Background: Lipoprotein lipase (LPL) polymorphisms were suggested to be the risk factor for ischemic stroke (IS). However, controversial results were obtained. Our objective was to investigate the association of LPL… Click to show full abstract
Background: Lipoprotein lipase (LPL) polymorphisms were suggested to be the risk factor for ischemic stroke (IS). However, controversial results were obtained. Our objective was to investigate the association of LPL polymorphisms at Ser447Ter, HindIII (+/−), and PvuII (+/−) with IS risk. Methods: Literatures search were carried out on databases: PubMed, Web of science, the Cochrane database of system reviews, Chinese National Knowledge Infrastructure, and Embase. Pooled odds ratio (OR) with 95% confidence interval (CI) was calculated to detect the relationship between LPL polymorphisms and the risk of IS. Results: No significant association was detected between LPL Ser447Ter and IS in allelic, dominant, or recessive models (P > .05). Significant lower frequencies of allelic and dominant models of LPL HindIII (+/−) and PvuII (+/−) in cases were detected (HindIII (+/−): allelic model: P = .0002, OR[95%CI] = 0.80 [0.71, 0.90]; dominant model: P = 0.003, OR[95%CI] = 0.80 [0.69, 0.92]; PvuII (+/−): allelic model: P < 0.0001, OR[95%CI] = 0.75[0.65–0.86]; dominant model: P = 0.02, OR[95%CI] = 0.67[0.48–0.93]). And the recessive model of PvuII (+/−) was significantly associated with the IS risk (P = .01, OR[95%CI] = .71[0.55–0.93]). Subgroup analysis stratified by ethnicity showed that the frequencies of allelic, dominant, and recessive models of HindIII (+/−), as well as dominant model of PvuII (+/−) were significant lower in Asian cases (HindIII (+/−): allelic model: P < .00001, OR[95%CI] = 0.69 [0.59, 0.79]; dominant model: P < .0001, OR[95%CI] = 0.69 [0.58, 0.83]; recessive model: P = .005, OR[95%CI] = 0.66 [0.50, 0.89]; PvuII (+/−): dominant model: P = .0008, OR[95%CI] = 0.66 [0.51–0.84]), but not in Caucasian cases (P > .05). In addition, the frequencies of allelic and recessive models of PvuII (+/−) significantly decreased in Caucasian cases (P < .05). Conclusion: the HindIII (+/−) and PvuII (+/−), but not the Ser447Ter might be the protective factors for IS.
               
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