Ronghua Song

Diabetes self-management education reduces risk of all-cause mortality in type 2 diabetes patients: a systematic review and meta-analysis.

BackgroundDiabetes self-management education is an essential part of diabetes care, but its impact on all-cause mortality risk of type 2 diabetes patients is unclear. A systematic review and meta-analysis aiming to elucidate the impact of diabetes self-management education on all-cause mortality risk of type 2 diabetes patients was performed.MethodsRandomised controlled trials were identified though literature search in Medline, Embase, CENTRAL, conference abstracts, and reference lists. Only randomised controlled trials comparing diabetes self-management education with usual care in type 2 diabetes patients and reporting outcomes after a follow-up of at least 12 months were considered eligible. Risk ratios with 95 %CIs were pooled. This study was registered at PROSPERO with the number of CRD42016043911.Results42 randomised controlled trials containing 13,017 participants were included. The mean time of follow-up was 1.5 years. There was no heterogeneity among those included studies (I2 = 0 %). Mortality occurred in 159 participants (2.3 %) in the diabetes self-management education group and in 187 (3.1 %) in the usual care group, and diabetes self-management education significantly reduced risk of all-cause mortality in type 2 diabetes patients (pooled risk ratios : 0.74, 95 %CI 0.60–0.90, P = 0.003; absolute risk difference: −0.8 %, 95 %CI −1.4 to −0.3). Both multidisciplinary team education and nurse-led education could significantly reduce mortality risk in type 2 diabetes patients, and the pooled risk ratios were 0.66 (95 %CI 0.46–0.96, P = 0.02; I2 = 0 %) and 0.64 (95 % CI 0.47– 0.88, P = 0.005; I2 = 0 %), respectively. Subgroup analyses of studies with longer duration of follow-up (≥1.5 years) or larger sample size (≥300) also found a significant effect of diabetes self-management education in reducing mortality risk among type 2 diabetes. Significant effect of diabetes self-management education in reducing mortality risk was also found in those patients receiving diabetes self-management education with contact hours more than 10 h (pooled risk ratio: 0.60, 95 %CI 0.44–0.82, P = 0.001; I2 = 0 %), those receiving repeated diabetes self-management education (pooled RR: 0.71, P = 0.001; I2 = 0 %), those receiving diabetes self-management education using structured curriculum (pooled risk ratio: 0.72, P = 0.01; I2 = 0 %) and those receiving diabetes self-management education using in-person communication (pooled risk ratio: 0.75, P = 0.02; I2 = 0 %). The quality of evidence for the effect of diabetes self-management education in reducing all-cause mortality risk among type 2 diabetes patients was rated as moderate according to the Grading of Recommendations Assessment, Development, and Evaluation method, and the absolute risk reduction of all-cause mortality of type 2 diabetic patients by diabetes self-management education was estimated to be 4 fewer per 1000 person-years (from 1 fewer to 6 fewer).ConclusionsThe available evidence suggests that diabetes self-management education can reduce all-cause mortality risk in type 2 diabetes patients. Further clinical trials with longer time of follow-up are needed to validate the finding above.

Antibiotic Exposure in Early Life Increases Risk of Childhood Obesity: A Systematic Review and Meta-Analysis

A number of studies have previously assessed the impact of antibiotic exposure in early life on the risk of childhood obesity, but no systematic assessment is currently available. A systematic review and meta-analysis was performed to comprehensively and quantitatively elucidate the risk of childhood obesity caused by antibiotic exposure in early life. Literature search was performed in PubMed, Embase, and Web of Science. Random-effect meta-analysis was used to pool the statistical estimates. Fifteen cohort studies involving 445,880 participants were finally included, and all those studies were performed in developed countries. Antibiotic exposure in early life significantly increased risk of childhood overweight [relative risk (RR) = 1.23, 95% confidence interval (CI) 1.13–1.35, P < 0.001] and childhood obesity (RR = 1.21, 95% CI 1.13–1.30, P < 0.001). Antibiotic exposure in early life also significantly increased the z-score of childhood body mass index (mean difference: 0.07, 95% CI 0.05–0.09, P < 0.00001). Importantly, there was an obvious dose–response relationship between antibiotic exposure in early life and childhood adiposity, with a 7% increment in the risk of overweight (RR = 1.07, 95% CI 1.01–1.15, P = 0.03) and a 6% increment in the risk of obesity (RR = 1.06, 95% CI 1.02–1.09, P < 0.001) for each additional course of antibiotic exposure. In conclusion, antibiotic exposure in early life significantly increases risk of childhood obesity. Moreover, current analyses are mainly taken from developed countries, and therefore the impact of antibiotic exposure on risk of childhood obesity in vulnerable populations or developing countries still needs to be evaluated in future studies.

