Leptin and thyroid hormones in beta-thalassemia major: A cross-sectional study

Thyroid-stimulating hormone (TSH) is secreted by the pituitary gland and promotes thyroid growth and function, with increased TSH levels typically associated with hypothyroidism. By consulting the literature, we found that the TSHR, PAX8, and PDE4B genes are associated with thyroid function. Recently, copy number variations (CNVs) have been used as genetic markers to investigate inter-individual variation. Therefore, we investigated the relationship between the TSHR, PAX8, and PDE4B gene CNVs and TSH abnormalities, by calculating variations in gene copy number. Four hundred and eighty-one participants, 232 healthy controls and 249 patients with TSH abnormalities, were selected from three distinct areas in China with different iodine statuses. RT-PCR was used to detect CNVs. Urinary iodine concentrations (UIC) were measured by As3+-Ce4+ catalytic spectrophotometry. There was an association between a CNV at the TSHR gene and TSH abnormalities (p = 0.002). The distribution of PAX8 and PDE4B gene CNVs between patients with TSH abnormalities and healthy controls was not significantly different. UIC > 200μg/l (OR = 1.49, 95% CI = 1.01-2.22) and the TSHR gene (OR = 6.01, 95% CI = 1.96-18.41) were found to be risk factors for TSH abnormalities. PAX8 and PDE4B gene CNVs were not significantly associated with TSH abnormalities. There was no significant interaction between UIC and any of the examined CNVs. In conclusion, the TSHR gene CNV was associated with the development of TSH abnormalities. No significant associations were revealed between urinary iodine levels and candidate gene CNVs.

Pesticides can act as endocrine disruptors by different mechanisms including inhibition of iodine absorption, increases in thyroid hormone clearance, decreased cellular uptake of thyroid hormones, or changes in expression of thyroid hormone regulated genes. This study examined how exposure to pesticides impacts thyroid hormone levels, thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), free T3 (FT3), and free T4 (FT4) by comparing conventional (n = 195) and organic farmers (n = 222), and by evaluating which types of pesticides might be associated with changes in thyroid hormone levels. Questionnaires were used to collect information about farmer characteristics, self-reported stress, agricultural activities, and history of pesticide use. Conventional farmers were asked to report the type and quantity of pesticides used each day. The TSH, FT3, T3, and T4 levels of conventional farmers were 1.6, 1.2, 1.3, and 1.1 times higher than those of organic farmers, respectively, after adjusting for covariates. Several specific herbicides had a significant relationship between the amount applied and an increase in thyroid hormone levels, after covariate adjustment. They included: paraquat (TSH, FT3 and T3); acetochlor (FT4); atrazine (TSH, FT3 and T3); glyphosate (T4); diuron (TSH) and the “other” herbicides including alachlor, propanil, and butachlor (FT4 and T3). The most commonly used herbicide among conventional farmers was glyphosate, followed by paraquat, 2,4-dichlorophenoxyacetic acid (2,4-D). These findings suggest that exposure to pesticides could impact the development of metabolic diseases and other health outcomes by altering the endocrine system (the thyroid hormone levels) through the hypothalamic–pituitary–thyroid (HPT) axis. This work is a part of a longitudinal study which will evaluate the sub-chronic effects of repeated exposure to different types of pesticides on thyroid hormone levels.

The function of the thyroid gland is to produce the thyroid hormones T3 and T4, which regulate gene transcription throughout the body (1). In medical practice, the thyroid becomes an issue when its size or shape becomes abnormal or when it produces too much or too little hormone. Thus, we typically think of the thyroid with reference to the clinical states of goiter, or hyper- or hypothyroidism. But what is the physiology of the thyroid when the gland and the entire hypothalamic-pituitary-thyroid axis are intact? As first year medical students ask each year, Why exactly do we have a thyroid, at all?

