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The purpose of this study is to systematically analyze the development trend, research hotspots, and future development direction on the treatment of neuropathic pain (NP) with spinal cord stimulation through bibliometric method. We extracted the literature related to the treatment of NP with spinal cord stimulation from January 2004 to December 2023 from the Web of Science database. As a result, a total of 264 articles were retrieved. By analyzing the annual published articles, authors, countries, institutions, journals, co-cited literature, and keywords, we found that the count of publication in this field has been experiencing an overall growth, and the publications within the past 5 years accounted for 42% of the total output. Experts from the United States and the UK have made significant contributions in this field and established a stable collaborative team, initially establishing an international cooperation network. Pain is the frequently cited journal in this field. The study on spinal cord stimulation therapy for NP especially the study on spinal cord stimulation therapy for back surgery failure syndrome (FBSS) and its potential mechanisms are the research hotspots in this field, while the study on novel paradigms such as high-frequency spinal cord stimulation and spinal cord burst stimulation represents the future development directions. In short, spinal cord stimulation has been an effective treatment method for NP. The novel paradigms of spinal cord stimulation are the key point of future research in this field. [ABSTRACT FROM AUTHOR]

Recent epidemiological studies suggested that proton pump inhibitor (PPI) use was associated with an increased risk of biliary tract cancer (BTC), however, confounders were not adequately controlled. Our study aimed to evaluate PPI use and subsequent risk of BTC and its subtypes in three well‐established cohorts. We conducted a pooled analysis of the subjects free of cancers in UK Biobank (n = 463 643), Nurses' Health Study (NHS, n = 80 235) and NHS II (n = 95 869). Propensity score weighted Cox models were used to estimate marginal HRs of PPIs use on BTC risk, accounting for potential confounders. We documented 284 BTC cases in UK Biobank (median follow‐up: 7.6 years), and 91 cases in NHS and NHS II cohorts (median follow‐up: 15.8 years). In UK biobank, PPI users had a 96% higher risk of BTC compared to nonusers in crude model (HR 1.96, 95% CI 1.44‐2.66), but the effect was attenuated to null after adjusting for potential confounders (HR 0.95, 95% CI 0.60‐1.49). PPI use was not associated with risk of BTC in the pooled analysis of three cohorts (HR 0.93, 95% CI 0.60‐1.43). We also observed no associations between PPI use with risk of intrahepatic (HR 1.00, 95% CI 0.49‐2.04), extrahepatic bile duct (HR 1.09, 95% CI 0.52‐2.27) and gallbladder cancers (HR 0.66, 95% CI 0.26‐1.66) in UK Biobank. In summary, regular use of PPIs was not associated with the risk of BTC and its subtypes. [ABSTRACT FROM AUTHOR]

Some studies reported that mildly elevated serum bilirubin levels were associated with decreased risk of cardiovascular disease (CVD) and diabetes. Whether these are causal relationships remains unclear. This study aims to examine the causal effects of bilirubin on CVD, diabetes and their subtypes. The data we used in this study includes individual data from the UK Biobank cohort with 331,002 white British participants, and summary data from published genome wide associations studies (GWAS) findings. We used individual data to perform logistic regression for the observational study and two-stage least squares method for the Mendelian randomization (MR) study. We also performed several traditional MR methods and MR-TRYX by summary data. The observational study supported the association relationships between bilirubin and CVD and diabetes and their subtypes. Results of MR showed strong evidence for negative causal associations of log e total bilirubin with CVD [OR 0.92, 95%CI 0.88–0.95, p -value 2.15 × 10−6], coronary heart disease [OR 0.90, 95%CI 0.85–0.96, p -value 1.54 × 10−3] and hypertensive diseases [OR 0.91, 95%CI 0.88–0.95, p -value 5.89 × 10−6], but no evidence for diabetes [OR 0.94, 95%CI 0.86–1.02, p -value 0.14] and its subtypes. We also obtained similar results for direct bilirubin. We found that blood pressure, cholesterol, C-reactive protein, alcohol and white blood cell count played important roles in the causal pathway from bilirubin to CVD. Two sample MR and sensitivity analyses showed consistent results with one sample MR. Genetically determined bilirubin was negatively associated with the risk of CVD but had no evident causal association with diabetes in the UK Biobank cohort of white British. • Genetic determined bilirubin is negatively associated with the risk of cardiovascular disease (CVD). • Bilirubin has no evident causal association with diabetes in white British. • We identified the mediators of the causal pathway from bilirubin to CVD. [ABSTRACT FROM AUTHOR]

