Systematic review of the risk of urolithiasis following parathyroidectomy in patients with primary hyperparathyroidism.

OBJECTIVE: Parathyroidectomy (PTX) is the conclusive therapy for primary hyperparathyroidism (PHPT), but its effect on the risk of urolithiasis is inconclusive. We comprehensively reviewed the currently available research to investigate the impact of PTX on the likelihood of urolithiasis among individuals suffering PHPT. METHODS: Internet-based articles in English language released on Cochrane, PubMed, Scopus, Web of knowledge, and Embase up to September, 2023 were comprehensively reviewed. Each publication in contrast to the incidence, occurrence, or recurrence of urolithiasis after PTX versus medical treatment in PHPT patients was included. The outcome with pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) was examined employing DerSimonian and Laird's model of random effects. To determine the range of the real effect size of a future study in 95% of all populations, a prediction interval (PI) was also established. RESULTS: Finally, ten studies involving 74,190 patients were included. Results from randomized-controlled trials (RCTs) and observational studies (OSs) both revealed that PTX did not substantially lessen the vulnerability of urolithiasis among individuals with PHPT (RCTs: pooled relative risk [RR] 0.42, 95%CI 0.13-1.41, p = 0.163; OSs: pooled RR 1.37, 95%CI 0.96 to 1.97, p = 0.084). The PI (RCT: 0.03 to 5.96; OSs: 0.44-4.20) containing 1.0 suggested the possibility of consistent results in future studies. Subgroup and sensitivity analyses supported the above findings, and no evidence showed publication bias. CONCLUSION: Our analysis from the available RCTs or OSs did not give adequate or exact proof that the average effect of PTX lowers the incidence of urolithiasis among PHPT persons based on the random-effects model. Future research shall take into account the common effect of PTX as well as the prerequisites of preventive stone procedures, which will further help us assess the effectiveness of PTX in reducing kidney calculus comorbidity and develop techniques to avoid stone sequelae in these individuals.

Polyunsaturated fatty acid status and risk of type 1 diabetes in infants and children: a systematic review and meta-analysis.

Introduction: The existing findings about the association between polyunsaturated fatty acid (PUFA) status (especially long-chain n-3 PUFAs) and the risk of preclinical or clinical type 1 diabetes (T1D) in children are controversial. This review aimed to evaluate the definite association. Material and methods: Three databases were systematically viewed until July, 2019 to identify relevant articles, without language restriction. Any observational study or randomized controlled trial reporting the risk estimates of preclinical or clinical T1D for PUFA status in infants and children was enrolled. Regardless of the statistical heterogeneity assessed by the I2 statistic, we pooled the odds ratios (ORs), relative risks (RRs) or hazard ratios (HRs) with 95% confidence intervals (CI) through random-effects models. Results: Five observational studies were enrolled in the meta-analysis. The status of n-3 PUFAs was negatively and significantly associated with the risk of preclinical, but not clinical, T1D (pooled RR = 0.85; 95% CI: 0.73-0.99) with substantial heterogeneity (I2 = 72.2%). However, no such association was found between n-6 PUFA status and the risk of preclinical or clinical T1D. Conclusions: The meta-analysis suggests that n-3 PUFA might play a potential protective role in the cause of preclinical T1D, and n-3 PUFA intake may be beneficial, since the n-3 PUFA status was associated with a significant decrease in the risk of preclinical T1D in children. Nevertheless, more well-designed prospective studies are necessary to determine whether dietary or supplemental intake of specific n-3 PUFA alters the risk of preclinical T1D.

Association of hypoglycaemia with the risks of arrhythmia and mortality in individuals with diabetes - a systematic review and meta-analysis.

