Fibrotic repair is an innate protective mechanism activated following tissue injuries to promote structural stability and adaptability. However, when this process persists beyond appropriate temporal and spatial limits, it becomes pathological, culminating in irreversible cellular damage and organ dysfunction-similar to a sponge losing its flexibility due to excessive adhesions. These pathological alterations fundamentally rely on myofibroblast-mediated intercellular transition and the accumulation of extracellular matrix (ECM). Increasing evidence indicates that myofibroblasts can originate from multiple cellular sources, with macrophage-myofibroblast transition (MMT) as a key factor. MMT significantly impacts fibrotic processes in the liver, heart, kidneys, and lungs, with emerging evidence in skeletal muscle, involving several molecular signaling pathways including TGF-β/Smad3, ALKBH5/IL-11, Src kinase, and Jmjd3/IRF4 axes. Organ-specific molecular pathways provide precision therapeutic targets for clinical intervention. This review consolidates current findings into the mechanistic roles of MMT in the progression of fibrosis across different organs, highlighting that therapeutically targeting MMT represents a promising strategy for reversing fibrosis and restoring the function of affected organs.

Subacute thyroiditis (SAT) is a self-limiting thyroiditis with an unclear pathogenesis. Human leukocyte antigen (HLA)-B*35 is considered a predisposing factor, and viral infection is believed to be a trigger. In recent years, elevated levels of thyroid-stimulating hormone receptor antibodies (TRAb) have been observed in some patients with SAT. Typically, these elevated TRAb levels may spontaneously revert to negative as the disease improves. The mechanism of TRAb production may be related to abnormalities in immune surveillance and viral infections. Critically, the presence of TRAb can influence clinical manifestations, complicate diagnosis, and affect recovery in SAT. There are three types of TRAb, yet studies on their changing patterns during SAT remain scarce. Both SAT and Graves’ disease (GD) can cause thyrotoxicosis, leading to difficulties in clinical differential diagnosis, especially when SAT presents with positive TRAb. Currently, studies on TRAb-positive SAT are relatively limited. Therefore, this article reviews the pathogenesis of TRAb-positive SAT and its differential diagnosis from GD, aiming to enhance the understanding of this disease among clinicians.

Background Chronic kidney disease (CKD) is associated with early menopause, and thereby reduced endogenous estrogen exposure (EEE) and elevated risk of cardiovascular disease (CVD). Methods Included were 138 154 naturally menopausal and 63 542 nonmenopausal women from the UK Biobank. To reflect cumulative EEE, duration of EEE was estimated as the time interval between age at menarche and current age (for nonmenopausal women) or age at menopause (for menopausal women). The relationship of menopausal status with incident CVD were assessed by CKD status, further considering cumulative EEE. Results Menopausal and nonmenopausal women had a comparable risk of CVD after accounting for age. Menopausal status interacted with CKD on risk of CVD (P for interaction=0.001). In the CKD group, menopausal women had a lower risk of CVD than nonmenopausal women (hazard ratio [HR], 0.75 [95% CI, 0.58–0.97]), predominantly for those with EEE ≥38 years (HR, 0.64 [95% CI, 0.47–0.88]) but not for those with shorter EEE (HR, 1.00). In the non‐CKD group, being menopausal was not associated with risk of CVD (HR, 1.00), but was associated with a suggestively lower risk among those with longer EEE (HR, 0.90 [95% CI, 0.81–1.00]) and a higher risk among those with shorter EEE (HR, 1.13 [95% CI, 1.02–1.25). Conclusions The association of menopausal status with risk of CVD appears to be varied by CKD status and further influenced by cumulative exposure to endogenous estrogen. These findings may have implications for more individualized CVD risk stratification and prevention in menopausal women.

Homocysteine (Hcy) is an important intermediate product in methionine metabolism which plays a key role in the methylation of DNA, RNA and proteins. High level of Hcy can induce endothelial cell damage, promote the release of inflammatory factors, stimulate oxidative stress and inhibit the fibrinolytic system. Numerous studies have confirmed the close relationship between hyperhomocysteinemia (HHcy) and the occurrence/development of various diseases such as cardiovascular diseases, neurological disorders, thrombotic diseases, and tumors. With the rising incidence of thyroid diseases, the relationship between Hcy and thyroid diseases has attracted widespread attention. It has been found that HHcy may be directly or indirectly associated with the development of hypothyroidism, but the findings with hyperthyroidism, chronic lymphocytic thyroiditis and reduced thyroid hormone sensitivity are controversial. This article reviews the research progress of Hcy and thyroid diseases, with a view to providing new ideas for the prevention and clinical treatment of diseases.

