Citations

Background/Aims Studies have shown that nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of chronic kidney disease (CKD). However, it is unknown whether severe liver fibrosis is associated with a higher prevalence of CKD among NAFLD. We examined the diagnostic performance of noninvasive fibrosis markers in identifying prevalent CKD among NAFLD. Methods This study represents an analysis of the National Health and Nutrition Examination Survey conducted in the USA between 1988 and 1994. NAFLD was defined by ultrasonographic evidence of hepatic steatosis without other liver diseases. CKD was defined by estimated glomerular filtration rate less than 60 ml/min/1.73 m2. The presence and severity of hepatic fibrosis were determined by the NAFLD fibrosis score (NFS), FIB-4 score, APRI score, and BARD score. Multiple logistic regression was performed to generate odds ratios (ORs) and receiver operating characteristic curves were used to assess the predictive values of each marker. Results A total of 4142 individuals with NAFLD were included; 200 (4.8%) had CKD. The area under the receiver operating characteristic curves was 0.77, 0.75, 0.62, and 0.51 for the multivariable equation with FIB-4, NFS, BARD, and APRI score, respectively. Compared with patients with a low probability of developing advanced liver fibrosis, individuals with a high probability of developing fibrosis showed significantly increased odds of CKD as estimated by NFS (adjusted OR: 4.92, 95% confidence interval: 2.96–8.15) and FIB-4 (adjusted OR: 2.27, 95% confidence interval: 1.05–4.52). Conclusion Advanced liver fibrosis, defined by NFS and FIB-4 scores, is associated independently with CKD among individuals with NAFLD. FIB-4 is the best predictor of an increased risk of prevalent CKD.

Background/objective Hepatitis C virus (HCV) infection is one of the most common infections worldwide. Recent epidemiologic studies have suggested that patients with HCV infection might be at an increased risk of Parkinson’s disease. However, the data on this relationship remain inconclusive. This meta-analysis was conducted with the aim to summarize all available evidence. Patients and methods A literature search was performed using MEDLINE and EMBASE database from inception to May 2017. Studies that reported relative risks, odd ratios (ORs), or hazard ratios comparing the risk of Parkinson’s disease among HCV-infected patients versus participants without HCV infection were included. Pooled OR and 95% confidence interval were calculated using a random-effect, generic inverse variance method. Results Of 468 studies, five studies with 323 974 participants met our eligibility criteria and were included in the analysis. We found a higher risk of Parkinson’s disease among patients with chronic HCV infection compared with participants without HCV infection with the pooled OR of 1.35 (95% confidence interval: 1.19–1.52). The statistical heterogeneity of this study was insignificant (I 2=3%). The main limitation of this meta-analysis was the limited accuracy of diagnosis in the primary studies as they were coding-based studies. Conclusion This study demonstrated a higher risk of Parkinson’s disease among HCV-infected patients. Further studies are required to clarify how this risk should be addressed in the clinical picture.

AbstractBackground/ObjectivesThe risk of renal cell carcinoma (RCC) in individuals who regularly drink coffee is controversial. Several antioxidant compounds in coffee have been proposed to reduce the risk of RCC, while the findings from several studies raise concerns regarding a potential increased risk of RCC with coffee consumption.AimThis meta‐analysis aims to evaluate the association between coffee consumption and RCC.MethodsA literature search was performed using MEDLINE, EMBASE and Cochrane Database of Systematic Reviews from inception until December 2016. Studies that reported odd ratios or hazard ratios comparing the risk of RCC in individuals who consumed a significant amount of coffee (at least one cup of coffee per day) versus those who did not consume coffee were included. Pooled risk ratios (RR) and 95% confidence intervals (CI) were computed using a random‐effect, generic inverse variance method.ResultsTwenty‐two observational studies (16 case–control and 6 cohort studies) were included in our analysis to assess the association between RCC and coffee consumption. The pooled RR of RCC in individuals consuming coffee was 0.99 (95% CI, 0.89–1.11). Subgroup analyses stratified by gender showed pooled RRs of RCC of 1.15 (95% CI, 0.85–1.55) in females and 0.87 (95% CI, 0.72–1.04) in males.ConclusionsOur study demonstrates no significant association between coffee consumption and RCC. Thus, coffee consumption is likely not a risk factor for RCC. Whether coffee consumption has a potential role in reduced risk of RCC, particularly in men, requires further investigations.

Background Hyperuricemia is a significant risk factor for nonalcoholic fatty liver disease (NAFLD). It may also have an impact on the histologic severity of NAFLD. However, data on this association are limited. We conducted this meta-analysis to investigate the relationship of serum uric acid with liver histologic severity as determined by NAFLD activity score (NAS) in patients with NAFLD. Patients and methods MEDLINE and EMBASE databases were searched through August 2016 for studies that investigated the association between hyperuricemia and NAS among patients with biopsy-proven NAFLD. Pooled odds ratio and 95% confidence interval were calculated using a random-effects model (generic inverse variance method). The between-study heterogeneity of effect size was quantified using the Q statistic and I 2. Results Five observational studies with 777 NAFLD patients were identified. Patients with NAFLD who had hyperuricemia had a high NAS (defined as score of ≥5) significantly more often than did those without hyperuricemia with a pooled odds ratio of 2.17 (95% confidence interval: 1.51–3.12). The statistical heterogeneity was low, with I 2 of 16% (P heterogeneity=0.31). Conclusion In patients with NAFLD, hyperuricemia is associated with a higher degree of histological liver damage. Further studies are required to establish the role of uric acid-lowering therapy among these patients.

