Serum T3 Levels Research Articles

Frequency of Pregnancy Induced Hypertension (PIH) in Patients Presenting with Hypothyroidism

Objective: Preeclampsia is a potentially fatal condition during pregnancy and following delivery. Numerous organs' functions can be influenced by preeclampsia. It is crucial, as this illness may be linked to abnormalities in thyroid function. Therefore, the aim of this study was to assess the frequency of thyroid dysfunction and its association with hypertension in pregnant women. Methodology: This descriptive cross sectional study was conducted at Obstetrics and Gynecology Unit-I, Civil Hospital, Karachi, using a non-probability consecutive sampling technique. The duration of the study was about six months from October 2022 till March 2023. A total of 80 pregnant women who were between the ages of 18 and 40, had gestational ages between 20 and 40 weeks, and had laboratory results that suggested hypothyroidism were included in this study. A chi-square test was applied to evaluate the association between maternal age, parity, gestational age, serum levels of TSH and T4 and pregnancy induced hypertension. Results: The study findings showed that most of the women 33(41.25%) were between 26 to 35 years of age. The mean age of the pregnant women was 29.43±4.64 years. The mean parity was 1.74±0.83 and the mean gestational age was 30.33±5.22 weeks, and the mean duration of hypothyroidism was 4.27±2.06 years. Concerning thyroid parameters, the mean T4 was 5.79±1.21 pmol/L, and the mean TSH was 6.28±2.03 mIU/L. Additionally, there was an insignificant association observed between pregnancy induced hypertension and maternal age, gestational age, parity, and thyroid hormone parameters. Conclusion: This study concluded that alterations in the thyroid function of pregnant women led to pregnancy induced hypertension. Only 25% of hypothyroid pregnant women had gestational hypertension. Furthermore, age, parity, gestational age, and thyroid parameters of pregnant women were insignificantly associated with pregnancy induced hypertension. Keywords: Pregnancy induced hypertension, hypothyroidism, gestational age.

Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation

The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction and/or exposure to IR resulted in a significant decrease in the serum levels of T3 and T4 associated with increased levels of lipid peroxidation end product, malondialdehyde (MDA), and nitrites (NO) in the brain tissue homogenate. Also, hypothyroidism and /or exposure to IR markedly enhance the endoplasmic reticulum stress by upregulating the gene expressions of the protein kinase RNA-like endoplasmic reticulum kinase (PERK), activated transcription factor 6 (ATF6), endoplasmic reticulum-associated degradation (ERAD), and CCAAT/enhancer-binding protein homologous protein (CHOP) in the brain tissue homogenate associated with a proapoptotic state which indicated by the overexpression of Bax, BCl2, and caspase-12 that culminates in brain damage. Meanwhile, the PTU and /or IR-exposed rats treated with MEE reduced oxidative stress and ERAD through ATF6. Also, the MEE treatment prevented the Bax and caspase-12 gene expression from increasing. This treatment in hypothyroid animals was associated with neuronal protection as indicated by the downregulation in the gene expressions of the microtubule-associated protein tau (MAPT) and amyloid precursor protein (APP) in the brain tissue. Furthermore, the administration of MEE ameliorates the histological structure of brain tissue. In conclusion, MEE might prevent hypothyroidism-induced brain damage associated with oxidative stress and endoplasmic reticulum stress.

Thyroid Hormone Status of School Going Children in An Urban Area of Chattogram, Bangladesh

Background: Thyroid gland is the endocrine organ that secretes hormones namely, Triiodothyronine (T3) and Thyroxine hormone (T4). T3 and T4 are released in relation to the message of tropic hormone TSH, by the anterior pituitary. Absences as well as excess of thyroid hormones have harmful impacts on the overall health condition like physical and mental impediment. Poor intelligence leading to poor academic performance is frequently observed in hypothyroid children. The study was aimed to estimate serum T3, T4 and TSH levels of a group of school going children in urban area of Chattogram, Bangladesh. Materials and methods: This cross-sectional observational study was conducted among school going children (Age: 7-12 years) of Chattogram city between January, 2022 and June 2022. Chattogram based three schools were selected by convenient sampling. A total of 500 blood samples of children were collected and serum T3, T4 and TSH levels were measured. Estimation of T3 and T4 were done by Radioimmunoassay (RIA) and estimation of TSH was done by Immunoradiometric assay (IRMA) in the in Vitro laboratory. Results: Among 500 children, the estimated mean ±SD serum T3 hormone level was2.46±0.79 (Range: 1.27-5.51) nmol/L, mean ±SD serum T4 hormone level was 141.99±32.77 (Range: 86.21-239.05) nmol/L and mean ±SD serum TSH hormone level was 1.58±1.04 (Range: 0.30-3.02) mIU/L. Conclusion: Thyroid hormone status of the study group children was found within normal limits. However, regular screening of children is suggested to identify the subclinical and unreported clinical cases, so that theiroptimum growth and development are ensured. IAHS Medical Journal Vol 5(2), Dec 2022; 67-69

