Influence Of Thyroid Hormones Research Articles

Reduced serum CLCF1 levels in hyperthyroidism patients and T3-treated mice.

Characteristic symptoms of hyperthyroidism include weight loss, heart palpitation and sweating. Thyroid hormones (TH) can stimulate thermogenesis through central and peripheral mechanisms. Previous studies have shown an association between dysfunction of Cardiotrophin-like cytokine factor 1 (CLCF1) and cold-induced sweating syndrome (CISS), with recent research also indicating a link between CLCF1 and brown adipose tissue (BAT) thermogenesis. However, it remains unclear whether CLCF1 and TH have synergistic or antagonistic effects on thermogenesis. This study aims to investigate the influence of thyroid hormone on circulating CLCF1 levels in humans and explore the potential role of thyroid hormone in regulating energy metabolism by modulating CLCF1 in mice. By recruiting hyperthyroid patients and healthy subjects, we observed significantly lower serum CLCF1 levels in hyperthyroid patients compared to healthy subjects, with serum CLCF1 levels independently associated with hyperthyroidism after adjusting for potential confounders. Tissue analysis from mice treated with T3 revealed a decrease in Clcf1 expression in BAT and iWAT of C57BL/6 mice. These findings suggest that TH may play a role in regulating Clcf1 expression in thermogenic adipose tissue and impacting thermogenesis.

Deciphering thyroid function and CIMT: a Mendelian randomization study of the U-shaped influence mediated by apolipoproteins.

Carotid Intima-Media Thickness (CIMT) is a key marker for atherosclerosis, with its modulation being crucial for cardiovascular disease (CVD) risk assessment. While thyroid function's impact on cardiovascular health is recognized, the causal relationship and underlying mechanisms influencing CIMT remain to be elucidated. In this study, Mendelian Randomization (MR) was employed to assess the causal relationship between thyroid function and CIMT. Thyroid hormone data were sourced from the Thyroidomics Consortium, while lipid traits and CIMT measurements were obtained from the UK Biobank. The primary analysis method was a two-sample MR using multiplicative random effects inverse variance weighting (IVW-MRE). Additionally, the study explored the influence of thyroid hormones on lipid profiles and assessed their potential mediating role in the thyroid function-CIMT relationship through multivariate MR analysis. The study revealed that lower levels of Free Thyroxine (FT4) within the normal range are significantly associated with increased CIMT. This association was not observed with free triiodothyronine (FT3), thyroid-stimulating hormone (TSH), or TPOAb. Additionally, mediation analysis suggested that apolipoprotein A-I and B are involved in the relationship between thyroid function and CIMT. The findings indicate a potential U-shaped curve relationship between FT4 levels and CIMT, with thyroid hormone supplementation in hypothyroid patients showing benefits in reducing CIMT. This research establishes a causal link between thyroid function and CIMT using MR methods, underscoring the importance of monitoring thyroid function for early cardiovascular risk assessment. The results advocate for the consideration of thyroid hormone supplementation in hypothyroid patients as a strategy to mitigate the risk of carotid atherosclerosis. These insights pave the way for more targeted approaches in managing patients with thyroid dysfunction to prevent cardiovascular complications.

Effect of probiotics or prebiotics on thyroid function: A meta-analysis of eight randomized controlled trials.

Microbiome-directed therapies are increasingly utilized to optimize thyroid function in both healthy individuals and those with thyroid disorders. However, recent doubts have been raised regarding the efficacy of probiotics, prebiotics, and synbiotics in improving thyroid function. This systematic review aimed to investigate the potential relationship between probiotics/prebiotics and thyroid function by analyzing the impact on thyroid hormone levels. We conducted a comprehensive systematic review and meta-analysis of randomized controlled trials that investigated the effects of probiotics, prebiotics, and synbiotics on free triiodothyronine (fT3), free thyroxine (fT4), thyroid stimulating hormone (TSH), and thyroid stimulating hormone receptor antibody (TRAb) levels. We searched for articles from PubMed, Scopus, Web of Science, and Embase up until April 1st, 2023, without any language restriction. Quantitative data analysis was performed using a random-effects model, with standardized mean difference (SMD) and 95% confidence interval as summary statistics. The methods and results were reported according to the PRISMA2020 statement. A total of eight articles were included in this review. The meta-analysis showed no significant alterations in TSH (SMD: -0.01, 95% CI: -0.21, 0.20, P = 0.93; I2: 0.00%), fT4 (SMD: 0.04, 95% CI: -0.29, 0.21, P = 0.73; I2: 0.00%) or fT3 (SMD: 0.45, 95% CI: -0.14, 1.03, P = 0.43; I2: 78.00%), while a significant reduction in TRAb levels was observed (SMD: -0.85, 95% CI: -1.54, -0.15, P = 0.02; I2: 18.00%) following probiotics/prebiotics supplementation. No indication of publication bias was found. Probiotics/prebiotics supplementation does not influence thyroid hormone levels, but may modestly reduce TRAb levels in patients with Graves' disease.