Non-thyroidal illness syndrome in patients with cardiovascular diseases: A systematic review and meta-analysis

BACKGROUND Non-thyroidal illness syndrome (NTIS) is characterized by decreased serum triiodothyronine level without increased thyroid-stimulating hormone level during critical illness. The summary data on the prevalence of NTIS in cardiovascular patients are lacking, and its prognostic role in cardiovascular patients is also unclear. METHODS We performed a systematic review and meta-analysis to comprehensively determine the prevalence and the prognostic role of NTIS in cardiovascular patients. The prevalence of NTIS was pooled using random-effect meta-analysis and the hazard ratios (HRs) for all-cause mortality, cardiac mortality and major adverse cardiovascular events (MACE) were also pooled. RESULTS Forty-one studies were finally included. The pooled prevalence of NTIS in cardiovascular patients was 21.7% (95% CI 18.4%-25.3%). Subgroup by the types of cardiovascular diseases showed the prevalence of NTIS was highest in patients with heart failure (24.5%), followed by acute myocardial infarction (18.9%) and acute coronary syndrome (17.1%). Meta-analysis of studies using strict diagnostic criteria of NITS showed that the pooled prevalence of NTIS in cardiovascular patients was 17.6% (95% CI 14.5%-21.2%). NTIS was independently associated with increased risks of all-cause mortality (HR=2.52, 95% CI 1.87-3.40, P<0.001) and cardiac mortality (HR=2.06, 95% CI 1.58-2.69, P<0.001) in cardiovascular patients. NTIS was also an independent predictor of MACE in cardiovascular patients (HR=1.73, 95% CI 1.32-2.26, P<0.001). CONCLUSION NTIS is very common in patients with cardiovascular diseases. NTIS is an independent prognostic factor in cardiovascular patients and is associated with increased risks of all-cause mortality, cardiac mortality and MACE.

The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases

Autoimmune thyroid diseases (AITD) are a group of both B cell- and T cell-mediated organ-specific autoimmune diseases. Graves’ disease and Hashimoto thyroiditis are the two main clinical presentations of AITD. Both genetic and environmental factors have important roles in the development of AITD. Epigenetics have been considered to exert key roles in integrating those genetic and environmental factors, and epigenetic modifications caused by environmental factors may drive genetically susceptibility individuals to develop AITD. Recent studies on the epigenetics of AITD have provided some novel insights into the pathogenesis of AITD. The aim of this review is to provide an overview of recent advances in the epigenetic mechanisms of AITD, such as DNA methylation, histone modifications, and non-coding RNAs. This review highlights the key roles of epigenetics in the pathogenesis of AITD and potential clinical utility. However, the epigenetic roles in AITD are still not fully elucidated, and more researches are needed to provide further deeper insights into the roles of epigenetics in AITD and to uncover new therapeutic targets. Although there are many studies assessing the epigenetic modifications in AITD patients, the clinical utility of epigenetics in AITD remains poorly defined. More studies are needed to identify the underlying epigenetic modifications that can contribute to accurate diagnosis of AITD, adequate choice of treatment approach, and precise prediction of treatment outcomes.