#6633 DIURETIC RESISTANCE PREDICTORS IN ACUTE DECOMPENSATED HEART FAILURE ADMISSIONS: A BROADER LOOK

Abstract Background and Aims Failing to relieve congestion portends a rise in mortality rate and length of stay in acute decompensated heart failure (ADHF) hospitalizations. That situation corresponds to diuretic resistance (RDIUR). We sought to evaluate clinical and biochemical predictors of RDIUR, including those non-conventional ones we noticed as relevant in prognosis in our clinical practice. Method We conducted an observational, analytical and cross-sectional study, with prospective and consecutive patient (P) data acquisition. We included P over 18 years-old, who were admitted to the Intensive Care Telemetry Unit in our Hospital in the period between July, 2011 and May, 2022 due to ADHF diagnosis. All P received diuretic IV therapy as part of pharmacological treatment. As mentioned in earlier presentations, urine output (UO) was registered in all P, and failure to achieve an UO ≥ 1.5 ml/kg/hour under a pre-established protocol that included and initial 100 mg of IV furosemide bolus followed by a 2 hours of a 5 mg/hour furosemide continuous infusion. Under failure to achieve the goal, furosemide dose was doubled for two additional hours. Failure to respond to this strategy was called “diuretic resistance”. P who received a heart transplant during index admission or those who were on chronic dialysis were excluded from this study. Clinical, epidemiological and biochemical variables were registered. Missing data was imputed by means of multiple regression with chained equations. We constructed a multivariate logistic regression, with selection of relevant predictors completed by resampling and regularization of a Lasso regression model. Statistical significance was considered with a 5% of alpha error. Analysis was conducted using R (R Core Team, 2021), with RStudio (RStudio Team, 2020) as Integrated Development Environment for R, and the tidymodels package (Silge and Kuhn, 2022). Results A total of 1359 P were included. RDIUR was observed in 177 P (13%). These P were younger (69 years old vs 72 p = 0.02), with a higher prevalence of diabetes (39.5% vs 28%; p = 0.002), admission creatinine levels (1.4 vs 1.1 mg/dl; p < 0.001), lower total T3 serum levels (0.56 ng/ml vs 0.7; p < 0.001), with higher incidence of cholestasis (61 vs 40%; p < 0.001), and anasarca as clinical phenotype of systemic congestion (17.5% vs 8.5% p < 0.001). In-hospital mortality was higher in P who developed RDIUR (32.8 vs 5.6%, p < 0.001), in the same way that inotropic support (62 vs 16, p < 0.001), worsening heart failure (48% vs 11; p < 0.001), and furosemide dose at 2nd admission day (175.4 vs 123.4 p < 0.001) were higher in these P. We found no differences in left ventricular ejection fraction (38 vs 41 p = 0.21), first day natriuresis (75.5 vs 78.4, p = 0.093), coronary etiology vs others (20% vs 22; p = 0.26) or one month readmission rate (33% vs 37; p = 0.27). In the adjusted model, inotropic support (OR 5.2; IC95% 3.4-8; p < 0.001), worsening heart failure (OR 3.4; IC95% 2.2-5.3; P < 0.001), furosemide dose at 2nd day (OR 1, IC95%1, P 0.001), admission creatininemia (OR 2.05; IC95% 1.7-2.6; p < 0.001), anasarca phenotype (OR 2.3; IC95 1.4-3.9; p = 0.002) and normal T3 levels (OR 0.05; IC95% 0.02-0.14; p < 0.001) were identified as independent predictors of RDIUR development. Model accuracy was 0.89 and ROC-AUC 0.87. In the same way, RDIUR (OR 2.57; IC95% 1.5-4.3; p < 0.001), worsening heart failure (OR 4.1 IC95% 2.4-7; p < 0.001), inotropic support (OR 3; IC95% 1.7-5.2; p < 0.001) and cholestasis (OR 3.1; IC95% 1.9-5.2; p < 0.001) were found as independent predictors of in-hospital mortality. Conclusion Diuretic resistance is a serious event in patients hospitalized for ADHF, and considerably associated with mortality. A decreased renal reserve, low T3 levels, and anasarca at admission were significantly associated with diuretic resistance development. Considering “new” biochemical predictors as admission T3 levels might add strength to this subset of patients, opposed to information displayed by “classical” event predictors in ADHF patients, as ventricular function or etiology of cardiac disease. Due to clinical potential implications these observational results should be confirmed under evidence based protocols.