ISEE-0440 Background and Objective: Infants are exposed to chemicals that might interfere with thyroid function, such as perchlorate, thiocyanate, and nitrate. There are no studies available with individual measures of these chemicals and thyroid function in infants. We examined whether urinary perchlorate, nitrate, or thiocyanate is associated with urinary thyroxine (T4) and thyroid stimulating hormone (TSH) in infants. Because background perchlorate exposure has been associated with changes in thyroid hormone levels in adults, we specifically examined whether perchlorate was associated with higher TSH in infants with low iodide and in infant girls, as was seen in US females over age 12 years. Methods: The study was conducted at the Children’s Hospital of Philadelphia, the Hospital of the University of Pennsylvania, and affiliated clinics, among 92 full term infants (47 males and 45 females) between birth and 1 year of age. We used data from the Study of Estrogen Activity and Development, which was a partly cross-sectional, partly longitudinal study designed to assess hormone levels of full term infants over the first 12 months of life. We analyzed urine samples collected in that study. Main Outcome Measures: Urinary perchlorate, thiocyanate, nitrate, iodide, TSH and T4, and blood TSH and T4. Results: In models with single chemical agents, infants with higher perchlorate had higher TSH and T4. In models with all three chemical agents, infants with low iodide and higher perchlorate had higher T4 and TSH; infants with higher urinary thiocyanate or higher urinary nitrate had higher urinary TSH and T4. Conclusions: The association of perchlorate exposure with increased urinary TSH in infants with low urinary iodide is consistent with previous findings in females aged 12 and older. Higher thiocyanate and nitrate exposure is also associated with higher urinary TSH in infants. (Supported in part by the intramural research program of NIH.)

We examined the changes in thyroid hormone levels in patients with an acute clinical condition and compared these to levels in the healthy subjects. Serum total triiodothyronine (T3), thyroid stimulating hormone (TSH), and free thyroxine (fT4) measurements were recorded from 555 patients (mean age: 55.0 years, men: 65.9%) admitted to the emergency department (ED) 1–91 months (median: 34 months) after a regular health examination (HE). Serological data were analyzed; mean change in hormone levels was stratified by emergency classification system and quintiles of changes in inflammatory marker values, such as neutrophil lymphocyte ratio (NLR) and high-sensitivity C-reactive protein (CRP). The mean decrease in T3 levels from HE and ED samples was 10.6 ng/dL (p< 0.001). Mean decrease in T3 levels was 21.6 ng/dL among patients classified as having an infection status and 11.0 ng/dL among patients classified as having an urgency status. A decrease 3.7 ng/dL among emergency patients was observed. TSH and fT4 levels did not change across all groups. When patients were stratified into quintiles according to changes in NLR values, mean decreases in T3 were 6.21, 8.14, 14.37, 12.76, and 21.98 ng/dL and showed significant linear reduction (p<0.001). For quintiles of changed CRP values, mean decreased T3 levels were 10.57, 3.05, 4.47, 7.68, and 28.07 ng/dL. TSH and fT4 were not associated with significant changes (p = 0.100, p = 0.561, respectively). In this study, thyroid function changes in individuals with an acute condition revealed that T3 significantly decreased, more markedly in infectious diseases compared to their healthy counterparts, and decline in T3 measurements correlated with inflammatory markers. TSH and fT4 levels remained stable. It is necessary to consider the severity of acute conditions when abnormal T3 levels are detected in subjects with emergent status.

Antidepressant-Resistant Depression in Patients With Comorbid Subclinical Hypothyroidism or High-Normal TSH Levels.

