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Irfan Vardarli 5th Medical Department, Division of Endocrinology and Diabetes, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Susanne Tan Department of Endocrinology, Diabetes and Metabolism, Clinical Chemistry – Division of Laboratory Research Endocrine Tumor Center at WTZ/Comprehensive Cancer Center, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Rainer Görges Department of Nuclear Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Bernhard K Krämer 5th Medical Department, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Ken Herrmann Department of Nuclear Medicine, University Hospital Essen, University of Duisburg-Essen, Essen, Germany

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Christoph Brochhausen Institue of Pathology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

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Objective

The management of thyroid nodules with indeterminate cytology (ITN) is still a challenge. To evaluate the performance of commercial molecular tests for ITN, we performed this comprehensive meta-analysis.

Methods

We performed an electronic search using PubMed/Medline, Embase, and the Cochrane Library. Studies assessing the diagnostic accuracy of Afirma gene expression classifier (GEC), Afirma gene sequencing classifier (GSC), ThyroSeq v2 (TSv2), or ThyroSeq v3 (TSv3) in patients with ITN (only Bethesda category III or IV) were selected; Statistical analyses were performed by using Stata.

Results

Seventy-one samples (GEC, n = 38; GSC, n = 16; TSv2, n = 9; TSv3, n = 8) in 53 studies, involving 6490 fine needle aspirations (FNAs) with ITN cytology with molecular diagnostics (GEC, GSC, TSv2, or TSv3), were included in the study. The meta-analysis showed the following pooled estimates: sensitivity 0.95 (95% CI: 0.94–0.97), specificity 0.35 (0.28–0.43), positive likelihood ratio (LR+) 1.5 (1.3–1.6), and negative likelihood ratio (LR−) 0.13 (0.09–0.19), with the best performance for TSv3 (area under the ROC curve 0.95 (0.93–0.96), followed by TSv2 (0.90 (0.87–0.92)), GSC (0.86 (0.82–0.88)), and GEC (0.82 (0.78–0.85)); the best rule-out property was observed for GSC (LR−, 0.07 (0.02–0.19)), followed by TSv3 (0.11 (0.05–0.24)) and GEC (0.16 (0.10–0.28), and the best rule-in was observed for TSv2 (LR+, 2,9 (1.4–4.6)), followed by GSC (1.9 (1.6–2.4)). A meta-regression analysis revealed that study design, Bethesda category, and type of molecular test were independent factors.

Conclusion

We showed that in patients with ITN, TSv3 has the best molecular diagnostic performance, followed by TSv2, GSC, and GEC. As regards rule-out malignancy, GSC, and rule-in, TSV2 is superior to other tests.

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Shikai Gui Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Wanli Yu Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Jiabao Xie Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Lunshan Peng Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Yuanyuan Xiong Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China

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Zhen Song Nanchang University, Nanchang, Jiangxi Province, China
Department of Urology, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Haitao Luo Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Juexian Xiao Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China

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Shengtao Yuan Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing, Jiangsu Province, China

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Zujue Cheng Department of Neurosurgery, the 2nd affiliated hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China
Nanchang University, Nanchang, Jiangxi Province, China
Institute of Neuroscience, Nanchang University, Nanchang, Jiangxi Province, China

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Invasive pituitary neuroendocrine tumors (PitNETs) are the most prevalent types of intracranial and neuroendocrine tumors. Their aggressive growth and difficulty in complete resection result in a high recurrence rate. Cystine transporter solute carrier family 7 member 11 (SLC7A11) is overexpressed in various cancers, which contributes to tumor growth, progression, and metastasis by promoting cystine uptake and glutathione biosynthesis. We identified SLC7A11 as an invasive biomarker based on three Gene Expression Omnibus cohorts. This study aimed to investigate the role of SLC7A11 in invasive PitNETs. Cell proliferation was assessed using CCK-8 and colony formation assays, while cell apoptosis was estimated with flow cytometry. Wound healing assays and transwell assays were utilized to evaluate migration and invasion ability. Our findings demonstrated that SLC7A11 was markedly upregulated in invasive PitNETs, and was associated with the invasiveness of PitNETs. Knockdown of SLC7A11 could largely suppress tumor cell proliferation, migration, and invasion, while inducing apoptosis. Furthermore, SLC7A11 depletion was implicated in regulating epithelial–mesenchymal transition and inactivating the PI3K/AKT signaling pathway. These insights suggest SLC7A11 as a potential therapeutic target for invasive PitNETs.