Depleted uranium induces thyroid damage through activation of ER stress via the thrombospondin 1-PERK pathway

Depleted uranium (DU) can cause damage to the body, but its effects on the thyroid are unclear. The purpose of this study was to investigate the DU-induced thyroid damage and its potential mechanism in order to find new targets for detoxification after DU poisoning. A model of acute exposure to DU was constructed in rats. It was observed that DU accumulated in the thyroid, induced thyroid structure disorder and cell apoptosis, and decreased the serum T4 and FT4 levels. Gene screening showed that thrombospondin 1 (TSP-1) was a sensitive gene of DU, and the expression of TSP-1 decreased with the increase of DU exposure dose and time. TSP-1 knockout mice exposed to DU had more severe thyroid damage and lower serum FT4 and T4 levels than wild-type mice. Inhibiting the expression of TSP-1 in FRTL-5 cells aggravated DU-induced apoptosis, while exogenous TSP-1 protein alleviated the decreased viability in FRTL-5 cells caused by DU. It was suggested that DU may caused thyroid damage by down-regulating TSP-1. It was also found that DU increased the expressions of PERK, CHOP, and Caspase-3, and 4-Phenylbutyric (4-PBA) alleviated the DU-induced FRTL-5 cell viability decline and the decrease levels of rat serum FT4 and T4 caused by DU. After DU exposure, the PERK expression was further up-regulated in TSP-1 knockout mice, and the increased expression of PERK was alleviated in TSP-1 over-expressed cells, as well as the increased expression of CHOP and Caspase-3. Further verification showed that inhibition of PERK expression could reduce the DU-induced increased expression of CHOP and Caspase-3. These findings shed light on the mechanism that DU may activate ER stress via the TSP 1-PERK pathway, thereby leading to thyroid damage, and suggest that TSP-1 may be a potential therapeutic target for DU-induced thyroid damage.

Effects of Triiodothyronine Treatment in an Animal Model of Heart Failure with Preserved Ejection Fraction.

Background: Low levels of triiodothyronine (T3) are common in patients with heart failure (HF). Our aim was to evaluate the effects of supplementation with low and replacement doses of T3 in an animal model of HF with preserved ejection fraction (HFpEF). Methods: We evaluated four groups: ZSF1 Lean (n = 8, Lean-Ctrl), ZSF1 Obese (rat model of metabolic-induced HFpEF, n = 13, HFpEF), ZSF1 Obese treated with a replacement dose of T3 (n = 8, HFpEF-T3high), and ZSF1 Obese treated with a low-dose of T3 (n = 8, HFpEF-T3low). T3 was administered in drinking water from weeks 13 to 24. The animals underwent anthropometric and metabolic assessments, echocardiography, and peak effort testing with maximum O2 consumption (VO2max) determination at 22 weeks, and a terminal hemodynamic evaluation at 24 weeks. Afterwhile myocardial samples were collected for single cardiomyocyte evaluation and molecular studies. Results: HFpEF animals showed lower serum and myocardial thyroid hormone levels than Lean-Ctrl. Treatment with T3 did not normalize serum T3 levels, but increased myocardial T3 levels to normal levels in the HFpEF-T3high group. Body weight was significantly decreased in both the T3-treated groups, comparing with HFpEF. An improvement in glucose metabolism was observed only in HFpEF-T3high. Both the treated groups had improved diastolic and systolic function in vivo, as well as improved Ca2+ transients and sarcomere shortening and relaxation in vitro. Comparing with HFpEF animals, HFpEF-T3high had increased heart rate and a higher rate of premature ventricular contractions. Animals treated with T3 had higher myocardial expression of calcium transporter ryanodine receptor 2 (RYR2) and α-myosin heavy chain (MHC), with a lower expression of β-MHC. VO2max was not influenced by treatment with T3. Myocardial fibrosis was reduced in both the treated groups. Three animals died in the HFpEF-T3high group. Conclusions: Treatment with T3 was shown to improve metabolic profile, myocardial calcium handling, and cardiac function. While the low dose was well-tolerated and safe, the replacement dose was associated with increased heart rate, and increased risk of arrhythmias and sudden death. Modulation of thyroid hormones may be a potential therapeutic target in HFpEF; however, it is important to take into account the narrow therapeutic window of T3 in this condition.

Prognostic significance of thyroid hormone T3 in patients with septic shock: a retrospective cohort study.

