小儿社区获得性肺炎单核细胞/HDL-C比率变化及对心肌损伤的预测价值

The Change of Monocyte /HDL-C Ratio in Children with Community Acquired Pneumonia and Its Predictive Valuefor Myocardial Injury

目的 通过CAP患儿MHR变化探讨其与CAP患儿发生心肌损伤的关系及预测价值,为临床防治CAP患儿发生心肌损伤提供理论支持。方法 从2020年12月31日至2022年12月31日在某院诊治的CAP患儿中随机选取80例作为观察组,根据年龄、性别匹配同期健康体检儿童80例作为对照组。观察组入院时、对照组体检时均检测单核细胞、HDL-C,计算MHR。统计观察组住院期间心肌损伤发生情况。对比不同MHR水平患儿心肌损伤发生率。分析MHR与CAP患儿心肌损伤的独立关系,评估MHR预测CAP患儿心肌损伤的价值。应用RCS分析MHR与CAP患儿心肌损伤是否存在非线性相关。结果 观察组单核细胞、MHR高于对照组,HDL-C低于对照组(P<0.05);80例CAP患儿发生心肌损伤发生率为41.25%(33/80),随着MHR升高,心肌损伤发生率呈升高趋势;Logsitic回归模型分析,调整混杂因素后MHR水平仍与CAP患儿心肌损伤独立相关(P<0.05),MHR评估CAP患儿心肌损伤的AUC值为0.810,置信区间为0.707~0.889,Youden指数最高值为0.517,敏感度为87.88%,特异度为63.83%;MHR与CAP患儿心肌损伤率呈非线性剂量-反应关系(P=0.036),曲线大致呈“J”形,当MHR≥0.70时,MHR与CAP患儿心肌损伤率呈正相关(β=1.142,95%CI=1.189~8.253,P=0.034)。结论 CAP患儿MHR显著升高,且MHR升高越显著,患儿出现心肌损伤的风险越大,二者大致呈“J”形关系,当MHR≥0.70时,对心肌损伤具有较高预测效能。

Objectives To explore the relationship and predictive value of MHR changes with myocardial injury in children with CAP,provide theoretical support for clinical prevention and treatment of myocardial injury in children with CAP. Methods From December 31st, 2020 to December 31st, 2022, 80 children with CAP amongwho were diagnosed and treated in a certain hospital were randomly selected as the observation group, and 80healthy children matched according to age and gender during the same period were selected as the control group.Monocyte and HDL-C were detected in the observation group at admission and in the control group at physicalexamination, and MHR was calculated. The incidence of myocardial injury in the observation group duringhospitalization was statistically analyzed. The incidence of myocardial injury in children with different MHR levelswas compared. The independent relationship between MHR and myocardial injury in children with CAP wasanalyzed, and the value of MHR in predicting myocardial injury in children with CAP was evaluated. The restrictedcubic spline model (RCS) was used to analyze whether there was a nonlinear correlation between MHR andmyocardial injury in children with CAP. Results Monocyte and MHR in observation group were higher than controlgroup, while HDL-C was lower than control group (P< 0.05). The incidence of myocardial injury in 80 childrenwith CAP was 41.25% (33/80). With the increase of MHR, the incidence of myocardial injury showed anincreasing trend. According to Logsitic regression model analysis, MHR level was still independently correlated withmyocardial injury in children with CAP after adjusting for confounding factors (P<0.05). The AUC value of MHRwas 0.810, the confidence interval was 0.707-0.889, and the highest Youden index was 0.517. The sensitivitywas 87.88% and the specificity was 63.83%. There was a nonlinear dose-response relationship between MHR andthe myocardial injury rate in children with CAP (P=0.036), and the curve was roughly "J" shape. When MHR≥0.70, there was a positive correlation between MHR and the myocardial injury rate in children with CAP (β=1.142, 95%CI= 1.189-8.253, P=0.034). Conclusions MHR in children with CAP was significantly increased,and the more significant the increase in MHR, the greater the risk of myocardial injury in children, and the twoshowed a roughly "J" shaped relationship. When MHR≥0.70, the prediction of myocardial injury was higher.