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Shams Ali Baig S Ali Baig, University of Birmingham College of Medical and Dental Sciences, Birmingham, B15 2TT, United Kingdom of Great Britain and Northern Ireland

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Kashish Malhotra K Malhotra, Department of Surgery, Rama Medical College Hospital and Research Centre Hapur, Hapur, India

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Josh Banerjee J Banerjee, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Mukunth Kowsik M Kowsik, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Khushi Kumar K Kumar, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Fazna Rahman F Rahman, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Syeda Sabbah Batul S Batul, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Mohammed Faraaz Saiyed M Saiyed, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Vardhan Venkatesh V Venkatesh, University of Birmingham College of Medical and Dental Sciences, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Pranav Vishwanath Iyer P Vishwanath Iyer, University of Birmingham College of Medical and Dental Sciences, Birmingham, B296DR, United Kingdom of Great Britain and Northern Ireland

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Punith Kempegowda P Kempegowda, University of Birmingham, Birmingham, B15 2TT, United Kingdom of Great Britain and Northern Ireland

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YouTube® is one of the leading platforms for health information. However, the lack of regulation of content and quality raises concerns about accuracy and reliability. CoMICs (Concise Medical Information Cines) are evidenced-based short videos created by medical students and junior doctors and reviewed by experts to ensure clinical accuracy. We performed a systematic review to understand the impact of videos on knowledge and awareness about diabetes and PCOS. We then evaluated the quality of YouTube® videos about diabetes and PCOS using various validated quality assessment tools and compared these with CoMICs videos on the same topics. Quality assessment tools like DISCERN, JAMA benchmark criteria, and Global Quality Score (GQS) were employed. Some of the authors of this study also co-authored the creation of some of the CoMICs evaluated. Our study revealed that while videos effectively improve understanding of diabetes and PCOS, there are notable differences in quality and reliability of the videos on YouTube®. For diabetes, CoMICs videos had higher DISCERN scores (CoMICs vs YouTube®: 2.4 vs 1.6), superior reliability (p<0.01) and treatment quality (p<0.01), and met JAMA criteria for authorship (100% vs. 30.6%) and currency (100% vs. 53.1%). For PCOS, CoMICs had higher DISCERN scores (2.9 vs. 1.9), reliability (p<0.01), and treatment quality (p<0.01); and met JAMA criteria for authorship (100% vs. 34.0%) and currency (100% vs. 54.0%); and had higher GQS scores (4.0 vs 3.0). In conclusion, CoMICs outperformed other similar sources on YouTube® in providing reliable evidence-based medical information which may be used for patient education.

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Sun Fei Wuxi Medical College of Jiangnan University, Wuxi, China

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Min Liu Wuxi Maternity and Child Health Care Hospital, Wuxi, China

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Hu Shanshan Wuxi Maternity and Child Health Care Hospital, Wuxi, China

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Ruijie Xie Department of Microsurgery, University of South China, Hengyang, China

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Wu Danni Wuxi Medical College of Jiangnan University, Wuxi, China

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Zhou Ningying Wuxi Medical College of Jiangnan University, Wuxi, China

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Background

Depression has become a multifaceted global health issue, with complex connections to obesity. Weight-adjusted-waist index (WWI) can effectively evaluate central obesity, but the relationship between WWI and depression has not been well studied. The study aims to investigate the potential correlation between these two health parameters.

Methods

According to the data from National Health and Nutrition Examination Survey, this cross-sectional study used multiple regression analysis, subgroup analysis, and smooth curve fitting to explore the relationship between WWI and depression. The assessment ability of WWI was evaluated and compared to other obesity indicators using the receiver operating characteristic (ROC) curve.

Results

This study analyzed 38,154 participants. Higher WWI is associated with higher depression scores (β = 0.41; 95% CI, 0.36–0.47). After adjusting for various confounding factors, the positive correlation between WWI and depression remained significant (P for trend < 0.0001). Nonlinear positive correlation was detected with a breakpoint of 11.14. ROC analysis shows that compared to other obesity indicators (ROCWWI = 0.593; ROCBMI = 0.584; and ROCWC = 0.581), the correlation between WWI and depression has better discrimination and accuracy. DII mediated 4.93%, SII mediated 5.08%, and sedentary mediated 0.35% of the total association between WWI and depression.

