The HindIII and PvuII polymorphisms of lipoprotein lipase (LPL) gene reduce the risk of ischemic stroke (IS): A meta-analysis.
The HindIII and PvuII polymorphisms of lipoprotein lipase (LPL) gene reduce the risk of ischemic stroke (IS): A meta-analysis.
复制标题
脂蛋白脂肪酶（LPL）基因的印度和PVUII多态性降低了缺血性中风的风险（IS）：一项荟萃分析。
DOI：
10.1097/md.0000000000010483
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发表时间：
2018-05
期刊：
影响因子：
1.6
通讯作者：
Chen X
中科院分区：
文献类型：
--
作者：
Cao L;Li Q;Chen X
脂蛋白脂酶（LPL）基因多态性可能是缺血性脑卒中（IS）的危险因素。然而，获得了有争议的结果。我们的目的是研究LPL Ser 447 Ter、HindIII（+/−）和PvuII（+/−）多态性与IS风险的关系。检索数据库：PubMed、Web of science、科克伦系统综述数据库、中国国家知识基础设施和Embase。计算合并比值比（OR）和95%可信区间（CI），以检测LPL基因多态性与IS风险的关系。在等位基因、显性和隐性模型中均未检测到LPL Ser 447 Ter与IS之间的显著关联（P> 0.05）。 在病例中检测到LPL HindIII（+/−）和PvuII（+/−）的等位基因和显性模型的频率显著较低（HindIII（+/−）：等位基因模型：P = 0.0002，OR[95%CI]= 0.80 [0.71，0.90];显性模型：P = 0.003，OR[95%CI]= 0.80 [0.69，0.92]; PvuII（+/−）：等位基因模型：P <0.0001，OR[95%CI]= 0.75[0.65-0.86];显性模型：P = 0.02，OR[95%CI]= 0.67[0.48-0.93]）。 PvuII（+/−）的隐性模型与IS风险显著相关（P = 0.01，OR[95%CI]= 0.71 [0.55-0.93]）。 按种族分层的亚组分析显示，亚洲病例中HindIII（+/−）的等位基因、显性和隐性模型以及PvuII（+/−）的显性模型的频率显著较低（HindIII（+/−）：等位基因模型：P <.00001，OR[95%CI]= 0.69 [0.59，0.79];显性模型：P <.0001，OR[95%CI]= 0.69 [0.58，0.83];隐性模型：P =.005，OR[95%CI]= 0.66 [0.50，0.89]; PvuII（+/-）：显性模型：P =.0008，OR[95%CI]= 0.66 [0.51-0.84]），但在白人病例中并非如此（P>.05）。 此外，PvuII（+/-）等位基因和隐性模式的频率在白人病例中显著降低（P <0.05）。 Hind Ⅲ（+/-）和Pvu Ⅱ（+/-）可能是IS的保护因子，而Ser 447 Ter可能不是。
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. 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. 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). the HindIII (+/−) and PvuII (+/−), but not the Ser447Ter might be the protective factors for IS.