首页|冠心病合并Hp感染患者糖脂代谢和斑块特征及miR-146a、IL-33、ST2水平

冠心病合并Hp感染患者糖脂代谢和斑块特征及miR-146a、IL-33、ST2水平

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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.
Glycolipid metabolism and plaque characteristics in patients with coronary heart disease combined with Hp infection and miR-146a,IL-33 and ST2 levels
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 dis-ease(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 trea-ted in this hospital during the same period were selected as the infection group.Glucose metabolism related indica-tors[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 infec-tion.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 carotid intima-media thickness(IMT)and plaque area of the infection group were larger than those of the un-infection group(P<0.05).The infection group had fewer mixed and hard plaques,and more soft plaques than the un-in-fection group(P<0.05).The levels of miR-146a,serum IL-33 and ST2 in the infection group were higher than those in the un-infection group(P<0.05).With the aggravation of Hp infection in patients with coronary heart disease,the levels of miR-146a,serum IL-33 and ST2 increased(P<0.05).CONCLUSION Hp infection can lead to 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.

Coronary heart diseaseHelicobacter pyloriPlaque characteristicMiR-146aInterleukin-33Sup-pression of tumorigenicity 2

崔玉凤、马红岩、沈志方、常国栋

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商丘医学高等专科学校诊断教研室,河南商丘 476100

商丘市第一人民医院心血管内科,河南商丘 476100

冠心病 幽门螺杆菌 斑块特征 miR-146a 白细胞介素-33 致瘤性抑制因子2

河南省医学科技攻关计划

LHGJ20200931

2024

中华医院感染学杂志
中华预防医学会 中国人民解放军总医院

中华医院感染学杂志

CSTPCD北大核心
影响因子:1.885
ISSN:1005-4529
年,卷(期):2024.34(11)
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