Background: Autoimmune thyroiditis (AIT) is the most common autoimmune disease, affecting 3-5% patients worldwide. In recent years, approximately 200 articles on AIT have been published annually in various journals. However, to date, no article has systematically assessed the related literature. Therefore, we conducted a bibliometric analysis on AIT to reveal the dynamic scientific developments and help researchers gain a global perspective while exploring the hotspots and development trends.Methods: AIT-related articles and reviews from 2000 to 2022 were retrieved from the Web of Science Core Collection (WoSCC). The following search terms were used to extract document data: TS= (“ autoimmune thyroiditi*”) OR TI= (“chronic lymphocytic thyroiditi*”) OR TI=(hashimoto*) OR TI= (“postpartum thyroiditis”). We selected articles and reviews published in English from 2000 to 2022. Three software programs (VOSviewer, CiteSpace, Pajek) were employed to analyze the contribution and co-occurrence relationships of different references, countries/regions, institutes, journals and also keywords in this field.Results: This scientometric study included 2290 English papers published in 723 journals with 39661 co-cited references from 561 institutions in 120 countries/regions. Based on the reference and keyword analysis, researchers used to focus on “apoptosis”, “insulin resistance”, “encephalopathy”, “IFN-γ” related to AIT during the past 20 years. However, with the development of other novel directions such as “papillary thyroid cancer” (2018-2022), “Vitamin D” (2016-2022), “oxidative stress” (2018-2022), “polymorphism” (2019-2022) and “association” (2020-2022), researchers are more interested in the relationship between papillary thyroid carcinoma and AIT, the effect of vitamin D supplementation on AIT, the oxidative stress in thyroid disease as well as the influence of polymorphism.Conclusion: Bibliometric analysis of the outputs of AIT shows an overview of the current status of the research on AIT. The associations between papillary thyroid carcinoma, vitamin D, oxidative stress, polymorphism and AIT are major research frontiers. However, further research and collaboration are still required worldwide. Our findings can help researchers grasp the research status of AIT and quickly determine new directions for future research.

Thyroid dysfunction is a frequently found endocrine disorder among reproductively aged women. Subclinical hypothyroidism is the most common condition of thyroid disorders during pregnancy and is defined as manifesting a thyroid-stimulating hormone concentration exceeding the trimester-specific reference value, with a normal free thyroxine concentration. Here, we evaluated the prospective association between spontaneous miscarriage and first-trimester thyroid function. We conducted a case–control study (421 cases and 1684 controls) that was nested. Thyroid-stimulating hormone (TSH), free thyroxine (FT₄), thyroid-peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) status were measured. We found that higher TSH was related to spontaneous miscarriage (OR 1.21; 95% CI, 1.13–1.30, P < 0.001). Compared with women with TSH levels of 0.4–<2.5 mIU/L, the risk of miscarriage was increased in women with TSH levels of 2.5–<4.87 mIU/L (OR 1.47; 95% CI, 1.16–1.87) and TSH greater than 4.87 mIU/L (OR 1.97; 95% CI, 1.22–3.18). After controlling for the confounding factor, TPOAb positivity status and FT₄, the results were similar. The present study showed that higher TSH was associated with miscarriage in early pregnancy. In fact, TSH levels between 2.5 and 4.87 mIU/L increased the risk for miscarriage, with TSH greater than 4.87 mIU/L increasing the risk even further.