Conclusion

WWI levels were related to an increased likelihood of depression and showed a stronger relationship than BMI and waist circumference. Our findings indicated that WWI may serve as a simple anthropometric index to evaluate depression.

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Peiwen Zheng School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Fan Wang Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China

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Hui Li Psychosomatic Medicine Research Division, Inner Mongolia Medical University, Huhhot, China

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Hanlu Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Mengtong Li School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Haozheng Ma School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Jue He School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Li Chen School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Yanlong Liu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Haiyun Xu School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China

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Objective

This study aimed to reveal associations between metabolic hormones in cerebral spinal fluid (CSF) and cigarette smoking-induced weight gain and to explore the underlying mechanism.

Methods

A total of 156 adult men were included, comprising active smokers and nonsmokers. In addition to demographic information and body mass index (BMI), plasma levels of ApoA1 and ApoB, high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase in the participants were measured. Moreover, the metabolic hormones adiponectin, fibroblast growth factor 21 (FGF21), ghrelin, leptin, and orexin A, as well as the trace elements iron and zinc in CSF, were assessed.

Results

Compared to nonsmokers, active smokers showed higher BMI, and elevated CSF levels of FGF21, Zn, and Fe, but decreased levels of metabolic hormones adiponectin, ghrelin, leptin, and orexin A. Negative correlations existed between CSF FGF21 and ghrelin, between CSF Zn and ghrelin, as well as between CSF Fe and orexin A in active smokers. Furthermore, elevated CSF FGF21 and Zn predicted ghrelin level decrease in the smokers.

Conclusion

These data relate smoking-induced weight gain to its neurotoxic effect on the neurons that synthesize metabolic hormones such as adiponectin, ghrelin, leptin, or orexin A in the brain, by disrupting mitochondrial function and causing oxidative stress in the neurons.

Open access
Weiwei Liang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Yilin Zhang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China

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Yan Guo Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Pengyuan Zhang Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Jiewen Jin Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Hongyu Guan Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Yanbing Li Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China

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Background

Filamin A (FLNA) is a member of the filamin family and has been found to be critical for the progression of several cancers. However, its biological function in papillary thyroid cancer (PTC) remains largely unexplored.

Methods

Data from The Cancer Genome Atlas (TCGA) databases were utilized to analyze the FLNA expression level and its influence on the clinical implications of patients with PTC. Gene Expression Omnibus (GEO) and qRT-PCR was used to verify the expression levels of FLNA in PTC. Kaplan–Meier survival analysis was conducted to evaluate the prognostic value of FLNA in PTC. Transwell assays and wound healing were performed to examine the biological function of FLNA knockdown in PTC cells. Gene set enrichment analysis (GSEA) and Western blotting were conducted to investigate the potential mechanisms underlying the role of FLNA in PTC progression. In addition, the relationship between FLNA expression and the tumor immune microenvironment (TME) in PTC was explored.

Results

FLNA was significantly upregulated in PTC tissues. High expression levels of FLNA was correlated with advanced TNM stage, T stage, and N stage, as well as poor disease-free interval (DFI) and progression-free interval (PFI) time in PTC patients. Moreover, we found that FLNA knockdown inhibited the migration and invasion of PTC cells. Mechanistically, FLNA knockdown inhibited epithelial–mesenchymal transition (EMT) in PTC and affected the activation of the FAK/AKT signaling pathway. In addition, FLNA expression was associated with TME in PTC.

Conclusion

FLNA may be regarded as a new therapeutic target for PTC patients.

Open access
Ayse Nurcan Cebeci Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

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Vera Schempp Paediatric Endocrinology, University Hospital, Bonn, Germany

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Katharina Förtsch Paediatric Endocrinology, University Hospital, Düsseldorf, Germany

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Bettina Gohlke Paediatric Endocrinology, University Hospital, Bonn, Germany

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Michaela Marx Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

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Helmuth-Guenther Dörr Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

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Joachim Woelfle Paediatric Endocrinology, Department of Friedrich-Alexander University Hospital, Erlangen, Germany

