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Disease Markers
Volume 23, Issue 3, Pages 161-166

Lipoprotein Lipase Gene PvuII Polymorphism Serum Lipids and Risk for Coronary Artery Disease: Meta-Analysis

Penbe Cagatay,1 Belgin Susleyici-Duman,2 and Cavlan Ciftci3

1Istanbul University, Cerrahpasa Faculty of Medicine Department of Biostatistics, Istanbul, Turkey
2Istanbul Science University Medical Faculty, Department of Medical Biology and Genetics, Istanbul, Turkey
3Istanbul Science University Medical Faculty, Department of Cardiology, Istanbul, Turkey

Received 13 April 2007; Accepted 13 April 2007

Copyright © 2007 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Our aim was to determine whether lipoprotein lipase gene PvuII polymorphism can be considered as an independent risk factor for coronary artery disease (CAD) by conducting a meta-analysis of all available published trials, including our own study. In 7 seperate studies, 3289 subjects were screened for this substitution; meta-analysis included only some of these individuals. Among the 7 studies, 6 were performed on white subjects, whereas 1 was on patients with Saudi Arabic descent.Subgroup analysis indicated that individuals with PvuII substitution does not have an increased risk for CAD. The LPL-PvuII genotype and allele frequency distributions did not differ significantly between CAD patients and healthy controls. There was no difference in the distribution of LPL-PvuII genotypes between the healthy subjects and the patients with CAD. However, no significant differences in lipid variables (triglyceride and HDL-cholesterol) were determined for the PvuII polymorphisms in the patients with CAD. No significant differences were found in serum triglyceride and HDL-cholesterol levels for LPL-PvuII genotypes when the control and CAD groups were pooled. In conclusion, LPL-Pvu II polymorphism cannot be used as independent genetic risk factor for CAD.