The role of thyroid hormones is crucial in the response to stress and critical illness, which has been reported to be closely associated with a poor prognosis in patients admitted to the intensive care unit (ICU). This study aimed to explore the relationship between thyroid hormone and prognosis in septic shock patients. A total of 186 patients with septic shock were enrolled in the analytical study between December 2014 and September 2022. The baseline variables and thyroid hormone were collected. The patients were divided into survivor group and non-survivor group according to whether they died during the ICU hospitalization. Among 186 patients with septic shock, 123 (66.13%) were in the survivor group and 63 (33.87%) were in the non-survivor group. There were significant differences in the indictors of free triiodothyronine (FT3) (p=0.000), triiodothyronine (T3) (p=0.000), T3/FT3 (p=0.000), acute physiology and chronic health evaluation II score (APACHE II) (p=0.000), sequential organ failure assessment score (SOFA) (p=0.000), pulse rate (p=0.020), creatinine (p=0.008), PaO2/FiO2 (p=0.000), length of stay (p=0.000) and hospitalization expenses (p=0.000) in ICU between the two groups. FT3 [odds ratio (OR): 1.062, 95% confidence interval(CI): (0.021, 0.447), p=0.003], T3 (OR: 0.291, 95% CI: 0.172-0.975, p=0.037) and T3/FT3 (OR: 0.985, 95% CI:0.974-0.996, p=0.006) were independent risk factors of the short-term prognosis of septic shock patients after adjustment. The areas under the receiver operating characteristic curves for T3 was associated with ICU mortality (AUC = 0.796, p<0.05) and was higher than that for FT3 (AUC = 0.670, p<0.05) and T3/FT3 (AUC = 0.712, p<0.05). A Kaplan-Meier curve showed that patients with T3 greater than 0.48 nmol/L had a significantly higher survival rate than the patients with T3 less than 0.48 nmol/L. The decrease in serum level of T3 in patients with septic shock is associated with ICU mortality. Early detection of serum T3 level could help clinicians to identify septic shock patients at high risk of clinical deterioration.

Thyroid Dysfunction in Patient with Cirrhotic Liver Disease and its Relation to the Severity of Cirrhosis

Background: Liver carries its vital significance due to ability to control over excretion, metabolism and transportation of the thyroid hormone. Peripheral change of T4 to T3 occurs in the live leading to initiation of action and breakdown of the hormones. Any morbidity in the liver can result in the decrease in TSH level and leading to thyroid dysfunction. So it is necessary to determine this impact in cases with liver cirrhosis. Methodology: 115 cases of chronic liver disease who were not on the any therapy were involved in this research. The age of &gt;18 years and both genders were selected. Data was collected from Department of Medicine, Lahore General Hospital, and Lahore in a duration of one year. All the demographics and baseline information mandatory for the selection of the appropriate sample was recorded. The participants were informed about the purpose of the research and after their consent they were selected for this study. Finally, the collected data was analyzed using SPSS 23.inc. Practical implication: Thyroid dysfunction in patients with cirrhotic liver disease has practical implications for their management and outcomes. Regular screening and early intervention are important to detect and treat thyroid dysfunction promptly. Managing both cirrhosis and thyroid dysfunction requires a multidisciplinary approach involving hepatologists and endocrinologists. Patient education and support are crucial for raising awareness and ensuring adherence to treatment plans. Further research is needed to understand the relationship between thyroid dysfunction and cirrhosis severity and to explore potential therapeutic targets. Integrating thyroid evaluation into the overall management of cirrhosis can improve patient outcomes and quality of life. Results: Mean age of 51(9.81) years were involved in this research. The male cases were higher in number 81(70.4%). The body mass index value was 27.5(3.65). Child Pugh A class was noted in 37(32.2%), B in 32(27.8%) &amp; C in 46(40%). Serum T3 level was 2.05, serum T4 level was 8.69, serum FT3 level was 3.06, serum FT4 was 1.24 and TSH level was having a mean value 3.15. A significant inverse relationship noted in the severity of cirrhosis and thyroid profile levels. Conclusion: Thyroid function depends on the smooth functioning of the liver through its hormones. As the liver compromise some disease, this normal function disturbs and thyroid dysfunction occurs which increase with the harshness of liver disease. Keywords: Liver Disease, Thyroid Dysfunction, HCV, TSH

Nano-selenium relieved hepatic and renal oxidative damage in hypothyroid rats.

