scholarly journals Association between the interleukin (IL)-17A rs2275913 polymorphism and rheumatoid arthritis susceptibility: a meta-analysis and trial sequential analysis

2021 ◽  
Vol 49 (10) ◽  
pp. 030006052110532
Author(s):  
Ping Chen ◽  
Yuhao Li ◽  
Liangliang Li ◽  
Guixin Zhang ◽  
Feng Zhang ◽  
...  

Objective This meta-analysis was conducted to investigate the relationship between the interleukin (IL)-17A rs2275913 polymorphism and rheumatoid arthritis (RA) susceptibility. Methods Eligible studies were retrieved from PubMed, Embase, and Web of Science. The fixed- or random-effects model was used to calculate the pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) on the basis of heterogeneity. Results Overall, 11 studies containing 4019 RA patients and 4137 controls were included in this meta-analysis. The results suggested a significant association between the IL-17A rs2275913 polymorphism and RA susceptibility in the overall population (allelic model A vs. G: OR = 0.89, 95%CI: 0.83–0.95; heterozygote model GA vs. GG: OR = 0.87, 95%CI: 0.78–0.96; homozygote model AA vs. GG: OR = 0.82, 95%CI: 0.71–0.96; dominant model GA + AA vs. GG: OR = 0.86, 95%CI: 0.78–0.94). In the subgroup analyses, the IL-17A rs2275913 polymorphism was significantly associated with RA risk in Europeans (allelic model A vs. G: OR = 0.87, 95%CI: 0.78–0.97; heterozygote model GA vs. GG: OR = 0.79, 95%CI: 0.68–0.93; dominant model GA + AA vs. GG: OR = 0.79, 95%CI: 0.68–0.92), but not in Africans or Americans. Conclusion This study suggests that the IL-17A rs2275913 polymorphism is significantly associated with RA susceptibility in Europeans. INPLASY registration number: INPLASY202170056.

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Nisha Thakur ◽  
Suchitra Kumari ◽  
Ravi Mehrotra

Introduction: Association between Cyclin D1 (CCND1) single nucleotide polymorphism (SNP) rs9344 and cancer risk is paradoxical. Thus, we performed a meta-analysis to explore the association between CCND1 variant and overall cancer risk in Indian population. Methods: Data from 12 published studies including 3739 subjects were collected using Pubmed and Embase. RevMan (Review Manager) 5.3 was used to perform the meta-analysis. OR with 95%CI were calculated to establish the association. Results: Overall, the cumulative findings demonstrated that CCND1 polymorphism (rs9344) was not significantly associated with cancer risk in all the genetic models studied (dominant model: GG vs GA+AA: OR (95%CI) = 0.81 (0.60–1.09), P=0.17; recessive model: GG+GA vs AA: OR (95%CI) = 1.23 (0.96–1.59), P=0.11; co-dominant model: GG vs AA: OR (95%CI) = 1.35 (0.93–1.97), P=0.12; co-dominant model: (GG vs GA: OR (95%CI) = 1.16 (0.85–1.59), P=0.34; allelic model: A vs G: OR (95%CI) = 1.20 (1.14–2.85), P=0.23; allelic model: G vs A: OR (95%CI) = 0.83 (0.62–1.12), P=0.23). Subgroup analysis according to cancer types presented significant association of CCND1 polymorphism and increased breast cancer risk in dominant model (GG vs GA+AA: OR = 2.75, 95%CI = 1.54–4.90, P=0.0006) and allelic model (G vs A: OR = 1.63, 95%CI = 1.22–2.19, P=0.001). An increased esophageal cancer risk in recessive model (GG+GA vs AA: OR = 1.51, 95%CI = 1.05–2.16, P=0.03) and co-dominant model (GG vs AA: OR = 2.51, 95%CI = 1.10–5.71, P=0.03) was detected. A higher risk for colorectal cancer was detected under both the co-dominant models (GG vs AA: OR = 2.46, 95%CI = 1.34–4.51, P=0.004 and GG vs GA: OR = 1.74, 95%CI = 1.14–2.67, P=0.01). However, in case of cervical cancer risk a non-significant association was reported under the recessive model (GG+GA vs AA: OR = 1.52, 95%CI = 0.60–3.90, P=0.38) with reference to CCND1 polymorphism (rs9344). The trial sequential analysis (TSA) showed that the cumulative Z-curve neither crossed the trial sequential monitoring boundary nor reached the required information size (RIS). Thus, present meta-analysis remained inconclusive due to insufficient evidence. Conclusion:CCND1 polymorphism rs9344 may not have a role in overall cancer susceptibility in Indian population. However, this polymorphism acts as a crucial risk factor for breast, esophageal, and colorectal cancer but not for cervical cancer. Future studies with larger sample size are required to draw a reliable conclusion.