Background: Hypoglycaemia has been linked to an increased risk of cardiac arrhythmias by causing autonomic and metabolic alterations, which may be associated with detrimental outcomes in individuals with diabetes(IWD), such as cardiovascular diseases (CVDs) and mortality, especially in multimorbid or frail people. However, such relationships in this population have not been thoroughly investigated. For this reason, we conducted a systematic review and meta-analysis. Methods: Relevant papers published on PubMed, Embase, Cochrane, Web of Knowledge, Scopus, and CINHAL complete from inception to December 22, 2022 were routinely searched without regard for language. All of the selected articles included odds ratio, hazard ratio, or relative risk statistics, as well as data for estimating the connection of hypoglycaemia with cardiac arrhythmia, CVD-induced death, or total death in IWD. Regardless of the heterogeneity assessed by the I2 statistic, pooled relative risks (RRs) and 95% confidence intervals (CI) were obtained using random-effects models. Results: After deleting duplicates and closely evaluating all screened citations, we chose 60 studies with totally 5,960,224 participants for this analysis. Fourteen studies were included in the arrhythmia risk analysis, and 50 in the analysis of all-cause mortality. Hypoglycaemic patients had significantly higher risks of arrhythmia occurrence (RR 1.42, 95%CI 1.21-1.68), CVD-induced death (RR 1.59, 95% CI 1.24-2.04), and all-cause mortality (RR 1.68, 95% CI 1.49-1.90) compared to euglycaemic patients with significant heterogeneity. Conclusion: Hypoglycaemic individuals are more susceptible to develop cardiac arrhythmias and die, but evidence of potential causal linkages beyond statistical associations must await proof by additional specifically well planned research that controls for all potential remaining confounding factors.

Diabetes duration or age at onset and mortality in insulin-dependent diabetics: a systematic review and meta-analysis.

BACKGROUND: This meta-analysis was conducted given the contradictory findings from studies on the influence of diabetes duration or age at onset on mortality in patients with insulin-dependent diabetes mellitus (IDDM). METHODS: Electronic databases (PubMed, Embase, Cochrane, Web of Knowledge, Scopus, and CINHAL) were comprehensively searched to identify relevant studies until October 31, 2022. All of the selected articles contained statistics on hazard ratios, relative risks (RRs), or odds ratios, or data for estimating the association between diabetes duration or age at onset and total mortality in IDDM patients. Regardless the heterogeneity assessed by the I2 statistic, pooled RRs and 95% confidence intervals (CI) for total mortality were acquired via random effect meta-analysis with inverse variance weighting. RESULTS: This meta-analysis finally included 19 studies involving 122, 842 individuals. Both age at onset and diabetes duration were positively associated with an increased mortality rate in IDDM patients. Specifically, the pooled RRs for age at onset and diabetes duration were 1.89 (95%CI 1.43-2.50) and 1.89 (95%CI 1.16-3.09) respectively. Subgroup analyses revealed that only prepubertal onset was associated with a greater survival advantage than pubertal or postpubertal onset. CONCLUSIONS: The findings of this meta-analysis and systematic review suggest that a later age at onset or longer diabetes duration is associated with increased risk of total mortality in IDDM patients. However, this conclusion shall be interpreted with caution due to the possibility of residual confounding and be confirmed in the future by well-designed studies.

Prognostic and clinical significance of modified glasgow prognostic score in pancreatic cancer: a meta-analysis of 4,629 patients.

In this study, we evaluated the association of modified Glasgow Prognostic Score (mGPS) with prognosis in pancreatic cancer (PC) by performing a meta-analysis. Potentially eligible studies were shortlisted by searching PubMed, Embase, Web of Science, Scopus, and the Cochrane Library. A total of 4,629 patients with PC from 25 studies were finally included in this meta-analysis. Meta-analyses were performed using a random-effects model or fixed-effect model according to heterogeneity. We pooled the hazard ratios (HRs) with 95% confidence intervals (CIs) to estimate the association between mGPS and overall survival (OS). The results showed that elevated mGPS correlated with poor OS in patients with PC (HR=1.92, 95% CI=1.60-2.30, p<0.002). In addition, subgroup analysis indicated that increased mGPS remained a significant prognostic factor irrespective of the study design, region, disease status, treatment, survival analysis, cancer type, study center, or the Newcastle-Ottawa Scale (NOS) score (all p<0.05). There was a significant correlation between higher mGPS and male gender (Odds ratio [OR]=1.30, 95% CI=1.01-1.67, p=0.038). Elevated pretreatment mGPS is a marker of poor prognosis in patients with PC. As an easily available and cost-effective inflammatory parameter, mGPS can serve as a promising tool for prognostication in PC.