Effect of Acute Caffeine Exposure on Blood Glucose and Hepatic Glycogen Content in Normal and Thyroidectomized Male Wistar Rats.

Acute caffeine exposure had been shown to induce hyperglycemia however; the influence of thyroid hormones on the caffeine-induced hyperglycemia is yet to be established. The present study was therefore designed to investigate the effect of caffeine exposure on blood glucose and hepatic glycogen content in thyroidectomized rats. Sixty adult male Wistar rats were randomly divided into 10 groups as I-X (n=6). Rats in groups I, III, V, VII and IX were given normal saline, caffeine, prazosin + caffeine, propranolol +caffeine, combined prazosin+ propranolol+caffeine injections respectively while rats in groups II, IV, VI, VIII and X were thyroidectomized and treated in similar manner as the normal rats respectively. Surgical removal of the thyroid gland was done in the thyroidectomised groups while sham-operation was done in Normal group to serve as control. After healing and following an overnight fast, the rats were anaesthetized and the femoral vein and carotid artery were cannulated for drug administration and blood glucose measurement respectively. After stabilization, following basal measurements, rats from each group were injected normal saline or caffeine (6mg/kg) while another sets were pre-treated prazosin (0.2 mg/kg), propanolol (0.5 mg/kg) or their combination before caffeine administration. Blood glucose was then monitored for 60 minutes post-injection of caffeine at 5 minutes interval. Liver samples were collected at the end of the observation period for glycogen content determination. Caffeine caused significant increased blood glucose levels in both normal and thyroidectomized rats which were up to 210% and 180% respectively at the peak of their responses. Liver glycogen content of the thyroidectomized rats (3.11 ± 0.20 mg/100g tissue weight) was significantly higher than the normal rats (1.91 ± 0.43 mg/100g tissue weight). These glycogen contents were significantly reduced by caffeine in both normal (0.25 ± 0.04 mg/100g tissue weight) and thyroidectomized rats (1.65 ± 0.16 mg/100g tissue weight) when compared with their controls. The caffeine effects on blood glucose and hepatic glycogen content were abolished by pretreatment with propanolol or a combination of prazosin and propanolol in both normal and thyroidectomized rats but pretreatment with prazosin caused only significant reduction in hyperglycemic response to caffeine. The findings of this study suggest that caffeine-induced hyperglycemia in both normal and thyroidectomized rats are mediated through both alpha and beta adrenoceptors.

Thyroid Function Status of Female Nurses Working Night-shift at a Tertiary Care Hospital