2020 ◽  
Author(s):  
Ying Wang ◽  
Hui-chang Zhuo ◽  
Jiandong Lin

Abstract Background: This meta-analysis is performed to evaluate the effects of AA on the mortality over sepsis patients, focusing on the courses and initiation of treatment as well as AA doses.Methods: Randomized controlled trials concerning sepsis patients treated with intravenous AA were included when searching the database. The meta-analysis was performed using the random (M-H heterogeneity) model to produce summary odds ratio with 95% CI. Trial sequential analysis was applied to evaluated the effect of random errors.Results: The included 12 trials enrolled a total of 1232 patients. Intravenously administration of AA could not lower 28-day mortality over sepsis patients (OR = 0.81; 95% CI (0.54-1.23); p = 0.326). Subgroup analysis demonstrated that when administrating AA alone, in a dose ≥ 10 g/d, or within 6 h of admission, the result may turn to positive (OR = 0.36; 95% CI (0.15-0.86); p = 0.020, OR = 0.50; 95% CI (0.27-0.92); p = 0.025, OR = 0.49; 95% CI (0.27-0.89); p = 0.019, relatively). The quality of evidence is moderate.Conclusion: IV AA may have no effects to lower mortality over sepsis patients. However, when administrating AA alone, in a dose ≥ 10 g/d, or within 6 h of admission, the result may turn to positive. Due to a moderate GRADE certainty of evidence, further studies are required to fully elaborate the effectiveness of AA during the management of the sepsis patients.PROSPERO registration number: CRD 42020170825. 24 Feb, 2020 retrospectively registered.


PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258789
Author(s):  
Po-Jen Hsiao ◽  
Chih-Chien Chiu ◽  
Dung-Jang Tsai ◽  
Pi-Shao Ko ◽  
Ying-Kai Chen ◽  
...  

Background Several meta-analyses of the relationship between endothelial nitric oxide synthase (eNOS) T-786C gene polymorphism and chronic kidney disease (CKD) have been published. However, the results of these studies were inconsistent, and it is undetermined whether sample sizes are sufficient to reach a definite conclusion. Objective To elucidate the relationship between T-786C and CKD by combining previous studies with our case-control sample and incorporate trial sequential analysis (TSA) to verify whether the sample size is adequate to draw a definite conclusion. Methods PubMed and Embase databases were searched for relevant articles on eNOS T-786C and CKD before February 28, 2021. TSA was also incorporated to ascertain a conclusion. A total of 558 hemodialysis cases in the case-control study was recruited from nine dialysis centers in the northern area of Taiwan in 2020. Additionally, 640 healthy subjects of the control group, with estimated glomerular filtration rate (eGFR) ≥ 60 mL/min/1.73 m2, were selected from participants of the annual elderly health examination program at the Tri-Service General Hospital. The functional analysis was based on eQTL data from GTExPortal. Results After screening with eligibility criteria, 15 papers were included and eventually combined in a meta-analysis. The result of the TSA showed that the sample size for Caucasians was adequate to ascertain the correlation between eNOS T-786C and CKD but was insufficient for Asians. Therefore, we added our case-control samples (n = 1198), though not associated with CKD (odds ratio [OR] = 1.01, 95% confidence interval [CI] = 0.69–1.46), into a meta-analysis, which supported that eNOS T-786C was significantly associated with CKD in Asians (OR = 1.39, 95% CI = 1.04–1.85) by using an adequate cumulative sample size (n = 4572) analyzed by TSA. Data of eQTL from GTEx showed that T-786C with the C minor allele exhibited relatively lower eNOS mRNA expression in whole blood, indicating the hazardous role of eNOS T-786C in CKD. Conclusions eNOS T-786C genetic polymorphism was of conclusive significance in the association with CKD among Asians in our meta-analysis. Our case-control samples play a decisive role in changing conclusions from indefinite to definite.


2021 ◽  
Author(s):  
Yuqing Wang ◽  
Fanqiang Meng ◽  
Jing Wu ◽  
Huizhong Long ◽  
Jiatian Li ◽  
...  

Abstract Background: Adipokines gene polymorphisms are speculated to have associations with the risk of osteoarthritis (OA), but evidences remain conflicting. This study therefore aimed to examine the potential associations between adipokines gene polymorphisms and OA.Methods: A systematic search was performed on PubMed, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), and Wanfang up to March 31, 2020. Meta-analysis was carried out by focusing on associations between adipokines gene polymorphisms and OA with allele model, dominant model, recessive model, homozygote model, and heterozygote model.Results: The present meta-analysis included 13 studies containing 3,661 OA patients and 4,864 controls for analysis. Significant associations were observed between ADIPOQ rs2241766 and OA in Asians (dominant: OR = 1.35, 95% CI 1.03-1.78; heterozygote: OR = 1.43, 95% CI 1.07-1.19), between LEPR rs1137101 and OA in the overall population (recessive: OR = 0.40, 95% CI 0.21-0.79; homozygote: OR = 0.38, 95% CI 0.18-0.79), between VISFATIN rs4730153 and OA in Asians (allele: OR = 0.58, 95% CI 0.41-0.83; dominant: OR = 0.57, 95% CI 0.39-0.83; heterozygote: OR = 0.59, 95% CI 0.40-0.86), and between VISFATIN rs16872158 and OA in Asians (allele: OR = 1.84, 95% CI 1.26-2.68; dominant: OR = 1.94, 95% CI 1.31-2.89; heterozygote: OR = 1.97, 95% CI 1.31-2.95).Conclusions: Adipokines gene polymorphisms may be associated with OA. In particular, associations were observed in ADIPOQ rs2241766, LEPR rs1137101, VISFATIN rs4730153, and VISFATIN rs16872158 in the present study. PROSPERO registration number: CRD42020187664.


