Tags

Type your tag names separated by a space and hit enter

Meta-analysis for the Association of Apolipoprotein E ε2/ε3/ε4 Polymorphism with Coronary Heart Disease.
Chin Med J (Engl). 2015 May 20; 128(10):1391-8.CM

Abstract

BACKGROUND

Coronary heart disease (CHD) is a multifactorial disease and is thought to have a polygenic basis. Apolipoprotein E (APOE) gene is one such candidate with its common ε2/ε3/ε4 polymorphism in CHD. In recent years, numerous case-control studies have investigated the relationship of APOE polymorphism with CHD risk. However, the results are confusing.

METHODS

To clarify this point, we undertook a meta-analysis based on 14 published studies including 5746 CHD cases and 19,120 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were assessed for association using a random-effects or fixed-effects model using STATA version 10 (StataCorp LP, College Station, TX, USA).

RESULTS

Overall, the analysis showed that carriers of APOE ε2 allele decreased risk for CHD (ε2 allele vs. ε3 allele: OR = 0.82, 95% CI: 0.75-0.90, P < 0.001; ε2 carriers vs. ε3 carriers: OR = 0.81, 95% CI: 0.73-0.89, P < 0.001), compared with those carrying ε3 allele, especially in Caucasian population. However, those with ε4 allele had a significant increased risk for CHD (ε4 allele vs. ε3 allele: OR = 1.34, 95% CI: 1.15-1.57, P < 0.001), especially in Mongoloid population. Potential publication bias was observed in the genetic model of ε4 versus ε3, but the results might not be affected deeply by the publication bias. When we accounted for publication bias using the trim and fill method, the results were not materially alerted, suggesting the stability of our results.

CONCLUSIONS

Taken together, our meta-analysis supported a genetic association between APOE gene and CHD. ε4 increased the risk of CHD, whereas ε2 decreased the risk of CHD.

Authors+Show Affiliations

No affiliation info availableDepartment of Cardiovascular Disease, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Meta-Analysis
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25963363

Citation

Zhang, Yong, et al. "Meta-analysis for the Association of Apolipoprotein E Ε2/ε3/ε4 Polymorphism With Coronary Heart Disease." Chinese Medical Journal, vol. 128, no. 10, 2015, pp. 1391-8.
Zhang Y, Tang HQ, Peng WJ, et al. Meta-analysis for the Association of Apolipoprotein E ε2/ε3/ε4 Polymorphism with Coronary Heart Disease. Chin Med J (Engl). 2015;128(10):1391-8.
Zhang, Y., Tang, H. Q., Peng, W. J., Zhang, B. B., & Liu, M. (2015). Meta-analysis for the Association of Apolipoprotein E ε2/ε3/ε4 Polymorphism with Coronary Heart Disease. Chinese Medical Journal, 128(10), 1391-8. https://doi.org/10.4103/0366-6999.156803
Zhang Y, et al. Meta-analysis for the Association of Apolipoprotein E Ε2/ε3/ε4 Polymorphism With Coronary Heart Disease. Chin Med J (Engl). 2015 May 20;128(10):1391-8. PubMed PMID: 25963363.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Meta-analysis for the Association of Apolipoprotein E ε2/ε3/ε4 Polymorphism with Coronary Heart Disease. AU - Zhang,Yong, AU - Tang,Hai-Qin, AU - Peng,Wen-Jia, AU - Zhang,Bing-Bing, AU - Liu,Ming, PY - 2015/5/13/entrez PY - 2015/5/13/pubmed PY - 2016/3/16/medline SP - 1391 EP - 8 JF - Chinese medical journal JO - Chin Med J (Engl) VL - 128 IS - 10 N2 - BACKGROUND: Coronary heart disease (CHD) is a multifactorial disease and is thought to have a polygenic basis. Apolipoprotein E (APOE) gene is one such candidate with its common ε2/ε3/ε4 polymorphism in CHD. In recent years, numerous case-control studies have investigated the relationship of APOE polymorphism with CHD risk. However, the results are confusing. METHODS: To clarify this point, we undertook a meta-analysis based on 14 published studies including 5746 CHD cases and 19,120 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were assessed for association using a random-effects or fixed-effects model using STATA version 10 (StataCorp LP, College Station, TX, USA). RESULTS: Overall, the analysis showed that carriers of APOE ε2 allele decreased risk for CHD (ε2 allele vs. ε3 allele: OR = 0.82, 95% CI: 0.75-0.90, P < 0.001; ε2 carriers vs. ε3 carriers: OR = 0.81, 95% CI: 0.73-0.89, P < 0.001), compared with those carrying ε3 allele, especially in Caucasian population. However, those with ε4 allele had a significant increased risk for CHD (ε4 allele vs. ε3 allele: OR = 1.34, 95% CI: 1.15-1.57, P < 0.001), especially in Mongoloid population. Potential publication bias was observed in the genetic model of ε4 versus ε3, but the results might not be affected deeply by the publication bias. When we accounted for publication bias using the trim and fill method, the results were not materially alerted, suggesting the stability of our results. CONCLUSIONS: Taken together, our meta-analysis supported a genetic association between APOE gene and CHD. ε4 increased the risk of CHD, whereas ε2 decreased the risk of CHD. SN - 2542-5641 UR - https://www.unboundmedicine.com/medline/citation/25963363/Meta_analysis_for_the_Association_of_Apolipoprotein_E_ε2/ε3/ε4_Polymorphism_with_Coronary_Heart_Disease_ L2 - https://doi.org/10.4103/0366-6999.156803 DB - PRIME DP - Unbound Medicine ER -