Background & objective: Night shift work has well-known adverse effects on health like sleep disturbances and other medical conditions including thyroid diseases. Various studies have revealed that the effect of night shift work on healthis mainly related to its interference with circadian rhythm, which can also influence thyroid hormone levels in accordance with sleep patterns. Therefore, night work can modify thyroid function and increase the risk of thyroid disorders. The present study was therefore conducted to evaluate the impact of the night shift work on the thyroid function status of female nurses in a tertiary care hospital. Methods: This case-control study was conducted in the Department of Physiology, Dhaka Medical College, Dhaka over a period of 1 year from January 2021 to December 2021. All female nurses (in the age range of 25-50 years) working at Dhaka Medical College in different shifts were the study population. Of them, the case group consisted of 90 female nurses who worked the night shift in different wards from 8.00 pm. to 8.00 am and the control group consisted of 90female nurses who worked the morning shift in the Outpatient Department (OPD) from 8.00 am to 2.00 pm. However, nurses with a personal or family history of sleep disorder, taking medications that may interfere with sleep, history of diabetes mellitus, bronchial asthma, or diagnosed with any kind of thyroid disease, such as Hashimoto’s thyroiditis, and pregnant nurses were excluded from the study. While the exposure variable was shift-work, the outcome variable was thyroid function status, evaluated in terms of serum FT4, FT3, and TSH and the presence of thyroid disorders. Results: The cases and controls were almost alike in terms of age, BMI, and blood pressure. The mean age of the case and the control groups were between 34 and 35 years with no significant difference between the groups. While serum levels of free thyroxine (FT4) and free triiodothyronine (FT3) were somewhat reduced in the case group than those in the control group, the serum TSH was significantly elevated in the former group than that in the latter group – a picture typical of subclinical hypothyroidism. Overt hypothyroidism was also higher in the former group than that in the latter group. Subclinical and clinical hyperthyroidism was found in 2(2.2%) and 3(3.3%) subjects of the control group only. Overall, 60% of the cases had some form of thyroid disorders as opposed to 15% of the controls with the risk of having thyroid disorders in night shift nurses being > 8(95% CI = 4.1 – 17.5) times higher than that in morning shift nurses(p < 0.001). Conclusions: The study concluded that night shift nurses may have a higher risk of developing subclinical hypothyroidism due to significantly higher levels of TSH and normal FT3, and FT4 levels. About two-fifths of the nurses working night shifts are at increased risk of having thyroid disorders, primarily subclinical hypothyroidism. Ibrahim Card Med J 2022; 12 (2): 40-45

Contrast-enhanced ultrasonography of the thyroid gland in healthy dogs, hypothyroid dogs and dogs with non-thyroidal illness

Diagnosis of canine hypothyroidism remains challenging, as non-thyroidal illness (NTI)-syndrome and medical treatment can influence thyroid hormone concentrations. Conventional ultrasound may give additional hints, however high interobserver variability has been described. Contrast-enhanced ultrasound (CEUS) allows detection of changes in tissue perfusion. The purpose of the present study was to assess the possible diagnostic value of CEUS regarding diagnosis of hypothyroidism. CEUS of the thyroid gland was performed in 52 healthy dogs, 16 hypothyroid dogs, and 20 NTI patients. The following perfusion parameters were calculated: Thyroid/carotid artery (TG/CA) ratios for peak enhancement (PE) and area under the curve (AUC), time to peak (TTP) and wash-in and wash-out rates (WiR, WoR) of the thyroid gland. Impact of sedation on perfusion parameters was investigated in 8 calm healthy dogs which were examined before and after sedation using midazolam and butorphanol. Significantly higher median TG/CA ratios for PE were detected for the left and right thyroid lobe in dogs with hypothyroidism (0.97/0.96) compared to healthy dogs (0.85/0.85) and dogs with NTI (0.84/0.84). AUCs were also significantly increased in hypothyroid dogs when compared to other groups. Dogs with NTI showed significantly lower WiR and WoR compared to other groups. Values for TTP were not significantly different between groups. Sedation had only impact on results of TTP which was significantly prolonged in sedated dogs. In conclusion, CEUS of the thyroid gland can provide an additional tool for diagnosis of hypothyroidism in dogs and support its differentiation from NTI. Sedation has limited impact on CEUS results.

The Influence of Thyroid Hormones on Levels of Lipid Profile and Adipokine in Iraqi Women with Thyroid Disorders

Hypothyroidism and hyperthyroidism are prevalent endocrine diseases.These have significant implications for lipid synthesis, mobilization, and metabolism. Retinol-binding protein 4 is a new adipokine implicated in some physiological and pathological processes, such as metabolic and endocrine disorders. Its elevation aids in the diagnosis of thyroid problems. The present study includes 60 women with thyroid diseases; 30 of them have hypothyroidism and 30 have hyperthyroidism. This study includes 20 healthy women as a control group. For each participant anthropometric, biochemical Thyroid-stimulating hormone, triiodothyronine, Thyroxine, lipid profile, and retinol binding protein-4 are measured. The results show that hypothyroid women have significantly higher levels of total cholesterol, triglycerides, and lowdensity lipoprotein cholesterol as compared to the hyperthyroid or control group. The serum of total cholesterol, triglycerides, and low-density lipoprotein cholesterol are significantly lower in hyperthyroid women compared to the hypothyroid or control group. In addition, there are no significant differences in blood high-density lipoprotein cholesterol concentrations among the three groups. Furthermore, serum retinolbinding protein-4 levels were higher in the hyperthyroid group compared to the hypothyroid or control groups. According to the findings of this study, hypothyroidism causes dyslipidemia, which raises the risk of cardiovascular disease while hyperthyroidism causes abnormalities in lipid profiles. Additionally, hyperthyroidism causes an increase in serum retinol-binding protein-4 levels in the blood.

