ASSOCIATION BETWEEN OSTEOPROTEGERIN GENE
POLYMORPHISMS AND RISK OF CORONARY ARTERY
DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS
Jia P, Wu N, Jia D*, Sun Y*
*Corresponding Author: Professor Dalin Jia and/or Professor Yingxian Sun, Department of Cardiology, The First Affiliated
Hospital of China Medical University, 155th North Nanjing Street, Heping District, Shenyang 110001, Liaoning Province,
People’s Republic of China. Tel: +86-242-326-9477. Fax: +86-242-326-9477. Email: jdl2001@126.com and/or
yxsun@mail.cmu.edu.cn
page: 27
|
|
RESULTS
Results of the Literature Search. As shown in
Figure.1, 36 potentially eligible records were initially
identified through literature search. Thirty articles were
excluded, including seven articles that were duplicated,
five articles that were reviews, 12 articles that did not
involve CAD, four articles that did not conform to the
diagnostic criteria of CAD, one article that lacked normal
controls, and one article that did not provide sufficient data
for the distribution of the genotype. Finally, six articles
in accordance with the inclusion criteria were included in
this meta-analysis [12-16,19]. To be specific, two studies
involved the G209A polymorphism, three studies with
T245G polymorphism, three studies with T950C polymorphism,
and five studies with G1181C polymorphism. Characteristics of Included Studies. The characteristics
of the included studies are summarized in Table
1. Overall, four studies were conducted in Asians, and
the other two studies were carried out in Caucasians. The
polymerase chain reaction-restriction fragment length
polymorphism (PCR-RFLP) method was used to detect
the gene polymorphisms in five out of six studies. The
average score of NOS was at 9. The genotype distribution
of the controls in all studies was consistent with HWE.
Quantitative Data Synthesis. Meta-analysis of the
G209A polymorphism was involved with two studies consisting
of 215 CAD cases and 98 controls. There was no
association between the G209A polymorphism and the
risk of CAD when pooling all the data in the meta-analysis
(AA/AG vs. GG: OR = 1.005, 95% CI = 0.564-1.792, p
= 0.986) (Figure 2A) (Table 2). For the T245G polymorphism,
three studies with 393 CAD cases and 410 controls
were included for final meta-analysis, but the results
showed no relationship between the T245G polymorphism
and the risk of CAD either (TT/TG vs. GG: OR = 0.664,
95% CI = 0.247-1.785, p = 0.417) (Figure 2B) (Table 2).
For the T950C polymorphism, 1105 CAD cases and 906 controls were included in the meta-analysis. A significant
association was found between the T950C polymorphism
and risk of CAD under the dominant model (CC/CT vs.
TT: OR = 1.327, 95% CI = 1.090-1.617, p = 0.005) (Figure
2C), allele model (C vs. T: OR = 1.264, 95% CI = 1.108-
1.442, p <0.001), homozygote model (CC vs. TT: OR =
1.615, 95% CI = 1.242-2.100, p <0.001), recessive model
(CC vs. CT/TT: OR = 1.376, 95% CI = 1.097-1.726, p =
0.006) (Table 2). Meta-analysis of the G1181C polymorphism
was involved with five studies consisting of 1137
CAD cases and 1024 controls and the results indicated that
the G1181C polymorphism was significantly associated
with the risk of CAD under the dominant model (CC/CG
vs. GG: OR = 1.268, 95% CI = 1.064-1.511, p = 0.008)
(Figure 4D). In addition, a statistically significant association
also existed between the G1181C polymorphism and
risk of CAD under the heterozygote model (CG vs. GG:
OR = 1.243, 95% CI = 1.027-1.504, p = 0.026) (Table 2).
Sensitivity Analysis and Publication Bias. The
result of the sensitivity analysis showed that the pooled
ORs of the G209A, T245G, T950C and G1181C polymorphisms
were not considerably affected by eliminating any individual study (Figure 3). The funnel plots were symmetrical
by visual inspection (Figure 4) and Egger’s test
also suggested no publication bias (p >0.05). These results
confirmed that this meta-analysis was robust.
|
|
|
|
 |
Number 27
VOL. 27 (2), 2024 |
Number 27
VOL. 27 (1), 2024 |
Number 26
Number 26 VOL. 26(2), 2023 All in one |
Number 26
VOL. 26(2), 2023 |
Number 26
VOL. 26, 2023 Supplement |
Number 26
VOL. 26(1), 2023 |
Number 25
VOL. 25(2), 2022 |
Number 25
VOL. 25 (1), 2022 |
Number 24
VOL. 24(2), 2021 |
Number 24
VOL. 24(1), 2021 |
Number 23
VOL. 23(2), 2020 |
Number 22
VOL. 22(2), 2019 |
Number 22
VOL. 22(1), 2019 |
Number 22
VOL. 22, 2019 Supplement |
Number 21
VOL. 21(2), 2018 |
Number 21
VOL. 21 (1), 2018 |
Number 21
VOL. 21, 2018 Supplement |
Number 20
VOL. 20 (2), 2017 |
Number 20
VOL. 20 (1), 2017 |
Number 19
VOL. 19 (2), 2016 |
Number 19
VOL. 19 (1), 2016 |
Number 18
VOL. 18 (2), 2015 |
Number 18
VOL. 18 (1), 2015 |
Number 17
VOL. 17 (2), 2014 |
Number 17
VOL. 17 (1), 2014 |
Number 16
VOL. 16 (2), 2013 |
Number 16
VOL. 16 (1), 2013 |
Number 15
VOL. 15 (2), 2012 |
Number 15
VOL. 15, 2012 Supplement |
Number 15
Vol. 15 (1), 2012 |
Number 14
14 - Vol. 14 (2), 2011 |
Number 14
The 9th Balkan Congress of Medical Genetics |
Number 14
14 - Vol. 14 (1), 2011 |
Number 13
Vol. 13 (2), 2010 |
Number 13
Vol.13 (1), 2010 |
Number 12
Vol.12 (2), 2009 |
Number 12
Vol.12 (1), 2009 |
Number 11
Vol.11 (2),2008 |
Number 11
Vol.11 (1),2008 |
Number 10
Vol.10 (2), 2007 |
Number 10
10 (1),2007 |
Number 9
1&2, 2006 |
Number 9
3&4, 2006 |
Number 8
1&2, 2005 |
Number 8
3&4, 2004 |
Number 7
1&2, 2004 |
Number 6
3&4, 2003 |
Number 6
1&2, 2003 |
Number 5
3&4, 2002 |
Number 5
1&2, 2002 |
Number 4
Vol.3 (4), 2000 |
Number 4
Vol.2 (4), 1999 |
Number 4
Vol.1 (4), 1998 |
Number 4
3&4, 2001 |
Number 4
1&2, 2001 |
Number 3
Vol.3 (3), 2000 |
Number 3
Vol.2 (3), 1999 |
Number 3
Vol.1 (3), 1998 |
Number 2
Vol.3(2), 2000 |
Number 2
Vol.1 (2), 1998 |
Number 2
Vol.2 (2), 1999 |
Number 1
Vol.3 (1), 2000 |
Number 1
Vol.2 (1), 1999 |
Number 1
Vol.1 (1), 1998 |
|
|