TNFSF4 Gene Variations Are Related to Early-Onset Autoimmune Thyroid Diseases and Hypothyroidism of Hashimoto's Thyroiditis

The aim of the current study was to examine whether the polymorphism loci of the tumor necrosis factor superfamily member 4 (TNFSF4) gene increase the risk of susceptibility to autoimmune thyroid diseases (AITDs) in the Han Chinese population, and a case-control study was performed in a set of 1,048 AITDs patients and 909 normal healthy controls in the study. A total of four tagging single nucleotide polymorphisms (SNPs) in the TNFSF4 region, including rs7514229, rs1234313, rs16845607 and rs3850641, were genotyped using the method of ligase detection reaction. An association between GG genotype of rs3850641 in TNFSF4 gene and AITDs was found (p = 0.046). Additionally, the clinical sub-phenotype analysis revealed a significant association between GG genotype in rs7514229 and AITDs patients who were ≤18 years of age. Furthermore, rs3850641 variant allele G was in strong association with hypothyroidism in Hashimoto’s thyroiditis (HT) (p = 0.018). The polymorphisms of the TNFSF4 gene may contribute to the susceptibility to AITDs pathogenesis.

Proteomic analysis reveals aberrant expression of CALR and HSPA5 in thyroid tissues of Graves' disease.

OBJECTIVES To explore the proteomic changes in thyroid tissue from GD patients and find new biomarkers for the prevention, diagnosis as well as the treatment of GD. DESIGN AND METHODS Group1 included five thyroid specimens of GD cases and 5 normal thyroid tissue samples which were removed surgically and collected. The proteins were extracted from these thyroid tissues and then the differentially expressed protein spots were identified by MALDI-TOF-MS. The interested proteins were further validated in more specimens (group2: 11 pathological thyroid specimens and 7 normal thyroid tissue samples). RESULTS A total of 34 differentially expressed proteins were observed, and the majority of these proteins were involved in endoplasmic reticulum stress (ER-stress), oxidative stress, energy metabolism, cytoskeleton and movement. The overexpression of calreticulin(CALR) and heat shock 70kDa protein 5(HSPA5) was further validated. CONCLUSION Alltogether, abundant new candidate molecules, especially proteins related to ER-stress, were found to be involved in the pathogenesis of GD.

A case–control study of selenoprotein genes polymorphisms and autoimmune thyroid diseases in a Chinese population

BackgroundSelenium is an essential trace and there is a high selenium concentration in the thyroid gland. Selenium deficiency may impair the thyroid function. The aim of this study was to investigate the association between three selenoprotein genes polymorphisms and autoimmune thyroid diseases.MethodsWe genotyped six single-nucleotide polymorphisms (SNPs), rs6865453 in selenoprotein P gene (SELENOP), rs713041 rs2074451 rs3746165 in glutathione peroxidase 4 gene (GPX4) and rs28665122 and rs7178239 in selenoprotein S gene (SELENOS) by MassARRAY system using the chip-based matrix-assisted laser desorption ionization time-of-flight mass spectrometry technology in 1060 patients with autoimmune thyroid diseases and 938 healthy controls.ResultsMajor alleles in rs6865453 of SELENOP, rs713041, rs2074451, rs3746165 of GPX4 decreased while the major allele C in rs28665122 of SELENOS increased in AITD patients than in the control. The allele C and genotype CC in rs7178239 of SELENOS showed different trend in GD and HT patients when compared with the control. All the distribution difference showed nonsignificant. Analysis according to clinical features including ophthalmopathy, hypothyroidism and family history came out to be negative either.ConclusionsOur findings suggest non-association between three selenoprotein genes and AITD, conflicting to the positive result in another population. Different selenium nutrition status in different populations may contribute to conflicting results, the contribution of genetic variants in AITD mechanism may be another reason.

Prevalence and independent risk factors of depression in Chinese patients with type 2 diabetes: a systematic review and meta-analysis