The Microbiome-Thyroid Link: A Review of the Role of the Gut Microbiota in Thyroid Function and Disease

The gut microbiota has emerged as a potential regulator of thyroid homeostasis and disease. Recent studies suggest that the composition and diversity of intestinal bacteria can impact thyroid stimulating hormone levels, thyroid hormone synthesis & metabolism and the risk of thyroid conditions like hypothyroidism and autoimmune thyroiditis. However, the mechanisms through which the gut microbiota influences the thyroid remain poorly understood. This review aims to summarize the current evidence on the role of the gut-thyroid microbiome axis in thyroid physiology and pathophysiology. Studies investigating the association of gut dysbiosis with altered thyroid function and disorders like Hashimoto’s thyroiditis were discussed. Potential mechanisms through which gut bacteria may influence thyroid hormone levels and autoimmunity, such as interference with autoantigen presentation, induction of inflammation, and production of metabolites were evaluated. The impact of dietary and probiotic interventions targeting the gut microbiota for managing thyroid disease is assessed. Future research directions focusing on delineating key bacteria influencing thyroid health, characterizing longitudinal microbiota changes in thyroid conditions, and identifying novel microbiota-based therapies are proposed. A deeper understanding of the gut-thyroid axis may lead to microbiota-targeted strategies for managing thyroid disorders.

Advance in the Correlation between Diabetic Nephropathy and Abnormal Serum Thyroid Hormone Levels in Patients.

This study was developed to explore the correlation between diabetic nephropathy (DN) and abnormal serum thyroid hormone (TH) levels in patients, which can provide a reference for disease prevention and control in patients with DN. DN is the most serious complication of diabetes. The mortality rate of diabetic patients with DN is approximately 30 times higher than that of diabetic patients without DN. DN leads to high blood sugar, which causes vascular dysfunction in patients, causes cardiovascular disease, aggravates the disease and disease complexity, and thus increases the mortality of patients. DN patients often have oxidative stress and even fibrosis in severe cases. TH has a potential renal protective effect and can also regulate glucose metabolism and improve abnormal glucose tolerance and insulin resistance. Abnormal serum TH levels increase the risk of DN. Normal thyroid function plays an important role in regulating the physiological functions of the human body. Hormonal disorders promote the development of diabetes mellitus (DM) into DN. The pathogenesis, clinical manifestations, detection, and treatment methods of DN were reviewed in this study. The research progress of the influence of TH on DN was analyzed. This study is conducive to clinical research on DN and provides a reference.

Influence of thyroid hormones and effect of treatment choice on the quality of life of hyperthyroid patients.

Objective: To evaluate the influence of thyroid hormones as well as the effect of treatment choice on the quality of life of patients visiting / admitted in tertiary healthcare centers in Karachi, Sindh Pakistan. Study Design: Cross-sectional study. Setting: Rafae Aam General Hospital Federal Area Karachi, Sindh, Pakistan. Period: March 2022 to June 2022. Material & Methods: Patient’s data related to their socio-demographic and clinical details was collected by using a pre-tested written questionnaire. Brazilian version of 36-Item Short Form Health Survey questionnaire was completed by all the study participants. Results: Total 337 participants were included in the study. Mean age of the study participants was 34.03 ± 10.06. Majority of them were females while most of them belonged to the age group of 18-29 years. Most of our study participants were urban residents, married, having no any formal education and suffering from comorbidities. Based on clinical examination, 272 (80.7%) patients were found euthyroidism while 65 (19.3%) were hyperthyroid. Thus, hyperthyroid patients displayed a greater toll on the quality of life, particularly in areas of physical (59.62 vs. 82.81; p<0.05) as well as emotional (61.54 vs. 82.81; p<0.05) functioning. Conclusion: This study concludes that hyperthyroid patients have a significant quality of life impairment, particularly in the physical and emotional domains. Moreover, regardless of the findings of the serum thyroid hormone levels, quality of life of hyperthyroid patients is compromised.

