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PubMed2025

TSH Cutoffs and Recurrence Risk in Differentiated Thyroid Carcinomas: A Systematic Review and Meta-Analysis.

CONTEXT: The current American Thyroid Association (ATA) guidelines recommend tailored TSH suppression, considering the recurrence risk of differentiated thyroid cancer (DTC); however, the evidence is limited. OBJECTIVE: This meta-analysis aimed to investigate the risk of recurrence in patients with DTC, stratified by the ATA risk of recurrence, according to variable thyrotropin (TSH) cutoffs (0.1, 0.5, and 2.0 mIU/L). METHODS: We searched Ovid-Medline, EMBASE, and Cochrane databases for studies reporting the recurrence rate of DTCs based on TSH cutoffs through March 2024. The search terms used included "thyroid neoplasm" OR "cancer," "TSH" OR "thyroid stimulating hormone," "suppress" OR "supplementation," and "thyroidectomy". RESULTS: Two randomized controlled trials and 7 observational studies, including 5320 patients, were analyzed, with an overall recurrence rate of 18%. The pooled recurrence risk for DTCs at each TSH cutoff (0.1, 0.5, and 2.0 mIU/L) was not significant. In the subgroup analysis, the pooled hazard ratios (HRs) stratified by the ATA risk of recurrence (low- and high-risk DTCs) did not differ according to TSH levels. However, the risks of recurrence increased at serum TSH of 0.1 mIU/L or greater (HR 2.27; 95% CI, 1.29-3.99) and TSH of 2.0 mIU/L or greater (HR 1.36; 95% CI, 1.001-1.84) in a leave-one-out meta-analysis after removing the study that significantly influenced the analysis. Patients with distant metastases had a higher risk of recurrence (HR 3.3; 95% CI, 1.53-7.10) when maintaining a TSH greater than or equal to 0.1 mIU/L. CONCLUSION: The degree of TSH suppression did not affect the overall risk of DTC recurrence. However, TSH suppression may be beneficial in reducing the recurrence risk in high-risk patients with distant metastases.

Humans↗

PubMed2001

Regulation of thyroid cell proliferation by TSH and other factors: a critical evaluation of in vitro models.

TSH via cAMP, and various growth factors, in cooperation with insulin or IGF-I stimulate cell cycle progression and proliferation in various thyrocyte culture systems, including rat thyroid cell lines (FRTL-5, WRT, PC Cl3) and primary cultures of rat, dog, sheep and human thyroid. The available data on cell signaling cascades, cell cycle kinetics, and cell cycle-regulatory proteins are thoroughly and critically reviewed in these experimental systems. In most FRTL-5 cells, TSH (cAMP) merely acts as a priming/competence factor amplifying PI3K and MAPK pathway activation and DNA synthesis elicited by insulin/IGF-I. In WRT cells, TSH and insulin/IGF-I can independently activate Ras and PI3K pathways and DNA synthesis. In dog thyroid primary cultures, TSH (cAMP) does not activate Ras and PI3K, and cAMP must be continuously elevated by TSH to directly control the progression through G(1) phase. This effect is exerted, at least in part, via the cAMP-dependent activation of the required cyclin D3, itself synthesized in response to insulin/IGF-I. This and other discrepancies show that the mechanistic logics of cell cycle stimulation by cAMP profoundly diverge in these different in vitro models of the same cell. Therefore, although these different thyrocyte systems constitute interesting models of the wide diversity of possible mechanisms of cAMP-dependent proliferation in various cell types, extrapolation of in vitro mechanistic data to TSH-dependent goitrogenesis in man can only be accepted in the cases where independent validation is provided.

Animals↗

PubMed2026

The association between prenatal PM2.5 constituent exposure and gestational diabetes mellitus: Exploratory analysis of the potential modifying role of thyroid hormones.

The associations of PM2.5 constituents with blood glucose and GDM remain unclear, and the interplay between PM2.5 exposure and thyroid hormone levels in relation to GDM has not been well characterized. This retrospective cohort study included 1314 pregnant women with data collected through multiple methods. A generalized linear model analyzed PM2.5-glucose links, logistic regression assessed pollutant-GDM associations, and stratified analyses explored these relationships at different thyroid hormone levels. In the study population, first-trimester exposure to SO42- and BC correlated positively with FBG, as did PM2.5 and its components in the second trimester. First-trimester SO4²⁻ exposure (OR=1.26, 95% CI: 1.06, 1.51) and second-trimester exposures to PM2.5 (OR=1.67, 95% CI: 1.19, 2.35), NO3⁻ (OR=1.34, 95% CI: 1.06, 1.68), and NH4⁺ (OR=1.33, 95% CI: 1.06, 1.65) were associated with increased GDM risk. Stratified analyses showed that second-trimester BC and OM were positively correlated with FBG in the high-TSH and low-FT4 strata, respectively. In addition, first-trimester exposure to SO42- (high TSH: OR = 1.42, 95% CI: 1.10, 1.84; low FT4: OR = 1.35, 95% CI: 1.05, 1.74) and to PM2.5 (high TSH: OR = 1.93, 95% CI: 1.14, 3.27; low FT4: OR = 1.82, 95% CI: 1.46, 2.25) in the second trimester were associated with higher odds of GDM. These findings show that PM2.5 exposure was associated with glucose dysregulation and GDM in pregnant women differently by trimester and component. Across the separate TSH- and FT4-stratified analyses, women in the high-TSH and low-FT4 strata, respectively, appeared to show greater susceptibility to air pollution-related GDM. These subgroup findings should therefore be interpreted as exploratory and require validation in future studies.