Hypothyroidism can induce oxidative stress. Nano-selenium (Nano Sel) has antioxidant effects. The current research explored Nano Sel effects on hepatic and renal oxidative damage induced by hypothyroidism in rats. Animals were grouped into (1) Control; (2) Propylthiouracil (PTU) group which received water mixed with 0.05% of PTU; (3) PTU-Nano Sel 50; (4) PTU-Nano Sel 100; and (5) PTU-Nano Sel 150. Besides PTU, the PTU-Nano Sel groups were treated with 50, 100, or 150 μg/kg of Nano Sel intraperitoneally. Treatments were done for 6 weeks. The serum level of T4, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), albumin, total protein, creatinine, and blood urea nitrogen (BUN) was evaluated. Malondialdehyde (MDA) and total thiol concentration and the activity of catalase (CAT) and superoxide dismutase (SOD) in hepatic and renal tissues also were checked. Hypothyroidism induced by PTU significantly increased AST, ALT, ALP, creatinine, BUN, and MDA concentration and noticeably reduced albumin, total protein, total thiol level, and SOD and CAT activity. Administration of Nano Sel ameliorated the adverse effects of hypothyroidism on liver and kidney function. Nano Sel applied protective effects against hepatic and renal damage resulting from hypothyroidism via ameliorating the oxidative stress status. More cellular and molecular experiments need to be done to understand the exact mechanisms.

Novel Interactomes of Cardiac Noncoding RNA Transcriptome under Altered Thyroid Hormonal States

Background: Noncoding RNAs are emerging as key players in cardiovascular diseases. Both Hypothyroidism (HypoTH; low thyroid hormones [THs]) and hyperthyroidism (HyperTH; high THs) can be deleterious to the heart. We recently showed the involvement of long noncoding RNAs (lncRNAs) in HypoTH under caloric restriction. However, a comprehensive view of the cardiac transcriptome and its interactions under altered TH states is lacking. We hypothesized that cardiac noncoding interaction networks are significantly altered in the cardiac-TH regulatory axis. Methods: In this randomized, blinded study (2.5 mon), adult C57 mixed-sex mice (n=8-10/group; 5 females, 3-5 males) were divided into Control, HypoTH (low iodine diet with oral methimazole), HyperTH (1 microgram [ug]/gram Thyroxine, T4; intraperitoneal) and HypoTH+T3 (similar to HypoTH with oral 12 ug/kilogram/day Triiodothyronine, T3). Morphometrics, ultrasound, immunosorbent assay, Quantitative real-time PCR (qPCR) and whole transcriptome sequencing were performed. Statistical analyses were done by Tukey’s analysis of variance (with post hoc), Benjamini &amp; Hochberg and others using Prism, R, etc. RNA quality was validated by Nanodrop, gel electrophoresis and Bioanalyzer. Results: In mixed-sex mice, HypoTH showed significant cardiac atrophy (whole heart, LV and right ventricle), low serum total T3 and T4 levels (p&lt;0.001), low heart rate, (p&lt;0.01) diminished systolic LV posterior (p&lt;0.05) and septal wall thicknesses (p&lt;0.01) and fractional shortening (-34%; p&lt;0.01) compared to controls. T3 therapy showed feedback inhibition of T4 (p&lt;0.001) and restored all other parameters including LV systolic diameter (p&lt;0.05). Among others, HyperTH had cardiac hypertrophy and increased T3 and T4 (p&lt;0.05) compared to controls (p&lt;0.001). Similar significant results were obtained in males and females. qPCR of shorter-term treatment showed significantly altered lncRNAs in inflammatory and immune pathways. Whole transcriptome sequencing showed numerous differentially expressed, significantly altered and enriched ( GO and KEGG) targets across the groups among all RNA species studied (p-adjusted; padj&lt;0.05). These include novel and known lncRNAs, microRNAs (miRNAs) and messenger (m) RNAs that change in opposite directions in low vs high TH groups. These also include 11 novel circular RNAs (circRNAs; CIRI2) decreased with HyperTH (padj&lt;0.05). We also uncovered novel co-expression and interactions of miRNA-mRNA, miRNA-lncRNA, mRNA-lncRNA, circRNA-miRNA and miRNA-lncRNA-mRNA (including TH receptor alpha; miRanda, Cytoscape) and also splicing and base editing events (padj&lt;0.05). Conclusions: This is the first cross-disciplinary study reporting a comprehensive cardiac transcriptome-wide interactome network of circRNA, lncRNA, miRNA and mRNA in a TH-responsive manner. This offers significant translational potential to develop diadiagnostic and therapeutic targets for cardiac-endocrine co-morbid conditions. NYITCOM at A-State, ABI This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins.