A Causality between Thyroid Function and Bone Mineral Density in Childhood: Abnormal Thyrotropin May Be Another Pediatric Predictor of Bone Fragility.

Low bone mass can occur in children and adolescents with numerous chronic conditions; however, the influence of abnormal thyroid hormone and thyroid-stimulating hormone (TSH) levels on low bone mineral density (BMD) in children and adolescents remains controversial. Investigating the effects of excessive or deficient thyroid hormone and TSH levels on the risk of childhood bone fragility may provide a better understanding of the role of thyroid function on bone density in the pediatric population. The triiodothyronine (T3), thyroxine (T4), and TSH levels and BMD of 619 children diagnosed with various underlying conditions and whose treatment was completed were simultaneously assessed. The T3, free thyroxine (FT4), and TSH levels were subcategorized based on the age-matched reference range, and the lumbar spine BMD (LSBMD) data were compared. The mean LSBMD z-score was 0.49 ± 1.28, while T3, FT4, and TSH levels were 1.25 ± 0.29 ng/mL, 1.28 ± 0.19 ng/dL, and 2.76 ± 1.87 µU/mL, respectively. Both lumbar and femoral BMD z-scores were lower in children with abnormal TSH levels. TSH abnormality was the strongest risk factor for decreased LSBMD z-scores, and thus could be an early indicator of low BMD in children and adolescents with various underlying conditions.

Adverse thyroid hormone and behavioral alterations induced by three frequently used synthetic musk compounds in embryo-larval zebrafish (Danio rerio)

Synthetic musk compounds (SMCs) have been extensively used in numerous consumer products, such as perfumes, cosmetics, soap, and fabric softener. Due to their bioaccumulative nature, these compounds have often been detected in the aquatic ecosystem. However, their effects on endocrine and behavioral effects in freshwater fish have rarely been investigated. In the present study, thyroid disruption and neurobehavioral toxicity of SMCs were investigated using embryo-larval zebrafish (Danio rerio). Three frequently used SMCs, i.e., musk ketone (MK), 1,3,4,6,7,8-hexahydro-4,6,6,7,8,8-hexamethyl-cyclopenta [g]- benzopyran (HHCB), and 6-acetyl-1,1,2,4,4,7-hexamethyltetralin (AHTN), were chosen. Experimental concentrations for HHCB and AHTN were selected to include the maximum levels reported in the ambient water. The 5-day exposure to either MK or HHCB led to significant decrease of T4 concentration in the larval fish at the levels as low as 0.13 μg/L, even though compensatory transcriptional changes, e.g., up-regulation of hypothalamic crhβ gene and/or down-regulation of ugt1ab gene, were taken place. In contrast, AHTN exposure resulted in up-regulation of crhβ, nis, ugt1ab, and dio2 genes but did not alter T4 level, suggesting its lesser thyroid disrupting potential. All tested SMCs caused hypoactivity of the larval fish. Several genes related to neurogenesis or development, e.g., mbp and syn2a, were down-regulated, but the patterns of transcriptional changes were different among the tested SMCs. The present observations demonstrate that MK and HHCB can decrease T4 levels and cause hypoactivity of the larval zebrafish. It requires attention that HHCB and AHTN could influence thyroid hormone or behavior of the larval fish even at the levels close to those observed in the ambient environment. Further studies on potential ecological consequences of these SMCs in freshwater environment are warranted.