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While subclinical or overt hypothyroidism are common in Down syndrome (DS); Graves’ disease (GD) is rare (ranges 0.6–3%). We aimed to evaluate the clinical features, course, and treatment of GD in children with DS and compare them with those without DS. Among 161 children with GD, 13 (8 female, 5 male) had DS (8%). Data were collected retrospectively from patients’ medical records. The mean age at diagnosis was 10.6 ± 4.5 years, with a female-to-male ratio 1.6:1. The main symptoms were weight loss (n = 6), increased irritability (n = 3), and increased sweating (n = 3). None had orbitopathy. Seven of 11 patients with a thyroid ultrasound at diagnosis had a goitre. On admission, all had thyroid-stimulating hormone (TSH) <0.01 mU/L (normal range (NR): 0.51–4.30), free triiodothyronine, free thyroxine (mean ± s.d .), and thyrotrophin receptor antibodies (median, range) were 22.2 ± 10.2 pmol/L (NR: 3.5–8.1), 50.2 ± 18.7 pmol/L (NR 12.6–20.9), and 17.0 (2.89–159.0) U/L (NR <1), respectively. Patients were treated either with methimazole (n = 10) or carbimazole (n = 3), a dose of 0.54 ± 0.36 mg/kg/day. The treatment was ‘block and replace’ in ten patients and ‘dose titration’ in three patients, with a mean duration of 43.4 ± 11.0 months. Of 13 patients, four are still receiving primary treatment, three are in remission, one patient had two medically treated recurrences, three underwent surgery without complications, and two patients were lost to follow-up. Our data show that the clinical course of GD in patients with DS was similar to those without DS and suggest that a prolonged medical therapy should be the preferred option.

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Zhenyu Liu Department of Clinical Medicine, Beijing Luhe Hospital, Capital Medical University, Tongzhou District, Beijing, China

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Huixi Kong Department of Clinical Medicine, Beijing Shijitan Hospital, Capital Medical University, Haidian District, Beijing, China

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Baoyu Zhang Center for Endocrine Metabolism and Immune Diseases, Beijing Luhe Hospital, Capital Medical University, Tongzhou District, Beijing, China

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To optimize the treatment plan for patients with type 2 diabetes mellitus (T2DM) and hyperuricemia, this narrative literature review summarizes the effect of antidiabetic drugs on serum uric acid (SUA) levels using data from observational studies, prospective clinical trials, post hoc analyses, and meta-analyses. SUA is an independent risk factor for T2DM, and evidence has shown that patients with both gout and T2DM exhibit a mutually interdependent effect on higher incidences. We find that insulin and dipeptidyl peptidase 4 inhibitor (DPP-4i) except linagliptin could increase the SUA and other drugs including metformin, thiazolidinediones (TZDs), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), linagliptin, sodium–glucose cotransporter 2 inhibitors (SGLT2i), and α-glucosidase inhibitors have a reduction effect on SUA. We explain the mechanisms of different antidiabetic drugs above on SUA and analyze them compared with actual data. For sulfonylureas, meglitinides, and amylin analogs, the underlying mechanism remains unclear. We think the usage of linagliptin and SGLT2i is the most potentially effective treatment of patients with T2DM and hyperuricemia currently. Our review is a comprehensive summary of the effects of antidiabetic drugs on SUA, which includes actual data, the mechanisms of SUA regulation, and the usage rate of drugs.

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M Guftar Shaikh M Shaikh, Department of Paediatric Endocrinology, Royal Hospital for Children, Glasgow, United Kingdom of Great Britain and Northern Ireland

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Tim Barrett T Barrett, Department of Endocrinology, Birmingham Womens and Children’s Hospital, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Nicola Bridges N Bridges, Department of Paediatric Endocrinology, Chelsea and Westminster Hospital, London, United Kingdom of Great Britain and Northern Ireland

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Robin Chung R Chung, Head Office, Prader-Willi Syndrome Association UK, London, United Kingdom of Great Britain and Northern Ireland

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Evelien Gevers E Gevers, Centre for Endocrinology, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom of Great Britain and Northern Ireland

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Anthony P Goldstone A Goldstone, Metabolic and Molecular Imaging Group, Imperial College London, London, United Kingdom of Great Britain and Northern Ireland

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Anthony Holland A Holland, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom of Great Britain and Northern Ireland

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Shankar Kanumakala S Kanumakala, Paediatric endocrinology, Royal Alexandra Children’s Hospital, Brighton, United Kingdom of Great Britain and Northern Ireland