Dialysis/renal insufficiency patients are often accompanied by hypothyroidism due to renal damage, the mechanisms of which are complex. The use of thyroid hormone replacement therapy in such patients has become an important clinical issue. This article reviews the mechanism of hypothyroidism in dialysis/renal insufficiency patients and describes the importance and precautions of thyroid hormone replacement therapy to provide a reference for clinical diagnosis and treatment.

The energy needs of tubular epithelial components, especially proximal tubular epithelial cells (PTECs), are high and they heavily depend on aerobic metabolism. As a result, they are particularly vulnerable to various injuries caused by factors such as ischemia, proteinuria, toxins, and elevated glucose levels. Initial metabolic and phenotypic changes in PTECs after injury are likely an attempt at survival and repair. Nevertheless, in cases of recurrent or prolonged injury, PTECs have the potential to undergo a transition to a secretory state, leading to the generation and discharge of diverse bioactive substances, including transforming growth factor-β, Wnt ligands, hepatocyte growth factor, interleukin (IL)-1β, lactic acid, exosomes, and extracellular vesicles. By promoting fibroblast activation, macrophage recruitment, and endothelial cell loss, these bioactive compounds stimulate communication between epithelial cells and other interstitial cells, ultimately worsening renal damage. This review provides a summary of the latest findings on bioactive compounds that facilitate the communication between these cellular categories, ultimately leading to the advancement of tubulointerstitial fibrosis (TIF).

ObjectiveThe meta-analysis aimed to explore the cardiac adaptation in hypothyroidism patients by cardiac magnetic resonance.Research methods and proceduresDatabases including PubMed, Cochrane Library, Embase, CNKI, and Sinomed for clinical studies of hypothyroidism on cardiac function changes. Databases were searched from the earliest data to 15 June 2023. Two authors retrieved studies and evaluated their quality. Review Manager 5.4.1 and Stata18 were used to analyze the data. This study is registered with the International Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY), 202440114.ResultsSix studies were selected for further analysis. Five of them reported differences in cardiac function measures between patients with hypothyroidism and healthy controls, and three studies reported cardiac function parameters after treatment in patients with hypothyroidism. The fixed-effect model combined WMD values for left ventricular ejection fraction (LVEF) had a pooled effect size of -1.98 (95% CI -3.50 to -0.44], P=0.01), implying that LVEF was lower in patients with hypothyroidism than in healthy people. Analysis of heterogeneity found moderate heterogeneity (P = 0.08, I² = 50%). WMD values for stroke volume (SV), cardiac index (CI), left ventricular end-diastolic volume index(LVEDVI), left ventricular end-systolic volume (LESVI), and left ventricular mass index(LVMI) were also analyzed, and pooled effect sizes showed the CI and LVEDVI of patients with hypothyroidism ware significantly decrease (WMD=-0.47, 95% CI [-0.93 to -0.00], P=0.05, WMD=-7.99, 95%CI [-14.01 to -1.96], P=0.009, respectively). Patients with hypothyroidism tended to recover cardiac function after treatment [LVEF (WMD = 6.37, 95%CI [2.05, 10.69], P=0.004), SV (WMD = 7.67, 95%CI [1.61, 13.74], P=0.01), CI (WMD = 0.40, 95%CI [0.01, 0.79], P=0.05)], and there was no difference from the healthy controls.ConclusionHypothyroidism could affect cardiac function, although this does not cause significant heart failure. It may be an adaptation of the heart to the hypothyroid state. There was a risk that this adaptation may turn into myocardial damage. Cardiac function could be restored after treatment in patients with hypothyroidism. Aggressive levothyroxine replacement therapy should be used to reverse cardiac function.Systematic review registrationhttps://inplasy.com, identifier (INPLASY202440114).

