Relationship between peripheral arterial occlusive disease (PAOD) and chronic Chlamydophila (Chlamydia) pneumoniae infection

2005 ◽  
Vol 93 (06) ◽  
pp. 1153-1160 ◽  
Author(s):  
José Gutiérrez ◽  
Juan de Dios Luna ◽  
José Linares ◽  
María del Rosario Montes ◽  
Emilia Quesada ◽  
...  

SummaryWe carried out a meta-analysis of observational case-control studies published before May 2004 to assess the degree of association between Chlamydophila pneumoniae (Cp) infection and PAOD. A search of the Medline database was performed using atherosclerosis and "Chlamyd* pneumoniae" as keywords. Strict criteria were applied for the selection of case studies, which had to be studies of Cp seroprevalence or of Cp detection in patients versus controls. Forty-three published studies that met these criteria were selected. An association between PAOD and Cp was revealed by immunohistochemical analysis (OR=15.4, 95%CI=5.0–46.9) and nested PCR studies of arterial biopsies (OR=4.3, 95%CI=1.8–10), by PCR study of non-arterial samples (OR=2.9, 95%CI=1.2–7.0), by other direct-detection tests (OR=16.7, 95%CI=7.0–39.8), and by ELISA and MIF tests to detect high IgG (OR=2, 95%CI=1.1–3.5 and OR=1.7, 95%CI=1.0–2.9, respectively) and IgA (OR=1.9, 95%CI=1.1–3.4 and OR=1.5, 95%CI=1.1–2.0, respectively) titers. No significant association was found in simple PCR studies of arterial biopsies, MIF tests to detect low IgG titers or IgM, or ELISA studies to detect IgM. According to this review, the association between Cp infection and PAOD depends on the analytical method adopted. Establishing a relationship between Cp and PAOD will require a case-control study with an adequate number of cases and samples that uses a combination of direct and indirect techniques to identify the presence of the bacterium in different types of sample from the same subjects, correlating the results with the activity of the disease.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuen-Fann Ng ◽  
Ebonne Ng ◽  
Ee-Wei Lim ◽  
Kumar M. Prakash ◽  
Louis C. S. Tan ◽  
...  

AbstractWe evaluate the association of hypertension with PD in an Asian population and performed a meta-analysis on similar studies to address the effect of hypertension on PD risk. A matched case-control study involving 1342 Chinese subjects (671 PD and 671 age and gender-matched controls (with a mean age of 63.9 ± 9.7 and 63.5 ± 9.8 years, and identical proportion of gender distribution) was conducted. Hypertension increases PD risk by 1.9 times [OR 1.86 (1.46–2.38)]. The literature search identified 618 studies initially; however, only three matched case-control studies (all in Caucasians) met the inclusion criteria for meta-analysis. Overall analysis showed that hypertension decreases PD risk by 0.2 times [OR 0.80 (0.66–0.96)]. Hypertension increases PD risk by 1.9 times in our Asian population. However, a meta-analysis comprising of Caucasian populations showed a protective effect of hypertension suggesting that ethnic differences or other genetic or environmental factors may contribute to the divergent observation. Early diagnosis and treatment of hypertension may potentially reduce the risk of PD, at least in our population.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Seoung-Jin Hong ◽  
Sang Wook Kang ◽  
Su Kang Kim ◽  
Young Sik Kim ◽  
Ju Yeon Ban

Background. Interleukin-1β(IL-1β) plays an important role as a mediator of various inflammatory responses in chronic periodontitis. Several studies have investigated the potential relationship between IL-1βpolymorphism (rs16944) and susceptibility to chronic periodontitis; inflammatory process is involved, but conclusions is still controversial.Objective. The aim of this study was to determine whether the IL-1βpolymorphism (rs16944) is associated with susceptibility to chronic periodontitis.Material and Methods. For the case-control study, 51 patients with chronic periodontitis and 33 healthy control patients were recruited in the study. Genotyping was conducted by direct sequencing. SNPStats and SPSS 18.0 were used for the analysis of genetic data and to evaluate odds ratios, 95% confidence intervals, andPvalues; logistic regression models were used. And to perform meta-analysis, studies about IL-1βpolymorphism (rs16944) and chronic periodontitis were searched in PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases until July 2017.Results. In our case-control study, no significant relationship was revealed between IL-1βpolymorphism (rs16944) and chronic periodontitis (P>0.05in each model). When combined with the previous studies in the meta-analysis, the result was not associated with chronic periodontitis in any of the models (CC vs. CT + TT: OR = 0.97, 95% CI = 0.762–1.246; CC + CT vs. TT: OR = 0.90, 95% CI = 0.658–1.232; and C vs. T: OR = 0.93, 95% CI = 0.774–1.128). The subgroup analysis stratified by ethnicity showed a weak association between the IL-1βpolymorphism (rs16944) and chronic periodontitis in the Caucasian population (recessive model, OR = 1.34, 95% CI = 1.017–1.758,P=0.037).Conclusion. Evidences from a case-control study and the meta-analysis suggest that IL-1βpolymorphism (rs16944) is not associated with susceptibility to chronic periodontitis.