Context: The impact of abnormal thyroid hormone levels on the cardiovascular system has been explored for decades. Recent emerging evidence suggests that subclinical thyroid dysfunction, especially subclinical hypothyroidism (SCH), significantly affects cardiac indices. Objective: We aimed to determine whether levothyroxine (LT4), commonly used to treat hypothyroidism, affects cardiovascular indices in SCH patients. Methods: This is a systematic review and meta-analysis. We searched online databases for studies analyzing cardiac morphology and functional changes in SCH patients before and after LT4 supplementation. A total of 294 SCH patients participated and finished the follow-up. The standard mean difference and 95% CI were calculated in fixed or random-effects models. The clinical outcomes analyzed in this study included 18 indicators, mainly covering cardiac morphology, myocardial performance (including various indicators of systolic and diastolic function), mitral wave flow, and systemic vascular resistance. Results: A total of 11 studies met our search criteria. All studies explicitly mentioned that serum thyrotropin levels decreased to normal at follow-up. Our results suggest that the cardiac output (CO), left ventricular ejection fraction (LVEF), and the ratio of peak E velocity/peak A velocity were all significantly increased after LT4 supplementation compared with the baseline level. However, we found no clear evidence of significant morphological changes in the heart. Conclusion: Judging from the obvious changes in the CO, LVEF, and E/A ratio, LT4 supplementation can effectively improve the cardiac systolic and diastolic dysfunction prevalent in SCH patients. This study provides evidence of the recommendation for LT4 supplementation in adult SCH patients.

Background. Type 2 deiodinase (Dio2) is a selenoenzyme that is mainly expressed in the endoplasmic reticulum of the central nervous system, brown adipose tissue, and placenta and is responsible for outer ring deiodination of thyroxine (T4) to form biologically active triiodothyronine (T3). The Thr92Ala polymorphism of Dio2 has been found to be a potential risk factor for various diseases beyond the hypothalamus‐pituitary‐thyroid (HPT) axis. Methods. We searched the relevant studies in the PubMed, Embase, and Cochrane Library databases and Google Scholar. A systematic review and meta‐analysis of studies on the Thr92Ala polymorphism and metabolic parameters beyond the HPT axis (e.g., BMI, fasting glycemic traits, plasma lipid levels, and hypertension risk) were performed. Results. Six eligible studies that analyzed the relationship between the Thr92Ala polymorphism and metabolic parameters beyond the thyroid were identified. All selected studies excluded patients with thyroid dysfunction, and diabetic patients were also excluded when fasting glucose and fasting insulin levels were meta‐analyzed. The Thr92Ala polymorphism was found to be a significant risk factor for higher BMI (Std. mean difference 0.31 (0.01, 0.60), p = 0.04) and higher fasting glucose levels (Std. mean difference 1.18 (0.05, 2.31), p = 0.04). However, fasting insulin levels, plasma lipid levels, and hypertension risk showed a nonsignificant association with the Thr92Ala polymorphism. Conclusion. Compared with euthyroid noncarriers (Thr/Thr), euthyroid Ala92‐Dio2 carriers showed increased BMI levels, and Ala92‐Dio2 carriers also had higher fasting plasma glucose levels than matched euthyroid nondiabetic noncarriers.