Introduction: Despite the generally favorable prognosis of PTC (Papillary Thyroid Carcinoma), it can still exhibit aggressive behavior and lead to patient mortality. IPCEF1 (interaction protein for cytohesin exchange factors 1) has emerged as a critical player in cell signaling related to proliferation and migration in cancer progression. Objective: Our research aimed to determine whether IPCEF1 is a key gene in PTC, elucidate its possible molecular mechanisms and ultimately search for new targets. Methods: This research utilized four gene expression array datasets and TCGA database to examine the role of IPCEF1 in PTC. Differential gene expression analysis, survival analysis, KEGG and GO enrichment and immune cell infiltration correlations were realized by bioinformatic methods. The expressions of IPCEF1 in PTC tissues were examined by IHC and the proliferation, migration, cell cycles of PTC cells were examined by CCK8, transwell and flow cytometry. Results: IPCEF1 had lower expression in PTC tumor tissues and its lower expression might lead to worse T/N stage and DFS/ PFS, which is perhaps related to its regulation of the JAK/STAT signaling pathway and immune microenvironment (macrophage and Tregs). IPCEF1 reduced the proliferation and migration ability of PTC cells, which is consistent with our clinical observations. Besides, we also found that high expression level of IPCEF1 lead to cell cycle arrest in the S or G2 phase, which ultimately reduced cell growth and proliferation. Conclusion: IPCEF1 is a cancer suppressor gene in the progression of PTC, influencing patient survival and prognosis through modulation of immune infiltration and signaling pathways.

ObjectiveThe aim of the study was to evaluate the effect of dipeptidyl peptidase-4 inhibitors (DPP4i) on cardiac structure and function by cardiac magnetic resonance (CMR). Research Methods & Procedures: Database including PubMed, Cochrane library, Embase and SinoMed for clinical studies of DPP4i on cardiac structure and function by CMR were searched. Two authors extracted the data and evaluated study quality independently. Mean difference (MD) or standardized MD and 95% confidence intervals (CI) were used for continuous variables. Review Manager 5.3 was used to performed the analysis.ResultsTen references (nine studies) were included in this meta-analysis. Most of the studies were assessed as well quality by the assessment of methodological quality. For clinical control studies, the merged MD values of △LVEF by fixed-effect model and the pooled effect size in favor of DPP4i was 1.55 (95% CI 0.35 to 2.74, P=0.01). Compared with positive control drugs, DPP4i can significantly improve the LVEF (MD=4.69, 95%CI=2.70 to 6.69), but no such change compared to placebo (MD=-0.20, 95%CI=-1.69 to 1.29). For single-arm studies and partial clinical control studies that reported LVEF values before and after DPP4i treatment, random-effect model was used to combine effect size due to a large heterogeneity (Chi2 = 11.26, P=0.02, I2 = 64%), and the pooled effect size in favor of DPP4i was 2.31 (95% CI 0.01 to 4.62, P=0.05). DPP4i significantly increased the Peak filling rate (PFR) without heterogeneity when the effect sizes of two single-arm studies were combined (MD=31.98, 95% CI 13.69 to 50.27, P=0.0006; heterogeneity test: Chi2 = 0.56, P=0.46, I2 = 0%).ConclusionsIn summary, a possible benefit of DPP4i in cardiac function (as measured by CMR) was found, both including ventricular systolic function and diastolic function.

Background: Poorly differentiated thyroid cancer (PDTC) is a special type of thyroid cancer that threatens the life of the patients. Unfortunately, there are no effective treatments for PDTC right now, so it is urgent to search for new efficacious drugs. This experiment was designed to elucidate the effects of selenomethionine (SeMet) on PDTC in vitro and vivo. Methods: A xenograft animal model was used to assay the volume and weight of PDTC. LncRNA NOMMMUT014201 expression was detected by fluorescence in situ hybridization and Real-time quantitative PCR (qRT-PCR). In vitro experiments were carried on in WRO cells. The Cell Counting Kit-8 assay was performed to test the effect of SeMet on the proliferation of cells. And the migration and invasion of WRO cells by the wound-healing assay, Transwell migration and invasion assays. The cell apoptosis was measured by flow cytometry. In addition, genes related to proliferation, migration, invasion and apoptosis were detected through qRT-PCR and Western Blot. Results: SeMet inhibited the proliferation, migration and invasion and promoted the apoptosis of WRO cells in a dose-dependent manner. Then vivo, SeMet significantly suppressed the volume and weight of PDTC. And SeMet downregulated the expressions of Ki67, PCNA, MMP2, MMP9 and BCL2, but upregulated that of BAX and Cleaved-Caspase 3. Moreover, SeMet upregulated the level of LncRNA NOMMMUT014201 both vivo and in vitro. In addition, repression of LncRNA NOMMMUT014201 removed the inhibition effect of SeMet on WRO cell growth significantly (p<0.05). Further investigation showed that LncRNA NOMMMUT014201 downregulated the expression of miR-6963-5p in PDTC cells, but miR-6963-5p inhibited the level of Srprb. In addition, sh-LncRNA NOMMMUT014201 enhanced the proliferation, migration and invasion but inhibited the apoptosis of WRO cells. However, inhibited miR-6963-5p or overexpressed Srprb relieved the effects of sh-LncRNA NOMMMUT014201on WRO cells. Conclusion: Collectively, SeMet inhibits the growth of PDTC in a dose-dependent manner through LncRNA NONMMUT014201/miR-6963-5p/Srprb signal pathway, thus suggesting that SeMet might be a potential drug for PDTC treatment.