This study was conducted to determine the possible effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins (UCPs) in rats. Forty male Wistar Albino rats were divided into 4 groups with 10 animals in each group: control, sham, 10 and 100µM MOTS-c. Hypothalamus, blood, muscle, adipose tissues samples were collected for thyrotropin-releasing hormone (TRH), UCP1 and UCP3 levels were determined by the RT-PCR and western blot analysis. Serum thyroid hormone levels were determined by the ELISA assays. MOTS-c infusion was found to increase food consumption but it did not cause any changes in the body weight. MOTS-c decreased serum TSH, T3, and T4 hormone levels. On the other hand, it was also found that MOTS-c administration increased UCP1 and UCP3 levels in peripheral tissues. The findings obtained in the study show that central MOTS-c infusion is a directly effective agent in energy metabolism.

A PROSPECTIVE STUDY OF THYROID FUNCTION TEST IN GERIATRIC POPULATION AND ITS CLINICAL CORRELATION IN A TERTIARY TEACHING CARE CENTER

Aim: The objective of the present investigation was to investigate the clinical relationship between hypothyroidism and hyperthyroidism in the elderly population as well as the demographics of thyroid dysfunction in this population.Materials and Method: An extensive clinical examination and thyroid function (T3, T4, and TSH) testing were performed on 100 patients older than 60 who were believed to have thyroid problems as part of a prospective study in our tertiary care center. Other pertinent examinations, such as USG &amp; FNAC neck, were carried out when thyroid swelling or nodules were present in order to obtain an accurate diagnosis. As necessary, further analysis was conducted using PS for expert opinion and 2DECHO. The determination of serum T3, T4, and TSH levels using the chemiluminescence assay method served as the basis for the laboratory evaluation of thyroid functioning. Result: In this investigation, it was discovered that 28% patients had thyroid function tests that were abnormal, and 18% of these patients also showed clinical signs of thyroid problems. 22% of cases had hypothyroidism, and 6% had hyperthyroidism. The prevalence of thyroid disorders rises with advancing age. Conclusion: In the elderly, thyroid dysfunction is more common. Older people should have their thyroid function checked, and long-term follow-up should be advised. Thyroid diseases in older individuals should be treated gradually and carefully, as they always need lifelong monitoring.

ASSOCIATION OF THYROID HORMONE LEVELS AND CHRONIC KIDNEY DISEASE

Introduction- Normal thyroid hormone metabolism, breakdown, and excretion depend heavily on the kidney. We sought to assess the serum thyroid hormone levels in CKD patients in the current investigation because there is little data on the association between thyroid hormone levels and CKD. Methods- This cross-sectional and time bound study was conducted in department of General Medicine and Nephrology in NIMS&amp;R Hospital, Jaipur for 18 months. Results- Number of patients with low serum T3 levels increased proportionately with decreasing eGFR levels. Serum T4 and TSH levels were not signicantly related to worsening renal function. Conclusion- Low T3 syndrome was the commonest and subclinical hypothyroidism was the second most common thyroid abnormality detected. Hypothyroidism and severity of CKD did not correlate with each other.

Alterations of Thyroid Hormone Levels and the Risks of Diabetic Retinopathy in T2DM

Background: Diabetes mellitus and thyroid disease are linked endocrinopathies. The association between diabetes mellitus complications and thyroid function is characterized by a complicated interdependent interplay that is difficult to understand. Objective: We conducted this study to determine the association between diabetic retina disease (DRD) incidence and normal thyroid hormone levels in T2DM. Methods: Recruit patients in the study, 134 patients with type 2 diabetes and 36 healthy ones with no DM, were screened in the present case-control study. Diabetic retinopathy was tested for all patients, and anthropometric and thyroid functions were assessed. Regression analyses were employed to evaluate the relationship between thyroid hormones and the risk of developing DR. Results: There were significant differences in triiodothyronine (T3) and thyroxine (T4) serum levels among the DR groups and the healthy control. The levels in each TSH and T4 are positively significant between groups of PDR and NDR, while T3 was negatively associated with NPDR. A significant association was found between increasing levels of T3 and the development of severe DR; thus, PDR was less likely to occur in individuals with high T3 levels‎ [OR 0.014(95% CI, 0.001-0.34) P value is 0.009 after adjustment. The risk of PDR had an increased likelihood of developing PDR at the highest levels of serum TSH and T4 [OR 41.07(1.60-1053.1) P= 0.025, OR 65.91(2.10-2067) P= 0.017, respectively). Conclusion: Diabetes retinopathy in euthyroid Iraqi people may be associated with levels of T3 and T4 in the blood. Patients with higher TSH and T4 concentrations had a greater risk of developing sight-threatening PDR in type 2 diabetics.