Influence of carvedilol and thyroid hormones on inflammatory proteins and cardioprotective factor HIF-1α in the infarcted heart

Inflammatory pathways of Toll-like receptor 4 (TLR4) and NLRP3 inflammasome contribute to acute myocardial infarction (AMI) pathophysiology. The hypoxia-inducible factor 1α (HIF-1α), however, is a key transcription factor related to cardioprotection. This study aimed to compare the influence of carvedilol and thyroid hormones (TH) on inflammatory and HIF-1α proteins and on cardiac haemodynamics in the infarcted heart. Male Wistar rats were allocated into five groups: sham-operated group (SHAM), infarcted group (MI), infarcted treated with the carvedilol group (MI+C), infarcted treated with the TH group (MI+TH), and infarcted co-treated with the carvedilol and TH group (MI+C+TH). Haemodynamic analysis was assessed 15 days post-AMI. The left ventricle (LV) was collected for morphometric and Western blot analysis. The MI group presented LV systolic pressure reduction, LV end-diastolic pressure elevation, and contractility index decrease compared to the SHAM group. The MI+C, MI+TH, and MI+C+TH groups did not reveal such alterations compared to the SHAM group. The MI+TH and MI+C+TH groups presented reduced MyD88 and NLRP3 and increased HIF-1α levels. In conclusion, all treatments preserve the cardiac haemodynamic, and only TH, as isolated treatment or in co-treatment with carvedilol, was able to reduce MyD88 and NLRP3 and increase HIF-1α in the infarcted heart.

Tenocytes do not just lie in a vacuum: the role of lipids, glycemic metabolism and thyroid hormones in tendinopathy and tendon rupture. A narrative review

Purpose: Tendinopathies and tendon ruptures are a common cause of pain and disabilities. The pathogenesis is considered multifactorial, and currently described as the failed healing response. Traditionally, tendon injuries have been mostly referred to age, overuse or mechanical factors. Recently, some authors have focused their attention on the influence of metabolic diseases and hormones on tendon homeostasis, opening new perspectives. There are even more studies which show how systemic condition and pathologies are able to influence the proliferation of tenocytes, the synthesis of extracellular matrix proteins, and the organization and properties of the extra cellular matrix of the tendons. Methods: In this article, we reviewed the current knowledge about the influence of lipids, glucose and thyroid hormones on the pathogenesis of tendinopathy. Results: Beside the traditional extrinsic and mechanical risk factors, this article showed the importance of metabolism and hormones of tendon health, reinforcing the idea of their great influence on the pathogenesis of tendinopathy. Current literature indicates that hypercholesterolemia, obesity, diabetes mellitus and hypothyroidism are all risk factors for tendinopathies and tendon ruptures. Conclusions: The precise role of each predisposing factor remains incompletely understood, and further epidemiology and laboratory studies should be performed to establish the strength of the association with tendon pathologies and their pathogenetic mechanism. Keywords: inertial measurement unit; acceleration; max speed; metrics; team sports.

Thyroid stimulating hormone correlates with triglyceride levels but is not associated with the severity of acute ischemic stroke in patients with euthyroidism: a cross-sectional study.

Growing evidence suggests an association between thyroid stimulating hormone (TSH) and severity of acute ischemic stroke (AIS). However, few studies have ruled out the potential influences of abnormal thyroid hormones when assessing this association. This study aimed to investigate the association between TSH levels and the severity of AIS patients with euthyroidism, and to explore the potential mechanism of TSH on this disease by analyzing the correlation of TSH with lipid profiles. This retrospective study consisted of 345 patients with normal T3 and T4 levels admitted for first-ever cerebral ischemic stroke. Baseline data of participant were collecte. Laboratory data, including serum levels of TSH and lipid profiles were measured in our hospital's clinical laboratory on admission. Stroke severity was recorded using the National Institutes of Health Stroke Scale (NIHSS). Associations between TSH levels and disease severity were analyzed with logistic regression analysis. Correlations between TSH and lipid profiles were analyzed with Spearman's rank correlation analysis. Among the 345 patients with AIS, the median age was 63 years (63±12 years), 106 patients (30.7%) were female, 237 (68.7%) patients were mild-severity and 108 (31.3%) patients were severity. Data analysis showed that higher serum TSH levels were associated with the mild severity of patients with AIS (P=0.042 in Kruskal-Wallis test, P=0.025 in logistic regression analysis, and P=0.044 in multiple logistic regression), but not in AIS patients with euthyroidism (P=0.078, P=0.337, respectively). Furthermore, TSH levels were correlated with triglycerides (TG) levels not only in total patients (r=0.135, P=0.012) but also in the patients with euthyroidism (r=0.133, P=0.018). TSH levels are associated with the severity of AIS patients, but not in patients with euthyroidism, predicting that stratified management of TSH may be beneficial in patients with AIS. Moreover, TSH levels are correlated with TG levels in patients with AIS.