Proton pump inhibitors (PPIs) are commonly used for gastric acid-related disorders, but their safety profile and risk stratification for high-burden diseases need further investigation. Analyzing over 2 million participants from five prospective cohorts from the US, the UK, and China, we found that PPI use correlated with increased risk of 15 leading global diseases, such as ischemic heart disease, diabetes, respiratory infections, and chronic kidney disease. These associations showed dose-response relationships and consistency across different PPI types. PPI-related absolute risks increased with baseline risks, with approximately 82% of cases occurring in those at the upper 40% of the baseline predicted risk, and only 11.5% of cases occurring in individuals at the lower 50% of the baseline risk. While statistical association does not necessarily imply causation, its potential safety concerns suggest that personalized use of PPIs through risk stratification might guide appropriate decision-making for patients, clinicians, and the public., (© 2024. The Author(s).)

Background & Aims: Proton pump inhibitors (PPIs) have a major impact on gut microbiome and immune function, which in turn, may increase the risk of inflammatory bowel disease (IBD). Our aim in this study was to evaluate PPI use and subsequent risk of IBD and subtypes (ie, Crohn's disease and ulcerative colitis)., Methods: This was a pooled analysis of the Nurses' Health Study (NHS, n = 82,869), NHS II (n = 95,141), and UK Biobank (n = 469,397). We included participants with information on personal use of PPIs and free of IBD or cancer at baseline. We evaluated hazard ratios and 95% confidence intervals (CIs) with Cox regression adjusting for lifestyle factors, PPI indications, comorbidities, and other medications., Results: We documented 271 cases of IBD (median follow-up, 12 years) in the pooled NHS cohorts and 1419 cases (median follow-up, 8.1 years) in the UK Biobank. For both pooled NHS cohorts and UK Biobank, regular use of PPIs consistently showed a significantly positive association with IBD, Crohn's disease, and ulcerative colitis risk. Combined analyses of 3 cohorts showed that regular PPI users had an increased risk of IBD as compared with nonusers (hazard ratio, 1.42; 95% CI, 1.22-1.65; number needed to harm, 3770; 95% CI, 3668-4369). Direct comparison with H2 receptor antagonist, a less potent acid suppressor, showed that PPI use was also associated with higher IBD risk (hazard ratio, 1.38; 95% CI, 1.16-1.65)., Conclusions: Regular use of PPIs was associated with an increased risk of IBD and its subtypes. The findings should be interpreted with caution because the absolute risk was low and the clinical benefits of PPIs are substantial., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Background This Mendelian randomization study aims to investigate causal associations between genetically predicted insomnia and 14 cardiovascular diseases (CVDs) as well as the potential mediator role of 17 cardiometabolic risk factors. Methods and Results Using genetic association estimates from large genome-wide association studies and UK Biobank, we performed a 2-sample Mendelian randomization analysis to estimate the associations of insomnia with 14 CVD conditions in the primary analysis. Then mediation analysis was conducted to explore the potential mediator role of 17 cardiometabolic risk factors using a network Mendelian randomization design. After correcting for multiple testing, genetically predicted insomnia was consistent significantly positively associated with 9 of 14 CVDs, those odds ratios ranged from 1.13 (95% CI, 1.08-1.18) for atrial fibrillation to 1.24 (95% CI, 1.16-1.32) for heart failure. Moreover, genetically predicted insomnia was consistently associated with higher body mass index, triglycerides, and lower high-density lipoprotein cholesterol, each of which may act as a mediator in the causal pathway from insomnia to several CVD outcomes. Additionally, we found very little evidence to support a causal link between insomnia with abdominal aortic aneurysm, thoracic aortic aneurysm, total cholesterol, low-density lipoprotein cholesterol, glycemic traits, renal function, and heart rate increase during exercise. Finally, we found no evidence of causal associations of genetically predicted body mass index, high-density lipoprotein cholesterol, or triglycerides on insomnia. Conclusions This study provides evidence that insomnia is associated with 9 of 14 CVD outcomes, some of which may be partially mediated by 1 or more of higher body mass index, triglycerides, and lower high-density lipoprotein cholesterol.