AbstractObjectiveThe study's aims were (1) to investigate the prevalence and (2) to assess the risk of Helicobacter pylori (H. pylori) infection in kidney transplant recipients.MethodsA comprehensive literature search was performed from inception until September 2016. Studies that reported prevalence, relative risks, odd ratios, or hazard ratios of H. pylori among kidney transplant recipients were included. Pooled risk ratios and 95% CI were calculated using a random‐effect model.ResultsEleven observational studies with 2545 kidney transplant recipients were enrolled. Between year 1990 and 2000, the estimated prevalence of H. pylori among people with kidney transplant was 50% (95% CI: 31% to 68%), with a prevalence of 46% (95% CI: 23% to 70%) in high‐income countries and 55% (95% CI: 22% to 86%) in middle‐income countries, respectively. From year 2000 to 2016, the estimated prevalence of H. pylori among people with kidney transplant was 35% (95% CI: 26% to 45%), with a prevalence of 28% (95% CI: 19% to 37%) in high‐income countries and 45% (95% CI: 38% to 51%) in middle‐income countries. Data regarding prevalence of H. pylori infection in low‐income countries were limited. The pooled RR of H. pylori in kidney transplant recipients was 0.57 (95% CI: 0.33 to 1.00) when compared to people with non‐transplant.ConclusionsThere has been a decline in prevalence of H. pylori in kidney transplant recipients with the overall estimated prevalence of H. pylori in kidney transplant recipients of 35%, particularly in both high‐income and middle‐income countries. Also, our meta‐analysis demonstrates a potential decreased risk of H. pylori infection in kidney transplant recipients compared with non‐transplant populations.

Background and Aim Peri‐procedural bridging ( PPB ) with heparin is recommended for patients with high thromboembolic risk who need to withhold antithrombotic therapy for colonoscopic polypectomy. However, little is known about the bleeding risk from heparin‐bridging therapy itself. Methods MEDLINE and EMBASE databases were searched through January 2017 for studies that compared the risk of PPB in patients who received heparin‐bridging therapy in lieu of antithrombotic agents for colonoscopic polypectomy and those who discontinued antithrombotic agents without receiving heparin. Pooled odds ratio ( OR ) and 95% confidence interval ( CI ) were calculated using a random‐effects model, generic inverse variance method. Between‐study heterogeneity was quantified using the Q statistic and I 2 . Results A total of five studies consisting of 2601 patients were identified. A significantly increased risk of PPB among bridged patients compared to non‐bridged patients was demonstrated with a pooled OR of 8.29 (95% CI , 4.96–13.87). Statistical heterogeneity was low with I 2 of 0%. Conclusion The present study demonstrated a significantly increased risk of PPB among patients who underwent colonoscopic polypectomy and received heparin‐bridging therapy in lieu of antithrombotic agents compared to patients who did not receive it.

Background Uric acid is a natural antioxidant. Previous studies have suggested a protective role of hyperuricemia against liver fibrosis among patients with nonalcoholic fatty liver disease (NAFLD). However, the results were conflicting. Methods MEDLINE and EMBASE databases were searched through August 2016 for studies that investigated the association between hyperuricemia and fibrosis stage among patients with biopsy-proven NAFLD. Pooled odds ratio and 95% confidence interval were calculated using a random-effects model, generic inverse variance method of DerSimonian and Laird. The between-study heterogeneity of effect size was quantified using the Q statistic and I 2. Results A total of five observational studies with 749 NAFLD patients were identified. Patients with NAFLD who had hyperuricemia were not significantly more likely or less likely to have advanced liver fibrosis (defined as fibrosis stage of ≥3) compared with patients with NAFLD who had normal serum uric with the pooled odds ratio of 0.72 (95% confidence interval: 0.34–1.53). The statistical heterogeneity was low with an I 2 of 22% (P heterogeneity=0.27). Conclusion Significant protective role of hyperuricemia against the development of advanced liver fibrosis in patients with NAFLD was not observed in this meta-analysis.

Background/Objectives: Helicobacter pylori (H. pylori) is the most common chronic bacterial infection. Patients with H. pylori infection may be at an increased risk of nonalcoholic fatty liver disease (NAFLD) because of chronic inflammation and insulin resistance. Several epidemiologic studies attempting to determine this risk have yielded inconsistent results. This meta-analysis was conducted with the aims to summarize all available evidence and estimate the risk of NAFLD in patients with H. pylori infection. Methods: A literature search was performed using MEDLINE and EMBASE database from inception to June 2016. Studies that reported relative risks, odd ratios, or hazard ratios comparing the risk of NAFLD among patients with H. pylori infection versus without H. pylori infection were included. Pooled odds ratios and 95% confidence intervals were calculated using a random-effect, generic inverse variance method. Results: Six studies met our eligibility criteria and were included in this analysis. We found a statistically significant increased risk of NAFLD among patients with H. pylori infection with the pooled odds ratios of 1.21 (95% confidence interval, 1.07-1.37). The statistical heterogeneity was low with an I 2 of 49%. Conclusions: A significantly increased risk of NAFLD among patients with H. pylori infection was demonstrated in this meta-analysis. Further studies are required to clarify how this risk should be addressed in clinical practice.