Prognostic Role of Platelet-to-Lymphocyte Ratio in Patients With Bladder Cancer: A Meta-Analysis.

Background: Many studies have been reported that platelet-to-lymphocyte ratio (PLR) may be associated with the prognosis of bladder cancer, but the results are inconsistent. Therefore, we performed a meta-analysis to evaluate the effect of pretreatment PLR on the prognosis of bladder cancer. Methods: The databases PubMed, Embase, Cochrane Library, and Web of Science were searched. Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were used to analyze the relationship between PLR and prognosis. Pooled odds ratios (ORs) and 95% CIs were used to analyze the relationship between PLR and clinicopathological features. Publication bias was estimated using Begg's funnel plot asymmetry tests. Results: A total of 8 studies comprising 3,303 patients were included in this meta-analysis. An elevated PLR was significantly associated with poorer overall survival (OS) (HR = 1.26, 95% CI = 1.03-1.54, p = 0.026), but not with cancer-specific survival (CSS) (HR = 1.15, 95% CI = 0.95-1.38, p = 0.149), or recurrence-free survival (RFS) (HR = 1.72, 95% CI = 0.79-3.75, p = 0.175). In addition, high PLR was correlated with age ≥ 65 years (OR = 1.82, 95% CI = 1.24-2.67, p = 0.002), whereas was not significantly correlated with sex, tumor grade, tumor stage, distant metastasis, or tumor size. Conclusions: The pretreatment PLR could serve as a predicative biomarker of poor prognosis for patients with bladder cancer.

High-Mobility Group Box 1 (HMGB1) Promotes Angiogenesis and Tumor Migration by Regulating Hypoxia-Inducible Factor 1 (HIF-1α) Expression via the Phosphatidylinositol 3-Kinase (PI3K)/AKT Signaling Pathway in Breast Cancer Cells.

BACKGROUND High-mobility group box 1 (HMGB1) is an essential contributor towards initiation and progression of many kinds of cancers. Nevertheless, our understanding of the molecular etiology of HMGB1-modulated vasculogenesis, as well as invasion, of breast cancer is poor. This study explored HMGB1 expression in breast cancer and its role in the development and spread of malignancy. MATERIAL AND METHODS We enrolled 15 patients with breast cancer who received primary surgery at the Department of Thyroid and Breast Surgery in our hospital. HMGB1 was recorded and analyzed. RESULTS Our investigation successfully proves that HMGB1 is upregulated in breast cancer tissues in comparison to the surrounding non-malignant tissues. HMGB1 enhanced vessel formation in breast cancer tissues by regulating hypoxia-inducible factor 1 (HIF-1alpha), which in turn upregulates the expression of VEGF. Furthermore, HMGB1-mediated upregulation of HIF-1alpha relies on its ability to stimulate the phosphatidylinositol 3-kinase (PI3K) pathway to reinforce AKT subunit phosphorylation. HMGB1 overexpression reinforces the vasculogenesis in malignancies not only in vivo but also in vitro. Additionally, shRNA knockdown of HMGB1 prohibited the vessel-forming and invasive capabilities, downregulated VEGF and HIF-1alpha, and suppressed AKT phosphorylation in breast cancer cells. Most importantly, PI3K/AKT axis suppression eliminated the effect of HMGB1-modulated vascularization and invasion in breast cancer cells. CONCLUSIONS Our research indicates that HMGB1 serves as a crucial regulator of malignant cell-modulated vessel formation and is involved in the development of malignancy. Our findings indicate that HMGB1 is a promising target for breast cancer treatment.

The roles of IL-6, IL-8 and IL-10 gene polymorphisms in gastric cancer: A meta-analysis.

