黑龙江医学
黑龍江醫學
흑룡강의학
HEILONGJIANG MEDICAL JOURNAL
2014年
8期
878-882
,共5页
脂蛋白(a)%基因多态性%脑梗死
脂蛋白(a)%基因多態性%腦梗死
지단백(a)%기인다태성%뇌경사
Lipoproteins(a)%Gene polymorphism%Cerebral infarction
目的：分析研究LPA＋93C＞T基因多态性与Lp（a）水平及不同亚型脑梗死的关系。方法选取2007-12～2008-10间在中山大学附属第三医院神经内科住院治疗的150例大动脉粥样硬化性脑梗死（Large-Artery Atherosclerosis，LAA）患者和175例小血管闭塞性脑梗死（Small-Artery occlusion，SAO）患者作研究对象，与245例体检患者进行对照。采用聚合酶链反应-限制性片段长度多态性（ PCR-RFLP）分析LPA＋93位点的基因型。应用酶联免疫吸附试验（ ELISA）测定血浆Lp（ a）浓度。结果研究组（LAA组及SAO组）血浆Lp（a）中位数显著高于对照组。无论LAA组、SAO组还是对照组，携带突变LPA＋93T等位基因者血浆LP（a）水平较非携带者显著降低。在LAA组中携带＋93T等位基因的LPA频率显著低于对照组（OR＝0.58，95％CI＝0.38～0.87，P＝0.008），而SAO组与对照组比较无统计学差异（ P＝0.6）。但经多元显回归分析显示，携带＋93 T等位基因的 LPA对减少LAA发病风险无统计学意义（OR＝0.78，95％CI＝0.43～1.47，P＝0.42）。结论我们的研究结果支持高水平Lp（a）是LAA同时也是SAO独立危险因素。携带突变LPA＋93T等位基因者血浆LP（a）水平较非携带者显著降低，但不能减少LAA发病风险。
目的：分析研究LPA＋93C＞T基因多態性與Lp（a）水平及不同亞型腦梗死的關繫。方法選取2007-12～2008-10間在中山大學附屬第三醫院神經內科住院治療的150例大動脈粥樣硬化性腦梗死（Large-Artery Atherosclerosis，LAA）患者和175例小血管閉塞性腦梗死（Small-Artery occlusion，SAO）患者作研究對象，與245例體檢患者進行對照。採用聚閤酶鏈反應-限製性片段長度多態性（ PCR-RFLP）分析LPA＋93位點的基因型。應用酶聯免疫吸附試驗（ ELISA）測定血漿Lp（ a）濃度。結果研究組（LAA組及SAO組）血漿Lp（a）中位數顯著高于對照組。無論LAA組、SAO組還是對照組，攜帶突變LPA＋93T等位基因者血漿LP（a）水平較非攜帶者顯著降低。在LAA組中攜帶＋93T等位基因的LPA頻率顯著低于對照組（OR＝0.58，95％CI＝0.38～0.87，P＝0.008），而SAO組與對照組比較無統計學差異（ P＝0.6）。但經多元顯迴歸分析顯示，攜帶＋93 T等位基因的 LPA對減少LAA髮病風險無統計學意義（OR＝0.78，95％CI＝0.43～1.47，P＝0.42）。結論我們的研究結果支持高水平Lp（a）是LAA同時也是SAO獨立危險因素。攜帶突變LPA＋93T等位基因者血漿LP（a）水平較非攜帶者顯著降低，但不能減少LAA髮病風險。
목적：분석연구LPA＋93C＞T기인다태성여Lp（a）수평급불동아형뇌경사적관계。방법선취2007-12～2008-10간재중산대학부속제삼의원신경내과주원치료적150례대동맥죽양경화성뇌경사（Large-Artery Atherosclerosis，LAA）환자화175례소혈관폐새성뇌경사（Small-Artery occlusion，SAO）환자작연구대상，여245례체검환자진행대조。채용취합매련반응-한제성편단장도다태성（ PCR-RFLP）분석LPA＋93위점적기인형。응용매련면역흡부시험（ ELISA）측정혈장Lp（ a）농도。결과연구조（LAA조급SAO조）혈장Lp（a）중위수현저고우대조조。무론LAA조、SAO조환시대조조，휴대돌변LPA＋93T등위기인자혈장LP（a）수평교비휴대자현저강저。재LAA조중휴대＋93T등위기인적LPA빈솔현저저우대조조（OR＝0.58，95％CI＝0.38～0.87，P＝0.008），이SAO조여대조조비교무통계학차이（ P＝0.6）。단경다원현회귀분석현시，휴대＋93 T등위기인적 LPA대감소LAA발병풍험무통계학의의（OR＝0.78，95％CI＝0.43～1.47，P＝0.42）。결론아문적연구결과지지고수평Lp（a）시LAA동시야시SAO독립위험인소。휴대돌변LPA＋93T등위기인자혈장LP（a）수평교비휴대자현저강저，단불능감소LAA발병풍험。
Objective To analyze the relationship of LPA +93C>T gene polymorphism and LP(a) level and cerebral infarction of different subtypes.Metho ds Selecting a total of 325 consecutive patients with a diagnosis of ischemic stroke admitted to the department of neurology in the Third Affiliated Hospital of Sun Yat -sen University including 150 patients with LAA and 175 patients with SAO.245 pa-tients under physical examination were in the control group.Genotyping of the LPA C93T polymorphism was performed by means of PCR -RFLPs.Plasma Lp(a) was tested by ELISA.Results Median Lp(a) levels were significantly higher in patients with LAA and SAO than in control subjects.Subjects carrying at least one LPA+93T allele had lower Lp (a) levels.The prevalence rate of the 93T allele was sig-nificantly higher in control subjects than in LAA patients ,but there was no significant differences in allele frequencies of LPA between SAO patients and control subjects (P=0.6).In multivariate logistic regression analysis with covariates including traditional risk factors , the 93T allele was not independently associated with a reduced risk of LAA ( OR=0.78 ,95% CI=0.43~1.47 , P=0.42 ).Conclusion The re-sults support the hypothesis that elevated Lp (a) is an independent risk factor for ischemic stroke caused by both LAA and SAO.The 93T allele of the LPA gene is associated with low Lp ( a) levels,but may not be an independent low risk for LAA.
