scholarly journals Associations between vitamin D receptor genetic variants and tuberculosis: a meta-analysis

2019 ◽  
Vol 25 (5) ◽  
pp. 305-313
Author(s):  
Xun Xu ◽  
Minghao Shen

We performed a meta-analysis to evaluate potential associations between vitamin D receptor ( VDR) genetic variants and tuberculosis (TB). Systematic literature research was conducted in PubMed, Web of Science, and Embase. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) to estimate strength of associations in all possible genetic models, and P values ≤ 0.05 were considered to be statistically significant. In total, 42 studies were enrolled for analyses. Pooled overall analyses suggested that VDR rs1544410 (dominant model: P = 0.02; allele model: P = 0.03) and rs731236 (dominant model: P = 0.04; recessive model: P = 0.02; allele model: P = 0.01) variants were significantly associated with TB. Further subgroup analyses by ethnicity revealed that rs1544410 (dominant and allele models) and rs731236 (dominant, recessive, and allele models) variants were both significantly associated with TB in South Asians. When we stratified data by type of disease, positive results were detected for rs7975232 variant in EPTB (dominant, recessive, over-dominant, and allele models) subgroup, and for rs2228570 variant in PTB (dominant, recessive, and allele models) and EPTB (dominant, recessive, over-dominant, and allele models) subgroups. Our meta-analysis supported that rs7975232, rs1544410, rs2228570, and rs731236 variants might serve as genetic biomarkers of certain types of TB.

2021 ◽  
Author(s):  
Upendra Yadav ◽  
Pradeep Kumar ◽  
Vandana Rai

Abstract Background: Tuberculosis is one of the top ten causes of deaths worldwide. The deficiency of vitamin D was reported to be associated with the increased susceptibility of tuberculosis. Various previous reports were published to check the association of FokI polymorphism of the vitamin D receptor gene with tuberculosis risk. But their results were inconsistent so, we performed a meta-analysis to know the exact relation of the two.Methods: Different databases were screened up to November, 2020 with the keywords “Vitamin D receptor”, “VDR”, and “FokI”, along with “Tuberculosis” and “TB” to find the suitable articles. All the statistical analyses were performed by the Open Meta-Analyst program and all p-values were two-tailed with a significance level of 0.05.Results: No statistically significant association was observed in the allele contrast model (ORfvs.F= 1.11, 95%CI= 0.99-1.24, p= 0.05, I2= 73.46%), in the dominant model (ORff+Ffvs.FF= 1.11, 95%CI= 0.96-1.28, p= 0.14, I2= 71.39%), and in the co-dominant model (ORFfvs.FF= 1.05, 95%CI= 0.92-1.21, p= 0.41, I2= 65.97%). However, a significant association was found in the homozygote model (ORffvs.FF= 1.32, 95%CI= 1.03-1.69, p= 0.02, I2= 67.02%) and in the recessive model (ORFF+Ff vs.ff= 1.26, 95%CI= 1.03-1.54, p= 0.02, I2= 58.01%). Further analysis was performed on the bases of the ethnicity. In Asian population a significant association was found in the homozygote model (ORffvs.FF= 1.57, 95%CI= 1.12-2.21, p= 0.008, I2= 70.37%) and in the recessive model (ORFF+Ff vs.ff= 1.43, 95%CI= 1.08-1.89, p= 0.01, I2= 63.13%).Conclusion: In conclusion, a significant association of FokI with tuberculosis susceptibility was found in the overall analysis and in the Asian population.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Sai Liu

Abstract Background Gestational diabetes mellitus (GDM) is a common disease during pregnancy. The association of vitamin D receptor (VDR) polymorphisms with GDM is still controversial. This study aimed to assess the associations between VDR polymorphisms and GDM risk. Methods We searched Cochrane Library, PubMed, and Embase electronic database for all eligible studies published from Jan 1, 1980 to December 31, 2020 to conduct a Meta-analysis. We analyzed four VDR polymorphisms: BsmI (rs1544410), ApaI (rs7975232), TaqI (rs731236), and FokI (rs2228570). Inclusion Criteria: (1) The data can be evaluated; (2) case–control study; and (3) meeting the Hardy–Weinberg’s law. Exclusion criteria: (1) Insufficient or extractable data; (2) Severe publication bias in the data; and (3) duplicate publications. We eventually included 15 studies in seven articles, including 2207 cases and 2706 controls. Results We eventually included 15 studies in seven articles, including 2207 cases and 2706 controls. The data showed that ApaI (rs7975232) VDR gene polymorphism was related with the risk of GDM for the comparison of CC vs AA and recessive model in overall population and FokI (rs2228570) VDR gene polymorphism was associated with the risk of GDM for recessive model in overall population. BsmI (rs1544410) polymorphism was not related with the risk of GDM in overall population. However, in the analysis of subgroups grouped by race, BsmI (rs1544410) has certain correlations. And, the data suggested the TaqI (rs731236) polymorphism was not associated with GDM. Conclusion Based on the meta-analysis, VDR ApaI (rs7975232) and FokI (rs2228570) polymorphisms increase susceptibility to GDM. In the future, it can be used to diagnose and screen molecular biomarkers for GDM patients.