STUDY QUESTION: Does levothyroxine (LT4) treatment reduce adverse pregnancy outcomes in pregnant women with thyroid dysfunction? SUMMARY ANSWER: LT4 treatment significantly reduces the risks of pregnancy loss, preterm delivery, and gestational hypertension, with no significant impacts on rates of live birth, placental abruption, or gestational diabetes. WHAT IS KNOWN ALREADY: Multiple meta-analyses have examined the impact of LT4 on pregnancy outcomes, but quantitative confidence assessments are still lacking. Thus, an umbrella review is needed to systematically synthesize and assess the quality of this evidence. STUDY DESIGN, SIZE, DURATION: This umbrella review of systematic reviews and meta-analyses used PubMed, Embase, Web of Science, and the Cochrane Database of Systematic Reviews. Searches included studies published in English or Chinese up to 20 March 2025. PARTICIPANTS/MATERIALS, SETTING, METHODS: Included studies were systematic reviews or meta-analyses of randomized controlled trials assessing the effects of LT4 on pregnancy outcomes in women with subclinical hypothyroidism (SCH) or thyroid peroxidase antibody (TPOAb) positivity. A set of 24 associations across six pregnancy outcomes were analyzed: pregnancy loss, preterm delivery, live birth, placental abruption, gestational hypertension, and gestational diabetes. Methodological quality was assessed using AMSTAR 1, and evidence quality was graded using GRADE. Sensitivity analyses were conducted to confirm robustness. MAIN RESULTS AND THE ROLE OF CHANCE: Eleven meta-analyses were included. High-quality evidence showed that LT4 treatment reduced the risks of pregnancy loss (RR = 0.43; class III evidence), preterm delivery (RR = 0.56; class III evidence), and gestational hypertension (RR = 0.63; class IV evidence). Moderate-to-low-quality evidence indicated no significant impact on rates of live birth, placental abruption, or gestational diabetes. Of the 24 associations, 22 were rated as high confidence and two as medium confidence based on AMSTAR 1. Sensitivity analyses confirmed the robustness of the findings, but treatment effects varied according to the study population, treatment timing, and method. For pregnancy loss and preterm delivery outcomes, the risk was significantly reduced only when LT4 treatment was initiated in early pregnancy (pregnancy loss: RR = 0.60, P = 0.03; RR = 0.59, P = 0.003; preterm labor: RR = 0.58, P < 0.0001; RR = 0.46, P < 0.00001). Additionally, women with TSH levels greater than 4.0 mU/l derived greater benefits from LT4 treatment compared to those with TSH levels between 2.5 and 4.0 mU/l. LIMITATIONS, REASONS FOR CAUTION: Limitations include small sample sizes, potential biases (selection and reporting), and language restrictions to English and Chinese studies, which may affect generalizability. WIDER IMPLICATIONS OF THE FINDINGS: By integrating high-quality evidence, this study confirms that LT4 can reduce the risk of pregnancy loss and preterm delivery in pregnant women with thyroid dysfunction, supports its clinical application in specific populations, such as SCH patients with positive TPOAb or TSH > 4.0 mU/l, and warns against the risk of overtreatment. The results of this study provide an evidence base for clinical precision intervention. Future studies should address the heterogeneity through standardized large studies, clarify the dose threshold, and evaluate the long-term health effects of LT4 on mothers and infants, to further improve the guidelines and optimize risk stratification management. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by the National Key R&D Program of China (Grant No. 2023YFC2508300, 2023YFC2508303, and 2023YFC2508305), the National Science and Technology Major Project (Grant No. 2024ZD0533403), and the National Natural Science Foundation of China (Grant No. 82100831, 81570709, and 82470826). All authors declared no competing interests. REGISTRATION NUMBER: CRD42024586105.

Chemokines may promote the formation and instability of atherosclerotic plaque, which is the most common cause of acute coronary syndrome. The aim of this study was to clarify the function of monocyte chemotactic protein-3 (MCP-3) in the stability of atherosclerotic plaque, to determine the role of tissue factor pathway inhibitor (TFPI) on the development and stability of atherosclerotic plaques, and to further elucidate the anti-atherosclerotic mechanism of TFPI with the emphasis on chemokine MCP-3. We constructed an adenovirus-mediated shRNA against mouse MCP-3 (Ad-MCP-3-shRNA) and an adenovirus-containing TFPI (Ad-TFPI), and tranferred them in a model of vulnerable plaque in ApoE-/- mice respectively. Here, we reported that MCP-3-shRNA and TFPI could both reduce the plaque area and decrease the content of lipids and macrophages, on the contrary, the fibrous cap thickness and content of collagen and smooth muscle cells were increased. In addition, the expression of MCP-3 and CC chemokine receptor 2 (CCR2) was decreased by TFPI transfer. These data provide the first in vivo evidence that MCP-3 is a major contributor to the unstability of atherosclerotic plaque and TFPI may exert its anti-atherosclerotic effects and promote stabilisation of plaque at least partly through inhibiting MCP-3/CCR2 pathway, which may be a new therapeutic method for atherosclerosis.