Effect modification↗

PubMed2025

Thyroid disease and breast cancer, benign breast neoplasm: a two-sample Mendelian randomization study.

BACKGROUND: Breast cancer (BC) is a prevalent and significant health issue and a major contributor to global cancer incidence, accounting for 31% of all reported cases in women. Benign breast neoplasm, as a benign tumor with a high incidence in women, may play an important role in the development of BC. Previous studies have shown that thyroid dysfunction and thyroid cancer (TC) can lead to the occurrence of many cancers. Therefore, we conduct Mendelian randomization (MR) analysis to explore the causality of thyroid dysfunctions, TC, and breast neoplasm. METHODS: The data of the analysis from the genome-wide association study (GWAS) dataset. The exposure includes FT4, TSH, hypothyroidism, hyperthyroidism, and TC. Meanwhile, the outcome consists of BC, HER2-enriched BC, HER2-negative BC, and benign breast neoplasm. We used five methods (inverse variance weighted (IVW) random effects model, IVW fixed effects model, MR-Egger method, median weighted method, and the weighted mode method). We used the MR-PRESSO test and MR-Egger intercept test to detect horizontal pleiotropy and Cochran's Q test to detect heterogeneity. RESULTS: The IVW method showed a positive relationship between high FT4 levels and BC (OR = 1.210 p = 0.008) and an inverse association between TSH levels (OR IVW = 0.908 p = 0.007), hypothyroidism (OR IVW = 0.959, p = 0.014) and BC. For HER2-positive BC, an elevated FT4 level was associated with an increased risk (OR IVW = 1.314, p = 0.001). Genetically predicted high TSH levels (OR IVW = 0.899, p = 0.02) and hypothyroidism (OR IVW = 0.944, p = 0.003) were associated with a decreased risk of HER2-positive BC. Meanwhile, individuals with TC (OR = 1.003, p = 0.048), and hyperthyroidism (OR IVW = 1.127, p = 0.006) were associated with an increasing risk of development of benign breast neoplasm. Hyperthyroidism was associated with an elevated risk of benign breast neoplasm. CONCLUSIONS: The present MR study explains the association between thyroid diseases and BC (mainly in HER2-positive BC). Furthermore, it demonstrates that hyperthyroidism, low levels of TSH, and TC may contribute to the development of benign breast neoplasm.

Humans↗

PubMed2024

Advances in serum thyroid hormone levels and seizures.

Epilepsy, a common neurological disorder, is characterized by paroxysmal, short-term, repetitive, and stereotypical features, significantly impacting patients' quality of life. Currently, the pathogenesis of epilepsy remains incompletely understood. Changes in neuronal excitability, imbalances in glutamate and gamma-aminobutyric acid (GABA) levels, alterations in the activity of GABA receptors, and dysfunction of GABA receptors are considered closely related to its occurrence. Thyroid hormones, vital for human growth and development, also play a crucial role in the nervous system. They mediate oxidative stress, influence reactive oxygen species production, affect mitochondrial function and neuronal excitability, and modulate glutamate and GABA levels. Also, they combine with thyroid hormone receptors and exert genomic effects by regulating the expression of numerous genes. However, once there are defects in thyroid hormone signaling, these defects may lead to severe neurodevelopmental disorders that are associated with an increased frequency of seizures. The impact of antiseizure medications (ASMs) on serum thyroid hormone levels, particularly traditional ASMs, has been extensively studied. It is reported that conventional ASMs such as phenobarbital, phenytoin sodium, carbamazepine, and valproate sodium were more likely to induce subclinical hypothyroidism (elevated TSH with normal FT4) or isolated hypothyroidism (decreased FT4 with normal TSH). However, the new ASMs, such as levetiracetam, have no effect on thyroid hormone levels. Together, seizures not only affect thyroid hormone levels, but abnormal thyroid hormone levels can also influence seizures. However, the precise mechanism underlying the interaction between serum thyroid hormone levels and seizures remains unclear. This review aims to explore the relationship between thyroid hormone levels and seizures, along with the underlying mechanisms.

Humans↗

PubMed2025

Thyroid Hormones and Co-workers: An Overview.