BACKGROUND: Recently, the roles of interleukin-6 (IL-6), IL-8 and IL-10 gene polymorphisms in gastric cancer have been extensively studied, with conflicting results. Therefore, we conducted the present study to better assess the potential correlations between these interleukin gene polymorphisms and gastric cancer. METHODS: Eligible articles were searched in PubMed, Medline, Embase, Web of Science and CNKI. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to detect any potential associations between interleukin gene polymorphisms and the risk of gastric cancer. RESULTS: A total of 73 case-control studies were finally included. Significant associations with the risk of gastric cancer were only detected for the IL-8 rs4073 polymorphism in overall analyses. Further subgroup analyses according to ethnicity of participants revealed that the IL-6 rs1800796, IL-8 rs4073, IL-10 rs1800871, IL-10 rs1800872 and IL-10 rs1800896 polymorphisms were all significantly associated with the risk of gastric cancer in Asians. No positive results were found for any investigated interleukin gene polymorphisms in Caucasians. CONCLUSIONS: Our findings suggest that IL-6 rs1800796, IL-8 rs4073, IL-10 rs1800871, IL-10 rs1800872 and IL-10 rs1800896 polymorphisms may serve as genetic biomarkers of gastric cancer in Asians.

LncRNA CRNDE promotes cell proliferation, invasion and migration by competitively binding miR-384 in papillary thyroid cancer.

Thyroid cancer is one of the most prevalent endocrine neoplasm. The present study examined the effects of Colorectal Neoplasia Differentially Expressed (CRNDE) on the progression of papillary thyroid cancer (PTC), and explored the underlying molecular mechanisms. Quantitative real-time PCR was used to detect CRNDE, miR-384 and pleiotrophin (PTN) mRNA expression. Western blot was used to measure PTN protein levels. Cell proliferation, cell growth, cell invasion and migration of PTC cells were determined by CCK-8, colony formation, transwell invasion and migration assays, respectively. CRNDE was up-regulated in PTC tissues and cell lines. Overexpression of CRNDE promoted BCPAP cell proliferation, invasion and migration, while knock-down of CRNDE suppressed K1 cell proliferation, invasion and migration. CRNDE negatively regulated the expression of miR-384 in PTC cells, which was further confirmed by luciferase reporter assay. MiR-384 was down-regulated and inversely correlated with CRNDE expression in PTC tissues. MiR-384 suppressed cell proliferation, invasion and migration in PTC cells, and enforced expression of miR-384 attenuated the oncogenic effects of CRNDE in PTC cells. PTN was predicted as a downstream target of miR-384, which was confirmed by luciferase reporter assay, and PTN was up-regulated in PTC tissues, and was negatively correlated with miR-384 expression and positively correlated with CRNDE expression in PTC tissues. In summary, our results suggested that the CRNDE/miR-384/PTN axis may play an important role in the regulation of PTC progression, which provides us with new insights into understanding the PTC.

Clinical value of eukaryotic elongation factor 2 (eEF2) in non-small cell lung cancer patients.

BACKGROUND: The purpose of this study was to evaluate a new type of tumor biomarker, eukaryotic elongation factor 2 (eEF2), in serum for the early diagnosis, confirmative diagnosis as well as assessment of treatment of non-small cell lung cancer (NSCLC). METHODS: 130 patients with NSCLC and 50 healthy individuals undergoing physical examination in our hospital provided the observation and healthy control groups. An enzyme linked immune sorbent assay (ELISA) method was applied to determine serum eEF2 levels. Serum neuron specific enolase (NSE) and squamous cell carcinoma antigen (SCC) levels in the observation group were assessed with an automatic biochemical analyzer. RESULTS: The median levels of eEF2 in the serum of NSCLC patients was found to be significantly higher than the healthy control group (p < 0.01) and it was markedly higher in stages III, IV than stages I, II (p < 0.05). eEF2 was higher with tumor size ≥ 2 cm than <2 cm (P< 0.01). Furthermore, two weeks after surgery patients showed a significant trend for eEF2 decrease (p < 0.05). CONCLUSIONS: The eukaryotic elongation factor 2 (eEF2) has certain clinical values for early diagnosis, verification, and prognosis as well as classification of lung cancer patients.