation of 0.093 whereas HPLC showed 91.2% recovery with RSD 0.052. These findings underscore the biosensor's potential as a cost‐effective alternative to sophisticated chromatographic methods for liothyronine estimation in pharmaceutical tablets. This advancement lays the groundwork for the development of a user‐friendly point‐of‐care device.

Meta-analysis of experimental studies of the effect of melatonin monotherapy on the levels of thyroid hormones and glucocorticoids in rats kept under standard condition

Meta-analysis of experimental studies of the effect of melatonin monotherapy on the levels of thyroid hormones and glucocorticoids in rats kept under standard condition

Nonylphenol and Cetyl Alcohol Polyethoxylates Disrupt Thyroid Hormone Receptor Signaling to Disrupt Metabolic Health.

Surfactants are molecules with both hydrophobic and hydrophilic structural groups that adsorb at the air-water or oil-water interface and serve to decrease the surface tension. Surfactants combine to form micelles that surround and break down or remove oils, making them ideal for detergents and cleaners. Two of the most important classes of nonionic surfactants are alkylphenol ethoxylates (APEOs) and alcohol ethoxylates (AEOs). APEOs and AEOs are high production-volume chemicals that are used for many industrial and residential purposes, including laundry detergents, hard-surface cleaners, paints, and pesticide adjuvants. Commensurate with better appreciation of the toxicity of APEOs and the base alkylphenols, use of AEOs has increased, and both sets of compounds are now ubiquitous environmental contaminants. We recently demonstrated that diverse APEOs and AEOs induce triglyceride accumulation and/or pre-adipocyte proliferation in vitro. Both sets of contaminants have also been demonstrated as obesogenic and metabolism disrupting in a developmental exposure zebrafish model. While these metabolic health effects are consistent across models and species, the mechanisms underlying these effects are less clear. This study sought to evaluate causal mechanisms through reporter gene assay assessments, relative binding affinity assays, co-exposure experiments, and use of both human cell and zebrafish models. We report that antagonism of thyroid hormone receptor signaling appears to mediate at least a portion of the polyethoxylate-induced metabolic health effects. These results suggest further evaluation is needed, given the ubiquitous environmental presence of these thyroid disrupting contaminants and reproducible effects in human cell models and vertebrate animals.

A clinical review of early assessment for congenital hypothyroidism in newborns

Congenital hypothyroidism is a critical factor associated with stunting, as thyroid hormone deficiencies can impair growth starting in utero. Children with thyroid disorders, including conditions like hypoparathyroidism, often experience growth retardation due to congenital abnormalities and growth hormone deficiencies. For neonates, a lack of thyroid hormones can lead to long-term impacts, such as physical and mental disabilities, neurological disorders, and stunted growth. Early detection of congenital hypothyroidism is, therefore, essential and is typically part of newborn screening aimed at identifying congenital abnormalities. Implementing early screening protocols can diagnose and treat congenital hypothyroidism promptly, mitigating risks such as stunting and enabling better health outcomes for children. This literature review examines methods of early detection for congenital hypothyroidism across various global contexts. Three databases—PubMed, ScienceDirect, and Google Scholar—were searched using a systematic literature review approach, yielding five eligible studies with a combined study population of 920.441 newborns. These studies involved screenings for T4, TSH, 17-OHP, and G-6-PD, identifying hypothyroidism in 2.530 (27%) cases. Screening involved blood samples taken from the umbilical cord or heel within 48 to 72 hours after birth. Understanding early detection procedures for congenital hypothyroidism is essential for nurses, as it enables them to engage in early intervention and provide effective nursing care for affected infants. Early involvement can help prevent the adverse, long-term effects associated with congenital hypothyroidism, improving quality of life and supporting healthy growth trajectories for children at risk. Keywords: Congenital hypothyroidism; literature review; nursing assessment; paediatric nursing; prevention

Peripubertal exposure to oxyfluorfen, a diphenyl herbicide, delays pubertal development in the male rat by antagonizing androgen receptor activity.

We recently identified the herbicide oxyfluorfen as an inhibitor of iodide uptake by the sodium iodide symporter (NIS), a key step in thyroid hormone synthesis, using in vitro assays. We also observed a suppression of serum T4 and T3 in juvenile rats exposed orally to oxyfluorfen for 4-8 days. The purpose of the present study was to further evaluate effects of an extended 31-day oral exposure using a male pubertal rat study (15 to 500 mg/kg). Oxyfluorfen delayed puberty at all doses (1.3 -3.5 days) suppressing ventral prostate at 62.5 mg/kg and above and seminal vesicle weights at 31.25 mg/kg and above with no effect on testosterone or luteinizing hormone. Serum T4 and T3 were suppressed by all doses up to 80%, with a linear increase in serum TSH. Based on delayed puberty without changes in testosterone, we hypothesized that oxyfluorfen interferes with androgen receptor (AR) function. Results from our Hershberger study, with oxyfluorfen (62.5 and 125 mg/kg) co-treated with testosterone proprionate (TP , 1 mg/kg) for 10 days showed 3 of 5 of the androgenic tissue weights were suppressed compared to TP alone indicating AR antagonism. We next confirmed this effect in an in vitro AR transcriptional activation reporter assay (0-20 μM) with 125 pM 5αDH-11-ketotestosterone and found concentration-dependent inhibition of AR luminescence activity (EC50 1.75 µM) without cytotoxicity. Here, we confirmed the endocrine disrupting effects of oxyfluorfen using both in vitro and in vivo evaluations of the thyroid hormone and AR pathways. This abstract doesn't necessarily reflect U.S. EPA policy.