ODP535 Thyrotoxic Periodic Paralysis (TPP) in A Young African American Male: Post Exercise

Abstract Thyrotoxic periodic paralysis (TPP) is a rare fatal disorder with hypokalemia as the hallmark feature associated with thyrotoxicosis. Compared with existing studies that TPP is prevalent among younger men of Asian descent, this study intends to complement this area of study by addressing aspects currently not fully covered involving the existence of TPP among men of African descent. This study documents the case of a 37year old African American Man with no previous history of hyperthyroidism who presented with sudden onset lower extremity paralysis and hypokalemia. It is particularly important to note that while majority of patients with TPP have preexisting hyperthyroidism, our patient presented with no history of overactive thyroid. The finding of this work fills a gap in literature highlighting the importance of separating Familial Hypokalemic periodic paralysis (FPP) and TPP at its earliest detection. We find strong and robust evidence suggesting that patients may be easily termed FPP in view of its similarity to TPP thereby leading to a delay in the diagnosis and treatment. TPP has been linked with genetic mutations in specific ion channels (calcium channels and KIR) and increased Na-K ATPase pump activity. This leads to a massive intracellular shift in potassium causing hypokalemia under the influence of excess thyroid hormone. We find that both TPP and FPP have similar clinical presentations and same precipitants hence the need for a high index of suspicion in patients with hypokalemia and sudden onset paralysis with no history of hyperthyroidism to prevent lethal complications. Our results suggest that prompt correction of hypokalemia and treatment of hyperthyroidism is key in resolving attacks and preventing lethal complications. Presentation: No date and time listed

Effect of vitamin D on serum BDNF level in patients with hypothyroidism caused by autoimmune thyroiditis

Background. Hashimoto’s thyroiditis is a chronic autoimmune disease of the thyroid gland caused by an increase in thyroid antibodies. A growing body of research suggests that patients with Hashimoto’s thyroiditis may suffer from cognitive impairment. Therefore, it is important to identify risk factors that contribute to the development of cognitive impairment in patients with autoimmune thyroiditis to diagnose them early and treat. Given that the influence of thyroid hormones on the brain is undeniable, and their deficiency leads to a variety of neurological complications, early diagnosis and treatment of neurological disorders in thyroid diseases is crucial for preventing further progression of these complications. The purpose of the study is to determine the effect of vitamin D on the level of brain-derived neurotrophic factor (BDNF) in blood serum of patients with hypothyroidism caused by autoimmune thyroiditis. Materials and methods. Twenty-eight patients with hypothyroidism caused by autoimmune thyroiditis were included in the study. The serum level of BDNF was quantified using a solid-phase enzyme-linked immunosorbent assay with a highly sensitive Human BDNF ELISA Kit (Elabscience®, United States, Catalog No E-EL-H0010) on E.I.A. Reader Sirio S (Seac, Italy). Results. In our study, the administration of vitamin D and L-thyroxine led to a 7.4-fold increase in BDNF levels (p<0.001). In the group of patients who took only L-thyroxine, serum content of BDNF increased by 2.1 times. In patients who took cholecalciferol and L-thyroxine, the level of BDNF was 2.48 times higher compared to those who took only L-thyroxine (p<0.001). Conclusions. A positive effect of vitamin D on the serum level of BDNF was found in patients with hypothyroidism caused by autoimmune thyroiditis. Treatment of these individuals using additional administration of cholecalciferol on the background of L-thyroxine proved to be more effective compared to the administration of L-thyroxine alone (p<0.001).

ETIOPATHOGENESIS OF THYROID DISEASE AND ASSOCIATION WITH METABOLIC SYNDROME

In clinical practice, patients with metabolic syndrome and thyroid disease are often referred. It is noteworthy that based on the results of various population studies, there has been an increase in both thyroid disease and the incidence of signs of metabolic syndrome in adults. Therefore, there has been a dramatic increase in interest in the study of possible associations between these two pathological conditions. Based on the results of various papers, the close relationship between these two pathological conditions is due on the one hand to the influence of thyroid hormones on carbohydrate, lipid metabolism and on the other hand the zobogenic effect of insulin on thyroid tissue. However, despite many scientific papers and population studies, the relationship between thyroid disease and components of the metabolic syndrome is still a matter of research, but in clinical practice, the results of these studies help to diagnose thyroid disease.