2021 ◽  
Vol 41 (1) ◽  
Author(s):  
Jiakai Jiang ◽  
Sheng Zhang ◽  
Weifeng Tang ◽  
Zhiyuan Qiu

Abstract Previous studies suggested that miR-146a rs2910164 (C/G) locus was predicted to influence the risk of cancer. However, the relationship of miR-146a rs2910164 locus with colorectal cancer (CRC) susceptibility was controversial. We recruited 1003 CRC patients and 1303 controls, and performed a case–control study to clarify the correlation of miR-146a rs2910164 locus with CRC risk. Subsequently, a comprehensive meta-analysis was conducted to verify our findings. In the case–control study, we suggested that miR-146a rs2910164 variants did not alter CRC risk (CG vs. CC: adjusted P=0.465; GG vs. CC: adjusted P=0.436, CG/GG vs. CC: adjusted P=0.387 and GG vs. CC/CG: adjusted P=0.589), even in subgroup analysis. Next, we conducted a pooled-analysis to identify the correlation of miR-146a rs2910164 locus with CRC risk. In this pooled-analysis, 7947 CRC cases and 12,168 controls were included. We found that miR-146a rs2910164 polymorphism did not influence the risk of CRC (G vs. C: P=0.537; GG vs. CC: P=0.517, CG/GG vs. CC: P=0.520 and GG vs. CC/CG: P=0.167). Our findings suggest that miR-146a rs2910164 C/G polymorphism is not correlated with the susceptibility of CRC. In the future, more case–control studies are needed to confirm our results.


PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1646
Author(s):  
Qian He ◽  
Zheng-ce Wan ◽  
Xiao-bing Xu ◽  
Jing Wu ◽  
Guang-lian Xiong

Background.Several kinds of foods are hypothesized to be potential factors contributing to the variation of prostate cancer (PCa) incidence. But the effect of poultry on PCa is still inconsistent and no quantitative assessment has been published up to date. So we conducted this meta-analysis to clarify the association between them.Materials and Methods. We conducted a literature search of PubMed and Embase for studies examining the association between poultry consumption and PCa up to June, 2015. Pooled risk ratio (RR) and corresponding 95% confidence interval (CI) of the highest versus lowest poultry consumption categories were calculated by fixed-effect model or random-effect model.Results.A total of 27 (12 cohort and 15 case-control) studies comprising 23,703 cases and 469,986 noncases were eligible for inclusion. The summary RR of total PCa incidence was 1.03 (95% CI [0.95–1.11]) for the highest versus lowest categories of poultry intake. The heterogeneity between studies was not statistically significant (P= 0.768,I2= 28.5%). Synthesized analysis of 11 studies on high stage PCa and 8 studies on chicken exposure also demonstrated null association. We also did not obtain significant association in the subgroup of cohort study (RR = 1.04, 95% CI [0.98–1.10]), as well as in the subgroups of population-based case-control study and hospital-based case-control study. Then the studies were divided into three geographic groups: Western countries, Asia and South America. The pooled RRs in these areas did not reveal statistically significant association between poultry and PCa.Conclusions.This meta-analysis suggests no association between poultry consumption and PCa risk. Further well-designed studies are warranted to confirm the result.


2014 ◽  
Author(s):  
Bianca Souza ◽  
Leticia Brondani ◽  
Tais Assmann ◽  
Ana Paula Boucas ◽  
Andrea Carla Bauer ◽  
...  

2020 ◽  
Vol 17 (2) ◽  
pp. 105-111
Author(s):  
Haitao Liu ◽  
Wei Ge ◽  
Wei Chen ◽  
Xue Kong ◽  
Weiming Jian ◽  
...  

Objectives: Previous case-control studies have focused on the relationship between ALDH2 gene polymorphism and late-onset Alzheimer's Disease (LOAD), but no definite unified conclusion has been reached. Therefore, the correlation between ALDH2 Glu504Lys polymorphism and LOAD remains controversial. To analyze the correlation between ALDH2 polymorphism and the risk of LOAD, we implemented this up-to-date meta-analysis to assess the probable association. Methods: Studies were searched through China National Knowledge Infrastructure (CNKI), VIP Database for Chinese Technical Periodicals, China Biology Medicine, PubMed, Cochrane Library, Clinical- Trials.gov, Embase, and MEDLINE from January 1, 1994 to December 31, 2018, without any restrictions on language and ethnicity. Results: Five studies of 1057 LOAD patients and 1136 healthy controls met our criteria for the analysis. Statistically, the ALDH2 GA/AA genotype was not linked with raising LOAD risk (odds ratio (OR) = 1.48, 95% confidence interval (CI) = 0.96-2.28, p = 0.07). In subgroup analysis, the phenomenon that men with ALDH2*2 had higher risk for LOAD (OR = 1.72, 95%CI = 1.10-2.67, p = 0.02) was observed. Conclusions: This study comprehends only five existing case-control studies and the result is negative. The positive trend might appear when the sample size is enlarged. In the future, more large-scale casecontrol or cohort studies should be done to enhance the association between ALDH2 polymorphism and AD or other neurodegenerative diseases.


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