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Ruth E Krone R Krone, Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, University of Birmingham, Birmingham, United Kingdom of Great Britain and Northern Ireland

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Andreas Kyriakou A Kyriakou, Department of Paediatric Endocrinology, Makarios Children's Hospital, Nicosia, Cyprus

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E Anne Livesey E Livesey, Department of Paediatric Endocrinology, Royal Alexandra Children’s Hospital, Brighton, United Kingdom of Great Britain and Northern Ireland

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Angela Lucas-Herald A Lucas-Herald, Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom of Great Britain and Northern Ireland

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Christina Meade C Meade, Endocrinology, CHI at Tallaght University Hospital, Dublin, Ireland

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Susan Passmore S Passmore, Main Office, Prader-Willi Syndrome Association UK, London, United Kingdom of Great Britain and Northern Ireland

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Edna Roche E Roche, Department of Pediatrics, The National Children’s Hospital, University of Dublin, Trinity College, Dublin, Ireland

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Chris Smith C Smith, Endocrinology, Royal Alexandra Children’s Hospital, Brighton, United Kingdom of Great Britain and Northern Ireland

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Sarita Soni S Soni, Psychiatry, NHS Greater Glasgow and Clyde, Glasgow, United Kingdom of Great Britain and Northern Ireland

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Prader Willi syndrome (PWS) is a rare orphan disease and complex genetic neurodevelopmental disorder, with a birth incidence of approximately 1 in 10,000-30,000. Management of people with PWS requires a multi-disciplinary approach, ideally through a multi-disciplinary team (MDT) clinic with community support. Hypotonia, poor feeding and faltering growth are characteristic features in the neonatal period, followed by hyperphagia and risk of rapid weight gain later in childhood. Children and adolescents (CA) with PWS usually display developmental delay and mild learning disability, and can develop endocrinopathies, scoliosis, respiratory difficulties (both central and obstructive sleep apnoea), challenging behaviours, skin picking, and mental health issues especially into adulthood. This consensus statement is intended to be a reference document for clinicians managing children and adolescents (up to 18 years of age) with PWS. It considers the bio-psycho-social domains of diagnosis, clinical assessment, and management in the paediatric setting as well as during and after transition to adult services. The guidance has been developed from information gathered from peer-reviewed scientific reports and from the expertise of a range of experienced clinicians in the United Kingdom and Ireland involved in the care of patients with PWS.

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Yueyuan Yang Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

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Tingting Yu Department of Radiology, Renmin Hospital of Wuhan University, Wuhan, China

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Zhili Niu Department of Clinical Laboratory, Institute of translational medicine, Renmin Hospital of Wuhan University, Wuhan, China

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Ling Gao Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

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Objective

Uridine might be a common link between pathological pathways in diabetes and cardiovascular diseases. This study aimed to investigate the predictive value of plasma uridine for type 2 diabetes (T2D) and T2D with atherosclerosis.

Methods

Individuals with T2D and healthy controls (n = 218) were randomly enrolled in a cross-sectional study. Patients with T2D were divided into two groups based on carotid ultrasound: patients with carotid atherosclerosis (CA) (group DCA) and patients without CA (group D). Plasma uridine was determined using HPLC-MS/MS. Correlation and logistic regression analyses were used to analyze the results.

Results

Fasting and postprandial uridine were significantly increased in patients with T2D compared with healthy individuals. Logistic regression suggested that fasting and postprandial uridine were independent risk factors for T2D. The receiver operating characteristic (ROC) curve showed that fasting uridine had a predictive value on T2D (95% CI, 0.686–0.863, sensitivity 74.3%, specificity 71.8%). Fasting uridine was positively correlated with LDL-c, FBG, and PBG and negatively correlated with fasting C-peptide (CP-0h) and HOMA-IS. The change in postprandial uridine from fasting baseline (Δuridine) was smaller in T2D patients with CA compared with those without (0.80 (0.04–2.46) vs 2.01 (0.49–3.15), P = 0.010). Δuridine was also associated with T2D with CA and negatively correlated with BMI, CP-0h, and HOMA-IR.

Conclusion

Fasting uridine has potential as a predictor of diabetes. Δuridine is closely associated with carotid atherosclerosis in patients with T2D.

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