The Role of Cell and Gene Therapies in the Treatment of Infertility in Patients with Thyroid Autoimmunity.

There is a rising incidence of infertility worldwide, and many couples experience difficulties conceiving nowadays. Thyroid autoimmunity (TAI) is recognized as one of the major female infertility causes related to a diminished ovarian reserve and potentially impaired oocyte maturation and embryo development, causing adverse pregnancy outcomes. Growing evidence has highlighted its impact on spontaneously achieved pregnancy and pregnancy achieved by in vitro fertilization. Despite the influence of thyroid hormones on the male reproductive system, there is insufficient data on the association between TAI and male infertility. In past years, significant progress has been achieved in cell and gene therapies as emerging treatment options for infertility. Cell therapies utilize living cells to restore healthy tissue microenvironment and homeostasis and usually involve platelet-rich plasma and various stem cells. Using stem cells as therapeutic agents has many advantages, including simple sampling, abundant sources, poor immunogenicity, and elimination of ethical concerns. Mesenchymal Stem Cells (MSCs) represent a heterogeneous fraction of self-renewal, multipotent non-hematopoietic stem cells that display profound immunomodulatory and immunosuppressive features and promising therapeutic effects. Infertility has a genetic component in about half of all cases, although most of its genetic causes are still unknown. Hence, it is essential to identify genes involved in meiosis, DNA repair, ovarian development, steroidogenesis, and folliculogenesis, as well as those involved in spermatogenesis in order to develop potential gene therapies for infertility. Despite advances in therapy approaches such as biological agents, autoimmune disorders remain impossible to cure. Recent research demonstrates the remarkable therapeutic effectiveness of MSCs in a wide array of autoimmune diseases. TAI is one of many autoimmune disorders that can benefit from the use of MSCs, which can be derived from bone marrow and adipose tissue. Cell and gene therapies hold great potential for treating autoimmune conditions, although further research is still needed.

FGF21 Is Released During Increased Lipogenesis State Following Rapid-Onset Radioiodine-Induced Hypothyroidism.

BackgroundFGF21 pharmacological treatment reverses fatty liver and lowers serum triglyceride concentration but FGF21 serum level is increased in hepatic steatosis. FGF21 secretion is induced by thyroid hormones in vitro.PurposeTo determine the influence of thyroid hormones and metabolic changes secondary to thyroid dysfunction on FGF21 secretion in humans.Materials and MethodsThis was a case-control study. 82 hyperthyroid and 15 hypothyroid patients were recruited together with 25 healthy controls. Of those with hyperthyroidism, 56 received radioiodine treatment and 42 of them achieved hypothyroidism and then euthyroidism within one year following therapy. Radioiodine-induced hypothyroidism developed abruptly within a six week interval between clinic visits. FGF21 serum levels were determined with an ELISA method.ResultsSerum FGF21 levels did not differ in hyper- and hypothyroid patients in comparison to controls [median 103.25 (interquartile range, 60.90-189.48) and 86.10 (54.05-251.02) vs 85.20 (58.00-116.80) pg/mL P=0.200 and 0.503, respectively]. In hyperthyroid patients treated with radioiodine, serum FGF21 levels increased significantly in rapid-onset hypothyroidism in comparison to the hyperthyroid and euthyroid phase [median 160.55 (interquartile range, 92.48 - 259.35) vs 119.55 (67.78-192.32) and 104.43 (55.93-231.93) pg/mL, P=0.034 and 0.033, respectively]. The rising serum FGF21 level correlated positively with serum triglycerides (Spearman coefficient rs=0.36, P=0.017) and inversely with serum SHBG (rs=-0.41, P=0.007), but did not correlate with thyroid hormone levels.ConclusionsThere was a transient increase in FGF21 serum level during rapid-onset hypothyroidism following radioiodine treatment. There was no association between FGF21 serum level and thyroid hormones. In radioiodine-induced hypothyroidism, the rising serum FGF21 concentration correlated positively with rising serum triglycerides and negatively with falling SHBG, reflecting increased hepatic lipogenesis.