Effect of the obese phenotype on expression of hepatic T4–5’ deiodinase activity, T3 generation and thyroidal mediated actions in congenic LA/Ntul//–cprats

Parameters of thyroidal responses to diet and environment have long been shown to be impaired in the obese phenotype of the LA/Ntul//–cp rat. To characterize the effect of expression of the obese phenotype on activity of maximum T4–5’ deiodinase (T4–DI) activity on adiposity and aspects of metabolism, groups of lean and obese littermates were subjected to measures of resting metabolic rate (RMR, VO2) at thermal neutrality (30°C) after a brief fast, followed by dose response Norepinephrine (NE) stimulation. Hepatic T4–DI activity represents a major source of hormonally active T3 in plasma and is readily delivered to peripheral tissues. At 16 weeks of age animals were sacrificed by cervical dislocation, blood was collected, and liver tissue was dissected for measures of serum levels of T3 and T4, and measures of maximal tissue dithiolthreitol (DTT)–stimulated T4–DI activity determined. The retroperitoneal and dorsal white adipose (WAT) depots were also dissected to estimate the magnitude of adiposity present upon sacrifice in each phenotype. Measures of RMR and the VO2 response to NE were greater in lean than obese phenotype, and indicators of BW and adiposity were much greater in obese than lean (p=&lt;0.01). Measures of serum T3 were greater in lean than obese, but T4 was similar in both phenotypes. Measures of the rate of hepatic T4 DI activity were greater in lean than obese (p=&lt;0.05), and the T1/2 for T4 disappearance were also prolonged in the obese phenotype. These results are consistent with other studies of impaired nonshivering thermogenesis in this strain, and suggest that decreased activity of hepatic T4–5’ deiodinase activity may be a contributing factor in the impaired capacity for nonshivering thermogenesis and excess fat accretion in the obese phenotype of this strain.

Circulating Thyroid Hormone Levels among Patients with Cardiovascular, Gastrointestinal, and Hypertensive Disorders in the Population of Peshawar, Khyber Pakhtunkhwa: An Analytical Comparison

This research set out to determine the levels of TSH, T4, and T3 in various age groups, genders, and conditions such as heart disease, gastroenteritis, and hypertension. Chemiluminiscence immunoassay (CLIA) was used to measure the serum levels of TSH, T4, and T3 in stomach, heart, and hypertension patients of various age groups and genders. Gender differences were seen in thyroid hormone levels. Based on our findings, women have a wider TSH range than men. Women's mean T3 values are nearly identical to those of men, whereas women's T4 values are higher than men's. Hormone levels vary significantly across people with heart disease, hypertension, and gastrointestinal disorders. While the values of T3 and T4 are normal, the mean TSH value in several patients was somewhat higher than the normal range. Hormone levels are influenced by age in a similar manner.

Assessment of Thyroid Functions and its Relationship With Semen Quality in Men

Introduction: In recent years, a partial relationship has been discovered between thyroid hormones and the formation of germ cells and the process of spermatogenesis. The current study aimed to assess thyroid hormone levels and the relationship between those levels and semen quality. Methods: Forty-seven infertile males, as the treatment group, and 25 healthy individuals, as the control group, were enrolled in this study. Thyroid-stimulating hormone (TSH), triiodothyronine (T3) hormone, and tetraiodothyronine (T4) hormone were calculated, and the parameters of seminal fluid (count, motility, and morphology) were assessed for semen quality. Results: The results demonstrated that sperm counts, sperm motility%, and normal morphology% were significantly lower in the infertile male group compared with the healthy group. The results further represented a highly significant level of TSH and total T3, while the total T4 was negligible in the infertile male group in comparison with the healthy group. The infertile male group was divided into subgroups based on sperm abnormalities, including asthenozoospermia, oligozoospermia, and azoospermia. Based on the findings, there was a significant reduction in TSH, T3, and T4 levels in oligozoospermia compared with the other groups. However, the levels of TSH, T3, and T4 were significantly higher in asthenozoospermia compared with the other groups, demonstrating the existence of a relationship between thyroid indicators and Asthenozoospermia. Conclusion: Overall, the mean serum levels of TSH, T3, and T4 were significantly lower in the infertile male group compared with the healthy group. Thus, they were negatively associated with sperm counts, motility%, and normal morphology%. Hence, these negative impacts on thyroid hormones were associated with different sperm abnormalities and semen quality in the infertile males group.

