摘要
目的分析脂蛋白相关磷脂酶A2(Lp-PLA2)活性在妊娠期糖尿病中的变化,探讨妊娠期糖尿病导致不良妊娠结局的深层机制。方法测定89例孕妇的血浆Lp-PLA2活性,其中正常对照组25例、妊娠期糖尿病血糖控制良好组32例、血糖控制不良组32例。分析3组孕妇血浆Lp-PLA2活性及其与妊娠结局的关系。结果无论早产患者还是足月产患者,血糖控制不良组血浆Lp-PLA2活性均高于正常对照组及血糖控制良好组,差异有统计学意义;在血糖控制不良组中,主要不良妊娠结局的发生率均高于其余2组;以孕周作为自变量,血浆Lp-PLA2活性作为因变量进行回归分析,2者之间未见明显相关性。结论血浆Lp-PLA2活性在妊娠期糖尿病血糖控制不良组中明显升高;妊娠期糖尿病血糖控制不良组中主要不良妊娠结局发生率高;Lp-PLA2可能参与妊娠期糖尿病的血管病变发生。
Objective To analyze the changes of lipoprotein-associated phospholipase A2 activity in gestational diabetes mellitus,so as to explore the deep mechanisms of adverse pregnancy outcomes of gestational diabetes.Methods Lp-PLA2 activity in plasma was determined,including 25 cases of normal control group (group A),32 cases of good glycemic control group (group B) and 32 cases of poor glycemic control group (group C).The maternal plasma Lp-PLA2 activity in three groups and its relationship with pregnancy outcome were analyzed with non-parametric tests.Results The plasma Lp-PLA2 activity in poor glycemic control group (group C) was significantly higher than that of the good glycemic control group (group B) and normal control group (group A) both in premature or full-term patients.In poor glycemic control group,the incidence of major adverse pregnancy outcomes was higher than the rest of the two groups.Considering gestational age as an independent variable,plasma Lp-PLA2 activity as the dependent variable,no obvious correlation between the two indexes was found by regression analysis.Conclusion The plasma Lp-PLA2 activity level was significantly higher in the group with gestational diabetes in poor glycemic control.The incidence of major adverse pregnancy outcomes in the group with poor glycemic control was higher than those of other groups.Plasma Lp-PLA2 activity may be involved in the occurrence of the vascular disease of gestational diabetes.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2014年第8期738-741,共4页
Journal of China Medical University
关键词
妊娠期糖尿病
脂蛋白相关磷脂酶A2
胰岛素抵抗
血管内皮损伤
gestational diabetes mellitus
lipoprotein-associated phospholipase A2
insulin resistance
vascular endothelial injury