Background:Ferroptosis is a novel form of regulated cell death that involves in cancer progression. However, the role of ferroptosis-related long non-coding RNAs (lncRNAs) in papillary thyroid cancer (PTC) remains to be elucidated. The purpose of this paper was to clarify the prognostic value of ferroptosis-related lncRNAs in PTC. Methods:The transcriptome data and clinical information were downloaded from The Cancer Genome Atlas (TCGA) database. The correlation between ferroptosis-related genes (FRGs) and lncRNA was determined using Pearson correlation analysis. Multivariate Cox regression model (P < 0.01) was performed to establish a ferroptosis-related lncRNAs risk model. Kaplan-Meier survival analysis, receiver operating characteristic (ROC) curves, risk curve and nomograms were then performed to assess the accuracy and clinical applicability of prognostic models. The correlations between the prognosis model and clinicopathological variables, immune and m6A were analyzed. Finally, in vitro assays were performed to verify the role of LINC00900, LINC01614 and PARAL1 on the proliferation, migration and invasion in TPC-1 and BCPAP cells, as well as the relationship between three lncRNAs and ferroptosis. Results:A five-ferroptosis-related lncRNAs (PARAL1, LINC00900, DPH6-DT, LINC01614, LPP-AS2) risk model was constructed. Based on the risk score, samples were divided into the high- and low-risk groups. Patients in the low-risk group had better prognosis than those in high-risk group. Compared to traditional clinicopathological features, risk score was more accurate in predicting prognosis in patients with PTC. Additionally, the difference of immune cell, function and checkpoints was observed between two groups. Moreover, experiments showed that LINC00900 promoted the proliferation, migration and invasion in TPC-1 and BCPAP cells, while LINC01614 and PARAL1 revealed opposite effects, all of which were related to ferroptosis. Conclusions:In summary, we identified a five-ferroptosis-related lncRNAs risk model to predict the prognosis of PTC. Furthermore, our study also revealed that LINC00900 functioned as a tumor suppressor lncRNA, LINC01614 and PARAL1 as an oncogenic lncRNA in PTC.

ObjectiveEvaluate the effects of sodium-glucose cotransporter 2 inhibitor (SGLT2i) on cardiovascular and cerebrovascular diseases.MethodsArticles of SGLT2i on cardiovascular and cerebrovascular diseases were searched. Two authors independently screened the literature, extracted the data, assessed the quality of the study and performed statistical analyses using Review Manager 5.4.ResultsRandom-effect model was used to merge the OR values, and the pooled effect showed that SGLT2i had significant preventive effects on cardiovascular death (OR=0.76, 95%CI 0.64 to 0.89), myocardial infarction (OR=0.90, 95%CI 0.84 to 0.96), heart failure (OR=0.69, 95%CI 0.64 to 0.74) and all-cause mortality (OR=0.65, 95%CI 0.58 to 0.73). Empagliflozin, dapagliflozin and canagliflozin all reduced the incidence of heart failure (OR=0.72, 95%CI 0.64 to 0.82; OR=0.56, 95%CI 0.39 to 0.80; OR=0.62, 95%CI 0.53 to 0.73), but only dapagliflozin displayed a favorable effect on inhibiting stroke (OR=0.78, 95%CI 0.63 to 0.98). SGLT2i could prevent stroke (OR=0.86, 95%CI 0.75 to 0.99), heart failure (OR=0.63, 95%CI 0.56 to 0.70) and all-cause mortality (OR=0.64, 95%CI 0.57 to 0.72) compared to DPP-4i. Furthermore, SGLT2i could reduce the incidence of heart failure (OR=0.72, 95%CI 0.67 to 0.77) and cardiovascular death (OR=0.72, 95%CI 0.54 to 0.95) in patients with high-risk factors.ConclusionsSGLT2i affects cardiovascular death, myocardial infarction, heart failure and all-cause mortality. Only dapagliflozin displayed a favorable effect on inhibiting stroke. SGLT2i could prevent stroke, heart failure and all-cause mortality compared to DPP-4i. In addition, SGLT2i significantly reduced the development of heart failure and cardiovascular death in patients with high-risk factors.Systematic review registrationhttps://www.crd.york.ac.uk/prospero, identifier CRD42024532783.