Biochemical Assessments of Thyroid Profile and Renal Function Test in Chronic Kidney Disease

Introduction: CKD is a clinical syndrome which occurs due to irreversible loss of renal function leading to metabolic, endocrine, excretory and synthetic function resulting in accumulation of non – protein nitrogenous substances which leads to metabolic derangements and ends up with distinct clinical manifestations. Aim: To study thyroid function abnormalities in patients with chronic kidney disease. To correlate the thyroid function abnormalities with severity of renal failure. To differentiate primary hypothyroidism from thyroid dysfunction due to chronic kidney disease. Methodology: After selection of patients, fulfilling the above criteria, about 5 ml of blood sample is collected in non-heparinised serum bottle and sent for thyroid profile test. Components of thyroid profile included in our study and Quantitative determination of T3, T4 and TSH is done by Enzyme Linked Immunosorbent Assay. Result: In our study out of 50 patients, 33 patients had low serum T3 levels . 4 patients among low serum T3 value, they also had low T4 and high TSH suggesting primary hypothyroidism. So excluding 4 patients of hypothyroidism 29 patients had low T3 syndrome in our study. Low T4 levels in our study, out of which 4 patients had low T3 and high TSH suggesting primary hypothyroidism. Conclusion: In my study population, 50 CKD patients who were on conservative management were studied. Among them 66% of the patients had low T3 values. The change in the serum levels of T3 and T4 in patients with CKD can be considered as being protective, promoting conservation of protein. There is increase in incidence of hypothyroidism in patients with chronic kidney disease.

Hormonal and inflammatory modulatory effects of hesperidin in hyperthyroidism-modeled rats.

The goal of the current study was to investigate the hormonal modulatory efficiency of hesperidin, through its regulatory potential of immunological, inflammatory, and/or antioxidant changes in on hyperthyroidism modeled adult female albino rats. Both normal and hyperthyroidism modeled rats (140-160g) were randomly divided into four groups (10 animals each) as follows: 1) healthy animals were daily ingested with saline for six weeks, and served as control group, 2) healthy animals were intraperitoneally injected with hesperidin (50 mg/kg/day) for a similar period, 3) hyperthyroidism-modeled animals without any treatment acted as positive control, and 4) hyperthyroidism-modeled animals were treated intraperitoneally with hesperidin for a similar period. The findings showed that hesperidin significantly modulated hyperthyroidism deteriorations, this was evidenced by a remarkable decline in serum T4, FT4, T3, FT3, TNF-α, IL1β-, IL4-, IL-6, and IL-10 levels, with a minor increase in TSH and significant raise in CD4+ level. Similarly, valuable improvement was observed in the oxidative status; serum SOD, GPx, CAT, and GSH levels were dramatically enhanced, associated with remarkable drop in MDA and NO levels. Also, hesperidin demonstrated nephro-hepatoprotective and anti-atherogenic potential, this was achieved from the notable reduction in ALAT and ASAT activities as well as urea, creatinine, cholesterol, and triglyceride close to the corresponding values of healthy group. These findings were supported by histological and immunohistochemical ones that showed a notable decrease in the expression of the calcitonin antibody. In conclusion, hesperidin possesses anti-hyperthyroidism, immunoinflammatory regulatory, and antioxidant activities that evidenced from the improvement of physio-architecture of the thyroid gland, reduction of inflammation and restoration of the impaired oxidative stress. This effect might be mechanized through immunological, inflammatory, apoptotic, and/or antioxidant modulatory pathways.

The Effect of the Thyroid Gland on High Blood Pressure

The paper discusses the relationship between the thyroid gland and high blood pressure, specifically in the context of hyperthyroidism. It explains that hyperthyroidism, characterized by an increase in thyroid hormones, can lead to an acceleration of the heartbeat and an increase in its force, resulting in high blood pressure . The paper also mentions that high blood pressure resulting from other diseases, such as thyroid problems, is known as secondary hypertension. Treating this type of high blood pressure requires addressing the underlying medical condition causing it Additionally, the paper highlights that thyroid hormones play a role in regulating hemostasis, the process of blood clotting. Thyroxine, a thyroid hormone, is associated with the release of von Will brand factor and influences the synthesis of proteins involved in hemostasis. Thyroxine deficiency in hypothyroidism can lead to a deficiency in certain clotting factors Low serum levels of T3 can increase peripheral vascular resistance by up to 30%, leading to arterial stiffness and a decrease in cardiac output. This results in high blood pressure, particularly in systolic blood pressure, which returns to normal with treatment of the underlying thyroid dysfunction. Hypothyroidism is associated with high blood pressure, and the most common cardiovascular findings in hypothyroidism are bradycardia and high blood pressure. Thyroid hormone deficiency affects the contractility of cardiomyocytes, leading to an increase in peripheral vascular resistance and diastolic dysfunction. The presence of an antigen in patients with subclinical hypothyroidism may contribute to a potential hypercoagulable state, which can further impact blood pressure regulation.