Abstract Background Studies of the prevalence of depression in patients with type 2 diabetes in China have reported inconsistent findings. The purpose of this study was to assess the prevalence and independent risk factors of depression in patients with type 2 diabetes in China. Methods We did a systematic review and meta-analysis of papers published in PubMed (1980–2016), Embase (1980–2016), China National Knowledge Infrastructure (1999–2016), and Wanfang Medical database (1998–2016). We selected population-based, cross-sectional studies investigating the prevalence of depression in patients with type 2 diabetes in China. We used a random-effects meta-analysis to pool the prevalence and relative risks (RR) with 95% CIs. This study was registered at PROSPERO, number CRD42016039795. Findings 26 studies published between May, 2003, and February, 2016, were included. The studies included 66 475 patients with type 2 diabetes in China. A meta-analysis of six studies comparing the depression prevalence in diabetes patients and healthy controls suggested that type 2 diabetes was associated with a doubled risk of depression in Chinese people (RR 2·06; 95% CI 1·46–2·92; p 1c (RR 1·44, 95% CI 1·11–1·88; p=0·0068), and use of insulin (RR 2·08, 95% CI 1·28–3·37; p=0·0030). Interpretation We found a high prevalence of depression in Chinese patients with type 2 diabetes. Patients with diabetes and depression should receive more attention than at present in the medical settings of China and effective interventions to decrease depression risk in patients with diabetes are needed. Funding National Natural Science Foundation of China (number 81471004).

Polymorphisms of IKZF3 Gene and Autoimmune Thyroid Diseases: Associated with Graves’ Disease but Not with Hashimoto’s Thyroiditis

Background/Aims: The IKZF3 gene encodes a zinc-finger protein that plays an important role in the proliferation and differentiation of B lymphocytes. Autoimmune thyroid diseases (AITDs), mainly include Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), are probably caused by the aberrant proliferation of B cells. The objective of this study was to explore the association between IKZF3 polymorphisms and AITDs. Methods: We examined 915 AITD patients (604 GD and 311 HT) and 814 healthy controls. IKZF3 variants (rs2941522, rs907091, rs1453559, rs12150079 and rs2872507) were tested by PCR-ligase detection reaction. Results: It was manifested that that the minor alleles of the five loci increased susceptibility to GD (p<0.05 for rs2941522, and p<0.01 for rs907091, rs1453559, rs12150079 and rs2872507) but in HT patients, these loci showed no significant difference compared with controls. Similarly, the genotype distributions of GD patients manifested obvious differences in all these loci compared with the control group, whereas no statistical differences were observed between HT patients and controls. Furthermore, bioinformatics tools were used to analyze rs1453559, rs12150079 and rs907091. These variants were believed to be the transcription regulator. Conclusion: It is the first time we reported the association between the IKZF3 polymorphisms and GD, indicating that IKZF3 gene tends to bean important risk factor for the development of GD.

Copy number variations exploration of multiple genes in Graves’ disease

Background: Few previous published papers reported copy number variations of genes could affect the predisposition of Graves’ disease (GD). Herein, the aim of this study was to explore the association between copy number variations (CNV) profile and GD. Methods: The preliminary copy number microarray used to screen copy number variant genes was performed in 6 GD patients. Five CNV candidate genes (CFH, CFHR1, KIAA0125, UGT2B15, and UGT2B17) were then validated in an independent set of samples (50 GD patients and 50 matched healthy ones) by the Accucopy assay method. The CNV of the other 2 genes TRY6 and CCL3L1 was investigated in 144 GD patients and 144 healthy volunteers by the definitive genotyping technique using the Taqman quantitative polymerase-chain-reaction (Taqman qPCR). TRY6 gene-associated single nucleotide polymorphism (SNP), rs13230029, was genotyped by the PCR-ligase detection reaction (LDR) in 675 GD patients and 898 healthy controls. Results: There were no correlation of the gene copy number (GCN) of CFH, CFHR1, KIAA0125, UGT2B15, and UGT2B17 with GD. In comparison with that of controls, the GCN distribution of TRY6 and CCL3L1 in GD patients did not show significantly differ (P > 0.05). Furthermore, TRY6-related polymorphism (rs13230029) showed no difference between GD patients and controls. No correlation was found between CNV or SNP genotype and clinical phenotypes. Generally, there were no link of the copy numbers of several genes, including CFH, CFHR1, KIAA0125, UGT2B15, UGT2B17, TRY6, and CCL3L1 to GD. Conclusion: Our results clearly indicated that the copy number variations of multiple genes, namely CFH, CFHR1, KIAA0125, UGT2B15, UGT2B17, TRY6, and CCL3L1, were not associated with the development of GD.