Selenium, a non-metallic element, is a micronutrient essential for the biosynthesis of selenoproteins containing selenocysteine. In adults, the thyroid contains the highest amount of selenium per gram of tissue. Most known selenoproteins, such as glutathione peroxidase, are expressed in the thyroid and are involved in thyroid hormone metabolism, redox state regulation, and maintenance of cellular homeostasis. Some clinical studies have shown that lack of selenium will increase the prevalence of several kinds of thyroid diseases. Selenium treatment in patients with Graves’ orbitopathy has been shown to delay disease progression and improve the quality of life. Selenium supplementation in Hashimoto’s thyroiditis was associated with the decreased levels of anti-thyroid peroxidase antibody and improved thyroid ultrasound structure. In thyroid cancer, various selenium supplements have shown variable anticancer activity. However, published results remain the conflicting and more clinical evidence is still needed to determine the clinical significance of selenium. This article reviews the strong association between selenium and thyroid disease and provides new ideas for the clinical management of selenium in thyroid disease.

Aims: Diabetic kidney disease (DKD) is a severe microvascular complication frequently associated with type 1 and type 2 diabetes mellitus. The objective of this work was to evaluate the relevance of PI3K/Akt pathway polymorphisms and DKD susceptibility by a meta-analysis.Methods: Case-control studies related to the relationship between PI3K/Akt pathway polymorphisms and DKD risk were searched from Pubmed, Embase, Cochrane Library, SINOMED, CNKI, and Wanfang databases. Statistical analysis and heterogeneity test were conducted by Review Manager 5.4.Results: Totally, 52 eligible studies were enrolled, including seven single nucleotide polymorphisms (SNPs) for four genes in the PI3K/AKT pathway (GNB3: rs5443; eNOS: rs1799983, rs869109213, rs2070744; IL-6: rs1800795, rs1800796; TNF alpha: rs1800629). The "M " allele of eNOS rs1799983 was related to the increased risk of DKD under random effects model, especially in Asian population (Overall:M vs. W: I-2 = 75%, OR = 1.29, 95%CI 1.07-1.56; MM + WM vs. WW: I-2 = 75%, OR = 1.50, 95%CI 1.21-1.86). The "M " allele of eNOS rs869109213 was implicated with higher prevalence of DKD under random effects model, especially in Asian population (Overall:M vs. W: I-2 = 63%, OR = 1.43, 95%CI 1.22-1.68; MM + WM vs. WW: I-2 = 50%, OR = 1.36, 95%CI 1.16-1.58; MM vs. WM + WW: I-2 = 59%, OR = 2.20, 95%CI 1.41-3.43). The "M " allele of eNOS rs2070744 was implicated with higher prevalence of DKD under random effects model, especially in Indian population (Overall: M vs. W: I-2 = 47%, OR = 1.35, 95%CI 1.15-1.59; MM + WM vs. WW: I-2 = 45%, OR = 1.32, 95%CI 1.07-1.62; MM vs. WM + WW: I-2 = 65%, OR = 2.29, 95%CI 1.39-3.77). The "M " allele of IL-6 rs1800796 was predominately associated with higher DKD risks under random effects model, especially in Asian population (Overall: M versus W: I-2 = 23%, OR = 1.49, 95%CI 1.21-1.84; MM + WM vs. WW: I-2 = 1%, OR = 1.43, 95%CI 1.15-1.77; MM + WM vs. WW: I-2 = 71%, OR = 2.77, 95%CI 1.09-7.06).Conclusions: This meta-analysis indicated that polymorphisms in the PI3K/Akt pathway in eNOS rs1799983, rs869109213, rs2070744, and IL-6 rs1800796 were related to the increased risk of DKD.

