We systematically identified the prevalence of hyperuricemia and gout in mainland China and provided informative data that can be used to create appropriate local public health policies. Relevant articles from 2000 to 2014 were identified by searching 5 electronic databases: PubMed, Google Scholar, Chinese Wanfang, CNKI, and Chongqing VIP. All of the calculations were performed using the Stata 11.0 and SPSS 20.0 software. The eligible articles (n=36; 3 in English and 33 in Chinese) included 44 studies (38 regarding hyperuricemia and 6 regarding gout). The pooled prevalence of hyperuricemia and gout was 13.3% (95% CI: 11.9%, 14.6%) and 1.1% (95% CI: 0.7%, 1.5%), respectively. Although publication bias was observed, the results did not change after a trim and fill test, indicating that that impact of this bias was likely insignificant. The prevalence of hyperuricemia and gout was high in mainland China. The subgroup analysis suggested that the geographical region, whether the residents dwell in urban or rural and coastal or inland areas, the economic level, and sex may be associated with prevalence.

Key Points: Ischemic heart disease and stroke were the leading contributors to the cardiovascular-kidney-metabolic (CKM) syndrome–related burden in 2021. Regions with a middle sociodemographic index, such as Southeast Asia and the Western Pacific, faced the highest burden. The burden of CKM syndrome is substantial and projected to rise through 2046, highlighting the need for targeted interventions. Background: Cardiovascular-kidney-metabolic (CKM) syndrome highlights the interconnected nature of metabolic diseases, CKD, and cardiovascular diseases, representing a significant and growing public health burden. This study aimed to quantify the global burden of CKM syndrome by examining its key components, including high body mass index, diabetes, CKD, atrial fibrillation and flutter, lower extremity peripheral arterial disease, ischemic heart disease, and stroke. Methods: Data were derived from the Global Burden of Disease 2021 platform, which provided estimates for incidence, prevalence, mortality, years lived with disability, years of life lost, and disability-adjusted life years (DALYs). A decomposition analysis was performed to assess the contributions of population growth, aging, and epidemiologic changes to the burden of CKM syndrome. A NORDPRED model was used to project future trends in DALYs, years of life lost, and years lived with disability through 2046. Results: Globally, ischemic heart disease and stroke were the major contributors to the CKM syndrome–related burden in 2021. Regions with a middle sociodemographic index (SDI), such as Southeast Asia and the Western Pacific, experienced the largest burden. However, age-standardized DALY rates were inversely related to SDI, with regions of lower SDI exhibiting higher rates. From 1990 to 2021, DALYs for the seven key components of CKM syndrome increased, primarily driven by population growth and aging. However, age-standardized DALY rates varied across components, with stroke (−38.7% [95% uncertainty interval: −43.4% to −34.0%]), peripheral arterial disease (−30.1% [−33.5% to −27.2%]), and ischemic heart disease (−28.8% [−32.5% to −25.2%]) showing a declining trend, whereas diabetes (38.2% [29.7%–47.0%]) and high body mass index (25.5% [16.6%–33.7%]) exhibited an increasing trend. Further projection analysis suggested a consistent trend in the changes in CKM syndrome–related burden from 2022 to 2046, with increases ranging from 55.9% for stroke to 105.7% for atrial fibrillation and flutter. Conclusions: The findings of this study highlight the substantial and growing CKM syndrome–related burden.