The hypothalamus secretes the thyroid-releasing hormone (TRH) that induces the pituitary gland to release the thyroid-stimulating hormone (TSH) which stimulates thyroid follicular cells to release the thyroid hormones (THs), thyroxine (T4), and triiodothyronine (T3). The process of synthesizing T3 and T4 hormones involves various enzymatic steps, starting with the iodination of L-tyrosine residues present in the protein thyroglobulin. Thyroid hormones are released into the bloodstream, where they bind to thyroid hormone distributor proteins (THDPs) which transport them in the circulation. The conversion of T4 to T3 (the more biologically active hormone) in target tissues is facilitated by selenoprotein enzymes known as deiodinases. THs can bind to different molecules located on the plasma membrane, such as integrin αvβ3, through which they exercise regulatory non-genomic control. Nevertheless, most of thyroid hormone's actions are mediated intracellularly by binding to thyroid hormone receptors (TRs). Thyroid hormone receptors act as ligand-dependent transcription factors, Thyroid hormone receptors activate thyroid hormone response elements on gene promoters through canonical signaling. Thyroid hormones mediate several critical physiological processes including organ development, cell differentiation, metabolism, and cell growth and maintenance.

Humans↗

PubMed2026

Arrhythmia and cardiomyopathy risk in Taiwan with complementary biobank evidence on thyroid genetic susceptibility: an integrative population-based framework.

BACKGROUND: Arrhythmia-induced cardiomyopathy (AiCM) is a potentially reversible cause of ventricular dysfunction; however, only a subset of patients with arrhythmia develop cardiomyopathy. Emerging evidence suggests that endocrine factors, particularly thyroid dysfunction with genetic susceptibility, may contribute to inter-individual variability in arrhythmia-related myocardial outcomes. METHODS: We performed a dual-cohort population-based study using the National Health Insurance Research Database (NHIRD, 2000-2015) and the Taiwan Biobank (TWB). In NHIRD, we examined the association between newly diagnosed arrhythmia and incident cardiomyopathy using Cox proportional hazards models. In TWB, genome-wide data, thyroid-stimulating hormone (TSH), polygenic risk scores (PRSs), lifestyle factors, and metabolic comorbidities were analyzed using multivariable regression and interaction models to assess determinants of thyroid dysfunction. RESULTS: In the NHIRD cohort, arrhythmia was associated with a significantly increased risk of incident cardiomyopathy (adjusted hazard ratio (aHR): 2.49, 95% CI: 1.94-2.96), with atrial fibrillation showing the strongest association among arrhythmia subtypes. In the TWB cohort, a higher thyroid polygenic risk score was strongly associated with thyroid dysfunction (adjusted odds ratio (aOR): 6.64, 95% CI: 5.86-7.52). The association between genetic susceptibility and thyroid dysfunction was further modified by metabolic and lifestyle factors, including diabetes, hyperlipidemia, and dietary patterns. Genome-wide analysis identified multiple loci associated with thyroid-stimulating hormone regulation, consistent with a polygenic architecture of thyroid endocrine traits. CONCLUSION: Arrhythmia was associated with an increased risk of cardiomyopathy in a nationwide cohort, while thyroid genetic susceptibility was strongly associated with thyroid dysfunction in a biobank cohort and modified by metabolic and lifestyle factors. These findings provide complementary population-level evidence of parallel cardiovascular and endocrine-genetic associations. Because the two cohorts were not individually linked, causal inference cannot be established. The results support a systems-level framework of endocrine-cardiac interaction and suggest that integrated clinical and genetic risk assessment may help identify individuals who warrant closer monitoring.

arrhythmia↗

PubMed2026

Approaches to thyroid nodules in paediatric cancer predisposition syndromes.

OBJECTIVE: The objective of this work was to summarize current evidence and practical management considerations for thyroid nodules in children and adolescents with cancer predisposition syndromes (CPSs), focusing on follicular cell-derived nodules and non-medullary thyroid carcinoma (NMTC). METHODS: We synthesized current paediatric guideline recommendations and recent cohort, pathology, and molecular studies addressing CPS-associated nodular thyroid disease, including PTEN hamartoma tumour syndrome (PHTS), DICER1 syndrome, familial adenomatous polyposis, and related endocrine neoplasia syndromes. RESULTS: Evidence quantifying syndrome-stratified malignancy risk among paediatric CPS patients presenting with nodules remains limited and is largely derived from mixed-age or retrospectively ascertained cohorts with surveillance and verification bias. High-resolution ultrasound (US) is central to risk stratification. US-guided fine-needle aspiration (FNA) is a cornerstone of evaluation yet frequently yields indeterminate results, particularly in follicular-patterned and encapsulated lesions (e.g. PHTS and DICER1 syndrome), and sampling error is accentuated in polyclonal multinodular disease. Molecular testing may aid aetiologic clarification and, in selected settings, risk refinement. However, panels optimized for sporadic adult disease may have reduced 'rule-out' utility in CPSs. Biochemical assessment (TSH ± free thyroxine) complements imaging, while routine thyroglobulin is not recommended, and thyroid autoantibodies should be viewed as adjunctive rather than directive markers in CPSs. CONCLUSION: Management of thyroid nodules in paediatric CPSs is best approached through integrated, multidisciplinary risk assessment that combines expert ultrasound, context-aware cytology and molecular interpretation, and shared decision-making. This review proposes a CPS-adapted, multidisciplinary risk assessment framework and highlights the need for prospective multicentre registries and harmonized protocols to define syndrome-specific outcomes and evidence-based thresholds for surveillance and intervention.

Humans↗