2020 ◽  
Vol 26 (5) ◽  
pp. 398-402
Author(s):  
Haibo Ge ◽  
Shi Chen ◽  
Jia Zhu

This meta-analysis was conducted to assess the consistency and strength of the relationship between polymorphism of IL-2 -330T/G and susceptibility to pulmonary tuberculosis (TB). PubMed, Web of Knowledge and CNKI were searched to find eligible studies about the relationship between IL-2 -330T/G polymorphism and susceptibility to pulmonary TB. A total of eight studies comprising 971 cases and 1519 controls were grouped together for the purpose of elucidating the relationship between polymorphism of IL-2 -330T/G and pulmonary TB susceptibility. The allele model (G vs. T: odds ratio (OR) = 1.34; 95% confidence interval (CI) 1.05–1.71, Phet = 0.001) and the recessive model (GG+GT vs. TT: OR = 1.60; 95% CI 1.08–2.38, Phet = 0.0001) showed an increased risk of development of pulmonary TB. However, the homozygous model (GG vs. TT: OR = 1.74; 95% CI 0.98–3.09, Phet = 0.0005) and the dominant model (GG vs. TT + TG: OR = 1.30; 95% CI = 0.80-2.14, Phet =  0.001) failed to show an increased incidence of pulmonary TB. When analysis was stratified by ethnicity, no obvious associations were identified in the Caucasian subgroup under all four genetic models. Additionally, heterogeneity disappeared in the analysis of Caucasian subgroup. Our combined data suggested that there was no association between IL-2 -330T/G polymorphism and pulmonary TB among Caucasians.


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.


2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Xiaoliang Guo ◽  
Chenxi Li ◽  
Jiawei Wu ◽  
Qingbu Mei ◽  
Chang Liu ◽  
...  

Abstract Tumor necrosis factor-α (TNF-α) is involved in insulin resistance and has long been a candidate gene implicated in type 2 diabetes mellitus (T2DM), however the association between TNF-α polymorphisms -308G/A and -238G/A and T2DM remains controversial. The present study sought to verify associations between these polymorphisms and T2DM susceptibility using a meta-analysis approach. A total of 49 case–control studies were selected up to October 2018. Statistical analyses were performed by STATA 15.0 software. The odds ratios (ORs) and 95% confidence intervals were calculated to estimate associations. Meta-analyses revealed significant associations between TNF-α −308G/A and T2DM in the allele model (P=0.000); the dominant model (P=0.000); the recessive model (P=0.001); the overdominant model (P=0.008) and the codominant model (P=0.000). Subgroup analyses also showed associations in the allele model (P=0.006); the dominant model (P=0.004) and the overdominant model (P=0.005) in the Caucasian and in the allele model (P=0.007); the dominant model (P=0.014); the recessive model (P=0.000) and the codominant model (P=0.000) in the Asian. There were no associations between TNF-α −238G/A and T2DM in the overall and subgroup populations. Meta-regression, sensitivity analysis and publication bias analysis confirmed that results and data were statistically robust. Our meta-analysis suggests that TNF-α −308G/A is a risk factor for T2DM in Caucasian and Asian populations. It also indicates that TNF-α −238G/A may not be a risk factor for T2DM. More comprehensive studies will be required to confirm these associations.


2021 ◽  
Author(s):  
Zhihua Hu ◽  
Shaowen Cheng ◽  
Xini Liu ◽  
Lina Xian ◽  
Xinyuan Liang ◽  
...  