MAPK signaling inhibitor (MAPKi) therapies show limited efficacy for advanced thyroid cancers despite constitutive activation of the signaling correlates with disease recurrence and persistence. Understanding how BRAF pathway stimulates tumorigenesis could lead to new therapeutic targets. Here, through genetic and pathological approaches, we demonstrate that BRAF^V600E promotes thyroid cancer development by increasing myeloid-derived suppressor cells (MDSCs) penetrance. This BRAF^V600E-induced immune suppression involves re-activation of the developmental factor TBX3, which in turn up-regulates CXCR2 ligands in a TLR2-NFκB dependent manner, leading to MDSCs recruitment into the tumor microenvironment. CXCR2 inhibition or MDSCs repression improves MAPKi therapy effect. Clinically, high TBX3 expression correlates with BRAF^V600E mutation and increased CXCR2 ligands, along with abundant MDSCs infiltration. Thus, our study uncovers a BRAF^V600E-TBX3-CXCLs-MDSCs axis that guides patient stratification and could be targeted to improve the efficacy of MAPKi therapy in advanced thyroid cancer patients.

Background: Previous studies on the association between thyroid function and non‐alcoholic fatty liver disease (NAFLD) have contradicted. Acquired resistance to thyroid hormone theory might provide a reasonable explanation for these contradictions. We aimed to analyze the association between sensitivity to thyroid hormone indices with NAFLD.Methods: A total of 4,610 individuals from the health medical center of the First Hospital of China Medical University were included in this study. The previously used thyroid feedback quantile-based index (TFQI_FT4) was calculated. Also, we substituted free triiodothyronine (FT₃) into the TFQI formulas to get the TFQI_FT3 index. NAFLD was defined using abdominal ultrasound.Results: Study results showed that FT₃/FT₄ and TFQI_FT3 were positively correlated with the triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels (P<0.05) and negatively correlated with high-density lipoprotein cholesterol (HDL-C) level (P<0.05). In contrast, TFQI_FT4 was positively correlated with HDL-C level (P < 0.05). After adjustment for multiple confounders, FT₃, FT₃/FT₄, and TFQI_FT3 were positively associated with the risks of dyslipidemia and NAFLD (P < 0.05). TFQI_FT3 and FT₃/FT₄ performed better than TFQI_FT4 on ROC analyses for NAFLD prediction, although the diagnostic sensitivity and specificity at the optimal cut-points were low. However, no association was observed between TFQI_FT4 with the risks of dyslipidemia and NAFLD.Conclusion: TFQI_FT3 and FT₃/FT₄ can be used as new indicators for predicting dyslipidemia and NAFLD, although with low sensitivity and specificity at the optimal cut-points, while TFQI_FT4 has insufficient evidence in predicting dyslipidemia and NAFLD.

Autoimmune thyroid diseases (AITD) are common autoimmune disorders. A few studies have analyzed the association between serum vitamin D levels and AITD, and available data remain inconclusive. The aim of this study was to evaluate the association between serum vitamin D levels and 3 types of AITD, that is Graves' disease (GD), Hashimoto's thyroiditis (HT), and postpartum thyroiditis (PPT). Two independent case-control studies were designed. The first is a cross-sectional case-control study in which we examined the levels of 25(OH)D in patients with newly diagnosed GD or HT and in controls; the second is a nested case-control study in which we compared 25(OH)D levels in 610 women who developed PPT during the follow-up after delivery and those who did not. Compared with the controls, GD patients and HT patients had significantly lower 25(OH)D levels. PPT cases also had a lower serum 25(OH)D concentration than controls. Serum 25(OH)D levels were associated with neither antithyroid peroxidase antibody nor antithyroglobulin antibody in GD and HT. There was no significant relationship between thyroid-stimulating hormone and 25(OH)D levels. Every 5 nmol/L increase in serum 25(OH)D concentrations was associated with a 1.55-, 1.62-, and 1.51-fold reduction in GD, HT, and PPT risk, respectively. We observed a lower serum vitamin D levels in AITD patients compared with controls. The lower the vitamin D level is, not vitamin D deficiency per se, the higher the risk for developing AITD will be. However, vitamin D does not have strong association with the titers of thyroid antibodies or the levels of thyroid hormones.

Previous studies have reported a negative relationship between thyroid-stimulating hormone (TSH) and renal function in euthyroid individuals, but others have found that higher free thyroxine (FT4) ...