摘要
目的探究冠心病合并幽门螺杆菌(Hp)感染对糖脂代谢和斑块特征及微小RNA-146a(miR-146a)、白细胞介素-33(IL-33)、致瘤性抑制因子2(ST2)的影响.方法选择2018年6月-2022年6月商丘市第一人民医院就诊的单纯冠心病(未合并Hp感染)患者86例作为未感染组,另选取同期于医院治疗的冠心病合并Hp感染患者60例作为感染组;比较两组糖代谢相关指标[空腹血糖、胰高血糖素、胰高血糖素样肽-1(GLP-1)、生长抑素(SS)、胰岛素]、脂代谢相关指标[甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]、斑块特征、miR-146a及血清IL-33、ST2表达水平,对比不同感染程度患者以上指标.结果感染组空腹血糖、胰高血糖素、TG、TC较未感染组高,而SS、HDL-C较未感染组低(P<0.05);感染组颈动脉内膜中层厚度(IMT)、斑块面积比未感染组高(P<0.05);感染组混合斑、硬斑较未感染组少,软斑较未感染组多(P<0.05);感染组miR-146a、血清IL-33、ST2水平均高于较未感染组(P<0.05);随冠心病合并Hp感染者的感染程度增加,miR-146a及血清IL-33、ST2水平均增加(P<0.05).结论Hp感染可导致冠心病患者糖脂代谢出现紊乱,斑块稳定性下降,miR-146a及血清IL-33、ST2水平升高,促进病情进展.
OBJECTIVE To investigate the effects of coronary heart disease complicated with Helicobacter pylori(Hp)infection on glycolipid metabolism and plaque characteristics,microRNA-146a(miR-146a),interleukin 33(IL-33)and suppression of tumorigenicity 2(ST2).METHODS Eighty six patients with simple coronary heart disease(without Hp infection)admitted to the First People's Hospital of Shangqiu from Jun.2018 to Jun.2022 were selected as the un-infection group,and 60 patients with coronary heart disease complicated with Hp infection treated in this hospital during the same period were selected as the infection group.Glucose metabolism related indicators[fasting blood glucose,glucagon,glucagon-like peptide-1(GLP-1),somatostatin(SS)and insulin],lipid metabolism related indicators[triglyceride(TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C)and high-density lipoprotein cholesterol(HDL-C)],plaque characteristics,and the levels of miR-146a,serum IL-33 and ST2 were compared between the two groups and among patients with different severity of infection.RESULTS Fasting blood glucose,glucagon,TG and TC in the infection group were higher than those in the un-infection group, while SS and HDL-C were lower than those in the un-infection group (P<0. 05). The carotidintima-media thickness (IMT) and plaque area of the infection group were larger than those of the un-infectiongroup (P<0. 05). The infection group had fewer mixed and hard plaques, and more soft plaques than the un-infectiongroup (P<0. 05). The levels of miR-146a, serum IL-33 and ST2 in the infection group were higher thanthose in the un-infection group (P<0. 05). With the aggravation of Hp infection in patients with coronary heartdisease, the levels of miR-146a, serum IL-33 and ST2 increased (P<0. 05). CONCLUSION Hp infection can leadto the emergence of disturbances in glycolipid metabolism, decreased plaque stability, and elevated levels of miR-146a, serum IL-33 and ST2 in patients with coronary heart disease, which promote disease progression.
作者
崔玉凤
马红岩
沈志方
常国栋
CUI Yu-feng;MA Hong-yan;SHEN Zhi-fang;CHANG Guo-dong(Shangqiu Medical College,Shangqiu,Henan 476100,China;不详)
出处
《中华医院感染学杂志》
CAS
CSCD
北大核心
2024年第11期1649-1653,共5页
Chinese Journal of Nosocomiology
基金
河南省医学科技攻关计划基金资助项目(LHGJ20200931)。