Purpose: To explore changes in thyroid hormone levels of women with twin pregnancies in the third trimester under different pregnancy complications and pregnancy outcomes and to analyze their associated correlations.Methods: A total of 646 women with twin pregnancies who attended their first prenatal visit and received subsequent prenatal care in our hospital were enrolled in this study. Their thyroid hormone levels—free thyroxine (FT4), thyroid‐stimulating hormone (TSH), and thyroid peroxidase antibody (TPO‐Ab)—in the third trimester were collected for analysis of correlations with pregnancy complications and outcomes, using Spearman’s correlation and a logistic regression model.Results: Adverse events, such as premature birth, premature rupture of membranes, placental abruption, fetal distress, fetal growth restriction, neonatal asphyxia, pregnancy‐induced hypertension, gestational diabetes mellitus, and postpartum hemorrhage, occurred among the 646 women with twin pregnancies in the third trimester. The highest proportion of pregnancy outcomes was premature birth, accounting for 42.26%, and the top two pregnancy complications were gestational diabetes mellitus and pregnancy‐induced hypertension, accounting for 31.42% and 20.28%, respectively. Assisted reproduction and twin type correlated with fetal distress during the third trimester of pregnancy and neonatal asphyxia. Maternal age correlated with gestational diabetes mellitus in the third trimester of pregnancy and postpartum hemorrhage. FT4 levels varied in pregnant women with placental abruption, TSH levels varied in pregnant women with pregnancy‐induced hypertension, and TPO‐Ab levels varied in pregnant women with premature birth, placental abruption, and postpartum hemorrhage.Study Limitations: This study only analyzed thyroid hormone levels at a single timepoint (third trimester) during pregnancy. Dynamic changes in hormone levels across different gestational stages—such as TSH suppression patterns in the first trimester due to hCG elevation or FT4 adjustments in the second trimester—were not tracked. This limitation may hinder the understanding of how temporal hormonal variations contribute to complications like gestational diabetes mellitus or placental abruption. For instance, transient TSH fluctuations in early pregnancy or mid‐trimester FT4 instability might differently influence outcomes. Future studies should incorporate longitudinal monitoring at multiple intervals (e.g., first, second, and third trimesters) to capture hormonal trajectories and their phase‐specific associations with adverse outcomes. Additionally, the exclusion of women with preexisting thyroid conditions or medication use limits the generalizability of findings to high‐risk populations who may benefit most from thyroid monitoring. The single‐timepoint design also precludes causal inference—while correlations between third‐trimester hormones and complications are observed, it remains unclear whether these abnormalities initiate pathological processes (e.g., placental dysfunction) or arise as secondary consequences of existing complications. Furthermore, the homogeneity of the cohort (e.g., predominantly dichorionic twins) may underestimate risks in monochorionic pregnancies, which inherently carry higher placental vulnerability.Conclusion: Abnormal changes in thyroid hormones during pregnancy may correlate with adverse events such as pregnancy‐induced hypertension and placental abruption. Clinicians should prioritize routine third‐trimester monitoring of FT4, TSH, and TPO‐Ab levels in twin pregnancies, particularly for women with assisted reproduction or monochorionic placentation, to enable early risk stratification and tailored interventions.

Objective: Alcohol is one of the commonest psychoactive substances consumed globally. There are evidences suggesting its role in causing thyroid abnormality. It has been reported to have multiple effects on the hypothalamopituitary- thyroid axis. This study aimed to look at the thyroid function abnormalities in admitted male patients with alcohol dependence syndrome. Methods: Thyroid function parameters were compared among 30 male in-patients with Alcohol dependence syndrome (ADS) and 30 male in-patients with psychotic disorders as controls. Results: 23.3% of patients in the alcohol dependence group had thyroid stimulating hormone (TSH) abnormality compared to 3.3% among control (psychotic disorders) group. 23.3% in the ADS group and 10% of the control group had free T4 (FT4) abnormality. TSH abnormality was seen more in individuals whose age of onset of alcohol use was 20-30 years which was statically significant (p=0.01). TSH abnormality was noted more in patients who consumed alcohol for more than 15 years and with quantity exceeding>720 ml.

