Lipoprotein Lipase (LPL) Polymorphism and the Risk of Coronary Artery Disease: A Meta-Analysis

Overview

Journal Int J Environ Res Public Health

Publisher MDPI

Specialties Environmental Health
Public Health

Date 2017 Mar 10

PMID 28275220

Citations 11

Authors

Li Xie

You-Mei Li

Affiliations

Soon will be listed here.

Abstract

Background: In recent years, the lipoprotein lipase (LPL) polymorphism has been extensively investigated as a potential risk factor for coronary artery disease (CAD). However, the results of these studies have been inconsistent. Therefore, we performed this meta-analysis to explore the association between LPL polymorphism and CAD risk.

Methods: The literature was searched from electronic databases such as Embase, China Biological Medicine Database, PubMed, Knowledge Infrastructure, and China National Web of Science by the key words "coronary artery disease", "lipoprotein lipase" and "polymorphism". All of the studies included in this manuscript met the inclusion and exclusion criteria. An odds ratio (OR) analysis using a 95% confidence interval (CI) was employed to assess the association of the LPL polymorphism with CAD susceptibility.

Results: We performed a meta-analysis of 14 case-control studies including HindIII, Ser447X and PvuII polymorphism. A statistically significant increase in the risk of CAD was associated with LPL HindIII polymorphism. This included HindIII H⁺H⁺ genotype (OR = 1.28, 95% CI = 1.09-1.49, = 0.002, I² = 43%) and H⁺ allele genotype (OR = 1.27, 95% CI = 1.03-1.58, = 0.03, I² = 67%). Ser447X XX genotype (OR = 2.37, 95% CI = 1.33-4.24, = 0.004, I² = 53%) was also associated with CAD risk. However, PvuII polymorphism was found to have no significant association with CAD risk.

Conclusions: LPL HindIII polymorphism was significantly associated with the risk of CAD. For Ser447X polymorphism, it was found that only XX genotype was significantly associated with CAD risk. Furthermore, PvuII polymorphism had no significant association with CAD risk. It was considered that LPL HindIII polymorphism might serve as a potential biomarker for CAD risk.

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