ObjectiveTo explore the relationship between short-term rapid hypothyroidism and blood lipid levels in patients with differentiated thyroid cancer (DTC).MethodsSeventy-five DTC patients scheduled to receive radioactive iodine ablation were enrolled. Levels of thyroid hormone and serum lipids were tested at two time points: the euthyroid before thyroidectomy, and the hypothyroid (off thyroxine). Then the collected data were analyzed.ResultsTotally 75 DTC patients enrolled, among them, 5o were female (66.67%) and 25 were male (33. 33%), with an average age of 52.24 ± 1.24 years old. The short-term rapid severe hypothyroidism induced by thyroid hormone withdrawal significantly aggravated dyslipidemia, particularly in patients with dyslipidemia before thyroidectomy (All P < 0.01). However, there was no significant differences between blood lipid levels with different thyroid stimulating hormone (TSH) levels. And our study showed significant negative correlations between free triiodothyronine levels and the changes from euthyjroidism to hypothyroidism in total cholesterol (r=-0.31, P=0.03), triglycerides (r=-0.39, P=0.006), high density lipoprotein-cholesterol (HDL-C) (r=-0.29, P=0.042), and significant positive correlations between free thyroxine and the changes of HDL-C (r=-0.32, P=0.027) were identified in females, however, which were not observed in males.ConclusionShort-term rapids severe hypothyroidism caused by thyroid hormone withdrawal can lead to rapid significant changes in blood lipid levels. It is necessary to pay attention to dyslipidemia and its long-term effects after thyroid hormone withdrawal, especially in patients with dyslipidemia before thyroidectomy. Clinical trial registrationhttps://clinicaltrials.gov/ct2/show/NCT03006289?term=NCT03006289&draw=2&rank=1, identifier NCT03006289.

AimsResistance to thyroid hormone (RTH) and pituitary tumors are both rare diseases, and the differential diagnosis of these two diseases is difficult in some cases. There are also patients who have both conditions, making diagnosis more difficult. To better understand this aspect, we analyzed the clinical characteristics and gene mutations of RTH coexisting with pituitary tumors.MethodsDatabase retrieval was conducted in the PubMed, Cochrane Library, and SinoMed databases, and the search contents were case reports or case series of patients with RTH coexisting with pituitary tumors. The demographic, clinical manifestations, and imaging characteristics of pituitary tumors and gene mutations were summarized.ResultsThirteen articles involving 16 patients with RTH coexistent with pituitary tumors, consisting of 13 female patients, one male patient, and two patients with unknown sex, were included. The patients were 10 to 79 years old and most patients were 41-55 years old (43.75%). The 16 patients were from seven different countries and three continents (Asia, the Americas, and Europe). All the patients showed an abnormal secretion of TSH, and five patients underwent transsphenoidal surgery. Finally, four patients were pathologically confirmed to have TSHoma. A total of 11 different mutations occurred at nine amino acid sequence sites (251, 310, 344, 347, 383, 429, 435, 438, and 453). Two different mutations occurred in both the no. 435 and no. 453 amino acid sequences. Fourteen patients provided their treatment histories, and all had undergone different treatment regimens.ConclusionsPatients with both RTH and pituitary tumors had multiple clinical manifestations and different thyroid functions, imaging characteristics of pituitary tumors, genetic mutations of THRβ, and treatments. However, due to the limited number of cases, the patients were mainly women. Further studies with more cases that focus on the mechanism are still needed.

Objective:The relationship between serum selenium levels and papillary thyroid cancer (PTC), especially the pathological features, still remains controversial. We conducted this study to investigate the relationship between serum selenium levels and PTC in a Chinese population.Methods:Cross-sectional data of 284 patients with PTC were collected from the First Affiliated Hospital of Shandong First Medical University. The general clinical characteristics, serum selenium levels, and tumor pathological features were described in PTC. The association between serum selenium levels and pathological features in PTC was analyzed using SPSS 26.0 statistical software.Results:Our results showed that the median serum selenium level was 79.15 μg/L (IQR: 71.00 - 86.98 μg/L) in PTC patients. Serum selenium levels were lower in females than males (p = 0.035). Serum selenium levels were negatively correlated with the number of lymph node metastases (p = 0.048). High serum selenium (OR = 0.397, 95%CI: 0.217 - 0.725) and diastolic blood pressure (OR = 1.028, 95%CI: 1.005 - 1.051) were related factors for the incidence of bilateral tumors. High serum selenium (OR = 0.320, 95%CI: 0.166 - 0.617) and diastolic blood pressure (OR = 1.066, 95%CI: 1.031 - 1.103) were related factors for tumor multifocal incidence.Conclusions:The serum selenium levels of PTC patients in females were lower than males. High serum selenium levels might be a protective factor in PTC patients. Further research is necessary to better understand the influence of selenium on PTC progression.