Occupational Radiation Exposure and Changes in Thyroid Hormones in a Cohort of Chinese Medical Radiation Workers

PP-29-109 Background/Aims: Brominated flame retarded (BFR) released from e-waste activity might affect the health of local people. Assessing the effect of e-waste exposure via recycling, and dismantling and changes of thyroid hormone levels is an area of ongoing research. Methods: The processing of e-waste recycling was investigated. A total of 236 occupational exposure people and 89 nonoccupational exposure people from e-waste recycling sites were surveyed, and their thyroid hormone levels (T3 and T4), free thyroid hormones (fT3 and fT4), and thyroid stimulating hormone were assayed. The level of polybrominated diphenyl ethers congeners and Polybrominated biphenyl congeners in serum was determined here. Linear regression model was taken to analyze the relations between thyroid hormone levels and BFRs concentrations. Results: Lower level of T3 in exposure groups were observed (P < 0.01). BDE205 with T4 positively varied were confirmed by linear regression model (unstandardized regression coefficient, beta = 0.25, ρ = 0.001) and a weaker positively trend in BDE126 and T4 was found. Conclusion: BFRs exposure may contribute to the changes of thyroid hormone levels.

Changes in thyroid hormone levels are commonly recognized characters among the elderly, which were reported to potentially influence incident frailty. Therefore, we examined the cross-sectional associations of thyroid hormones (THs) with frailty as well as the five components characterizing frailty (fatigue, resistance, ambulation, number of illnesses, and loss of weight) among the oldest-old. Four hundred and eighty-seven community-dwelling oldest-old from a local community in Haidian District, Beijing, participated in our recruitment campaign between April 2019 and May 2020. The primary outcomes were a definitive diagnosis of frailty according to the FRAIL scale (Fatigue, Resistance, Ambulation, Illnesses, Loss of weight) and a positive score for each frailty subdomain. Demographic information (age, sex, marital status, and educational status), comorbidities, and details on the participants' lifestyles were recorded. Serum THs including free triiodothyronin (fT3), triiodothyronine (T3), free thyroxine (fT4), and thyroxine (T4) and thyroid stimulating hormone (TSH) levels were also measured at the beginning of our study. Logistic regressions were conducted to screen for potential risk factors for frailty and its subdomains. Among the total 487 subjects at enrollment, 60 (12.23%) of them were diagnosed with subclinical hypothyroidism and 110 (22.59%) of the total population scored positive for frailty. Logistic regression analyses adjusted for all potential confounders, showed that frailty was significantly associated with the serum TSH concentration (odds ratio [OR]: 1.06), fT3 concentration (OR: 0.54), and subclinical hypothyroidism score (OR: 2.18). The association between fT4 and frailty was absent in our observational study. The fT3/fT4 ratio characterizing peripheral hormone conversion was also tested to be correlated with frailty. Subclinical hypothyroidism, higher TSH level, lower fT3 level, and decreased fT3/fT4 ratio were all associated with frailty assessed by the FRAIL scale among the community-dwelling oldest-old, suggesting a relevant role of thyroid function in aging. Future longitudinal studies are warranted to determine the casual relationship between thyroid dysfunction and frailty in the oldest-old.

Thyroid bone disease

Background:Smoking can cause thyroid disorders; the aim of the present study was to investigate the association between smoking status and changes in thyroid hormone levels among adult males during a decade long follow-up of in the Tehran Thyroid Study (TTS).Methods:Data of 895 adult males (smokers=115, non-smokers=691, ex-smokers=89) participants of the TTS without any previously known thyroid disease were analyzed. To examine trends of changes in thyroid hormone levels in these three groups, generalized estimating equation models were used. The interaction between the smoking status and each phase of the study was checked in a separate model.Results:Age and BMI adjusted trends of free thyroxine (FT4) demonstrated a non-significant decrease in participants (P=0.121) and thyroid-stimulating hormone (TSH) gained a significant average increase value over time in the total population (adjusted marginal mean of TSH=1.15 mU/L in phase 1, vs. 1.75 mU/L in phase 4, P<0.0001). Of the three groups, non-smokers and ex-smokers showed statistically significant increases in TSH during the follow-up period, whereas the smoker group had lower increases in TSH levels, changes from phase 1 until phase 2 among smokers were 38.46%, vs 43.54% and 52.94% in the ex and non-smokers, respectively.Conclusion:TSH was lower and FT4 was higher in smokers compared with the other smoker groups, although TSH level shows no decreasing trend over time in this group. The increasing trend of TSH in smokers was similar to ex and non-smokers. No difference was seen in FT4 trends among the smoking groups.