BMJ Open ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. e032389 ◽  
Author(s):  
Naqash Sethi ◽  
Arushma Imran Naqash ◽  
Niklas Nielsen ◽  
Janus Christian Jakobsen

IntroductionFever is an integral part of the inflammatory response and has therefore likely a physiological role in fighting infections. Nevertheless, whether fever in itself is beneficial or harmful in adults is unknown. This protocol for a systematic review aims at identifying the beneficial and harmful effects of fever control interventions in adults.Methods and analysisThis protocol for a systematic review was conducted following the recommendations of Cochrane, GRADE and the eight-step assessment suggested by Jakobsen and colleagues for better validation of meta-analytical results in systematic reviews. We plan to include all relevant randomised clinical trials comparing any fever control intervention with placebo, sham or no intervention in adults. We plan to search CENTRAL, MEDLINE, Embase, LILACS, BIOSIS, CINAHL, Scopus and Web of Science Core Collection to identify relevant trials. Any eligible trial will be assessed and classified as either at high risk of bias or low risk of bias, and our primary conclusions will be based on trials at low risk of bias. We will perform our meta-analyses of the extracted data using Review Manager 5.3 and Trial Sequential Analysis. For all our outcomes, we will create a ‘Summary of Findings’ table based on GRADE assessments of the certainty of the evidence.Ethics and disseminationNo formal approval or review of ethics is required for this systematic review as individual patient data will not be included. This systematic review has the potential to highlight (1) whether one should believe fever to be beneficial, harmful or neither in adults; (2) the existing knowledge gaps on this topic; and (3) whether the recommendations from guidelines and daily clinical practice are correct. These results will be disseminated through publication in a leading peer-reviewed journal.PROSPERO registration numberCRD42019134006


2021 ◽  
Author(s):  
Sarah Jafrin ◽  
◽  
Md. Abdul Aziz ◽  
Mohammad Safiqul Islam

Review question / Objective: To assess the link of IL-1β rs1143634 (+3954C>T) Polymorphism with cancer. Condition being studied: The included studies must contain 1) genotypic information and detailed data of IL-1β rs1143634 (+3954C>T) polymorphism 2) case-control studies. Information sources: PubMed, Google Scholar, CNKI, Web of Science, and EMBASE.


Pathogens ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1600
Author(s):  
Hady Mohammadi ◽  
Mehrnoush Momeni Roochi ◽  
Masoud Sadeghi ◽  
Ata Garajei ◽  
Hosein Heidar ◽  
...  

Background and objective: Interleukins (ILs), as important biochemical mediators, control the host response to inflammation and are associated with bone resorption. In the present meta-analysis, we investigated the association between IL−1 polymorphisms and susceptibility to dental peri-implant disease (PID). Materials and methods: We searched Web of Science, Cochrane Library, Scopus, and PubMed/Medline databases for studies published until 9 September2021, without any restrictions. We calculated the crude OR and 95% confidence intervals (CI) to estimate the associations between IL−1 polymorphisms and PID risk in the five genetic models. We further performed the subgroup analysis, sensitivity analysis, meta-regression, trial sequential analysis, and calculated the publication bias. Results: Out of 212 retrieved records, sixteen articles were used in the meta-analysis. There was no association between IL−1A (–889), IL−1B (−511), IL−1B (+3953), and IL−1RN (VNTR) polymorphisms and the risk of dental PIDs, but there was an increased risk of IL−1B (+3954) in the patients with PIDs. In addition, an association of the composite genotype of IL−1A (−889)/IL−1B (+3953) was observed with the risk of PIDs, but not for the composite genotype of IL−1A (−889)/IL−1B (+3954). The publication year, the ethnicity, sample size, and the outcome were significantly influenced pooled estimates of some genetic models. Trial sequential analysis showed the lack of sufficient sample sizes in the studies. Conclusions: Among IL−1 polymorphisms evaluated in the meta-analysis, the composite genotype of IL−1A (−889)/IL−1B (+3953) and IL−1B (+3954) were the only polymorphisms associated with the risk of PID. The T allele and CT genotype of IL−1B (+3954) polymorphism were also associated with an elevated risk of PID.


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