Abstract Objective To assess the association between the Mannose-binding lectin (MBL) gene polymorphism and the susceptibility to sepsis using a meta-analysis.Methods The publications were searched on PubMed, Embase, and Web of Science databases up to December 1, 2019 for relevant literature. Results A total of 32 studies (21 adult and 11 pediatric studies) were selected for analysis. Overall, in the three models of MBL +54 A/B gene polymorphisms, namely the dominant model BB + AB vs. AA (p = 0.03), the recessive model BB vs. AB + AA (p < 0.00001), and the allele model B vs. A (p = 0.04), MBL +54A/B was significantly related to the risk of sepsis. In the adult group, the MBL A/O gene polymorphism was associated with the risk of sepsis in the dominant model AO + OO vs. AA (p = 0.006) as well as in the allele model O vs. A (p = 0.04). The MBL +54A/B gene polymorphism was significantly related to the risk of sepsis in the recessive model and, therefore, may increase the risk of sepsis. In the pediatric group, no polymorphic loci were significantly associated with sepsis in any of the three models. The results of the publication bias test demonstrated no publication bias in an unadjusted estimate of the relationship between MBL A/O and -211Y/X gene polymorphism and sepsis.


2019 ◽  
Vol 34 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Zongsheng Huang ◽  
Xianwen Guo ◽  
Guo Zhang ◽  
Liexin Liang ◽  
Bing Nong

Purpose: The correlation between patatin-like phospholipase domain-containing protein 3 ( PNPLA3) rs738409 polymorphism and hepatocellular carcinoma was investigated by several pilot studies, but the results of these studies were controversial. Therefore, we performed this study to better assess the relationship between PNPLA3 rs738409 polymorphism and the likelihood of hepatocellular carcinoma. Methods: Eligible studies were searched in PubMed, Medline, EMBASE, and Web of Science. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the relationship between PNPLA3 rs738409 polymorphism and hepatocellular carcinoma. Results: A total of 17 studies with 10,330 participants were analyzed. A significant association with the likelihood of hepatocellular carcinoma was detected for the PNPLA3 rs738409 polymorphism in dominant ( P = 0.0001; OR 0.66; 95% CI 0.53, 0.82), recessive ( P < 0.0001; OR 2.32; 95% CI 1.76, 3.06) and allele ( P < 0.0001; OR 0.64; 95% CI 0.53, 0.77) comparisons. Further subgroup analyses revealed that the PNPLA3 rs738409 polymorphism was significantly associated with the likelihood of hepatocellular carcinoma in Caucasians (dominant model: P < 0.0001, OR 0.57, 95% CI 0.45, 0.71; recessive model: P < 0.0001, OR 2.74, 95% CI 2.02, 3.71; allele model: P < 0.0001, OR 0.56, 95% CI 0.46, 0.67). However, no positive results were detected in Asians. Conclusions: Our findings indicated that the PNPLA3 rs738409 polymorphism may serve as a potential biological marker of hepatocellular carcinoma in Caucasians.


2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Ming Ming Yang ◽  
Jun Wang ◽  
Jiao Jie Fan ◽  
Tsz Kin Ng ◽  
Dian Jun Sun ◽  
...  

Leptin is a hormone protein regulating food intake and energy expenditure. A number of studies have evaluated the genetic effect of leptin (LEP) and leptin receptor (LEPR) genes on T2DM. This study aimed to investigate the association between these gene polymorphisms and T2DM by a systematic review and meta-analysis. Published studies were identified through extensive search in PubMed and EMBASE. A total of 5143 T2DM cases and 5021 controls from 14 articles were included in this study. Five functional variants inLEPRwere well evaluated. Meta-analysis showed that rs1137101 (p.R223Q) was significantly associated with T2DM in all genetic models: allele model (OR = 1.27, 95% confidence interval (CI) = 1.13–1.42), dominant model (OR = 1.19, 95% CI = 1.05–1.35), homozygote model (OR = 1.82, 95% CI = 1.38–2.39), and recessive model (OR = 1.75, 95% CI = 1.35–2.28), with minimal heterogeneity and no indication of publication bias. Similar associations with T2DM were also found for rs62589000 (p.P1019P) and 3′UTR ins/del, although the data was obtained from a small number of studies. For the other two polymorphisms rs1137100 (p.R109K) and rs8179183 (p.K656N), they were not significantly associated with T2DM. Our results provide robust evidences for the genetic association of rs1137101 (p.R223Q) inLEPRwith T2DM susceptibility.


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