Background: Alcohol use disorder(AUD) is associated with thyroid dysfunction. This study aimed to explore the changes of thyroid hormone levels in patients with AUD and alcohol-induced psychotic disorders(AIPD), gender differences, and the changes after withdrawal treatment. Methods In this retrospective case–control study we enrolled 283 patients with AUD (261 men, 22 women) admitted between 2021 and 2024, of whom 80 had AIPD. Baseline levels of thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), thyroxine (T4) and triiodothyronine (T3) were measured at the time of admission. A second measurement was performed three to four weeks after detoxification. Baseline values were compared with those of 300 age- and sex-matched healthy controls. Longitudinal changes within the AUD cohort and differences between AIPD and non-AIPD subgroups were analyzed by paired t-tests and chi-square tests as appropriate. Results Mean serum levels of FT4, FT3, T4 and T3 were significantly lower in AUD patients than in healthy controls, while TSH had no significant change. In the same comparison, the proportion of individuals with abnormal thyroid parameters was higher in the AUD group than in controls. Among AUD patients, women, showed a higher proportion of elevated TSH, and reduced FT4, FT3 and T3 than men with AUD. The level of thyroid hormone in patients with AIPD was higher than that in patients with Non-AIPD, and after detoxification treatment, thyroid function may not necessarily return to normal, but showed a trend of thyroid hormone decreased and TSH increased, which was more pronounced in AIPD patients. Conclusion AUD can lead to thyroid dysfunction. Patients with AUD should closely monitor their thyroid hormone levels to prevent the worsening of psychiatric and neurological symptoms.

Bisphenol A (BPA) is a type of endocrine-disrupting chemical utilized in the production of plastics like epoxy resins and polycarbonate polymers. BPA exhibits weak estrogenic and potent anti-androgenic effects, and prior research has linked it to disturbances in thyroid function. This study aims to assess the potential association between early childhood exposure to urinary bisphenol A and thyroid hormone levels in pubertal children from Korea. Participants were drawn from the Ewha Birth and Growth Cohort Study, encompassing individuals who visited Ewha Women's Mokdong Hospital between 2001 and 2005. The concentration of urinary BPA was repeatedly measured for each subject at ages 3-5 years and 7-9 years. Serum levels of free triiothyronine (T3), free thyroxine (T4), and thyroid-stimulating hormone (TSH) were measured at ages 10-12 years in a subgroup of 128 out of 164 subjects who had undergone repeated BPA concentration measurements. We utilized the SAS program to analyze possible links between childhood exposure to BPA and thyroid hormone function in adolescence. Additionally, we explored how exposure to BPA during two specific periods influenced changes in thyroid hormone levels. The study observed that urinary BPA levels at ages 3-5 years were not notably linked to thyroid hormone levels in adolescents aged 10-12 years. However, BPA levels at ages 7-9 years were significantly associated with free T3 levels in girls aged 10-12 years. Conversely, exposure to BPA did not result in significant differences in thyroid hormone levels among boys. The study did not find statistically significant connections between levels of urinary BPA and the other thyroid hormones, specifically TSH and free T4. There was a significant decrease in the concentration of free T3 in girls with higher BPA concentrations. BPA exposure in childhood affects thyroid function in adolescent girls. This relationship may contribute to an increased prevalence of thyroid disorders in adolescents due to environmental influences.