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血清 Sesrtain2 在合并心肌病的感染性休克患者中降低。

Serum Sestrin2 Was Lower in Septic Shock Patients with Cardiomyopathy.

机构信息

Shengli Clinical Medical College of Fujian Medical University, Fuzhou 350001, China.

Department of Emergency, Fujian Provincial Hospital, Fuzhou 350001, China.

出版信息

Dis Markers. 2022 Sep 1;2022:1390373. doi: 10.1155/2022/1390373. eCollection 2022.

DOI:10.1155/2022/1390373
PMID:36092963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9458382/
Abstract

BACKGROUND

To determine the clinical significance of variations in serum sestrin2 protein levels in the development of septic cardiomyopathy in septic shock patients.

METHODS

The serum sestrin2 concentrations of each sample were determined using ELISA in a total of 67 control persons and 188 patients with septic shock. Furthermore, using transthoracic echocardiography, septic shock patients were split into two groups based on whether or not cardiomyopathy had developed, and the differences in each index between the two groups were analyzed. We looked at the relationship between serum sestrin2 levels, norepinephrine dosage, and NTproBNP levels. The influencing variables for the prediction of septic cardiomyopathy linked with the development of septic cardiomyopathy and clinical prognosis in septic cardiomyopathy were determined using multivariate binary logistic regression.

RESULTS

Assessment of left ventricular systolic function by measurement of LVEF revealed that 61/188 (32.4%) of the 188 patients with septic shock included in the research satisfied the diagnostic criteria for septic cardiomyopathy. (1) Sestrin2 protein levels showed a significant difference between septic shock and healthy controls ( < 0.01). (2) Compared to the group without septic cardiomyopathy, the group with combined septic cardiomyopathy had lower serum sestrin2 protein levels ( < 0.05), lower systolic blood pressure ( < 0.05), and higher plasma NTproBNP levels ( < 0.01) and used greater norepinephrine dosages ( < 0.01). The levels of serum sestrin2 protein revealed a little negative relationship with NTproBNP and norepinephrine dose. However, a binary logistic regression analysis revealed that none of these factors was an independent predictor of septic shock. (3) Age, lactate level, SOFA score, positive bacteremia, and sestrin2 protein were shown to be substantial discrepancies in clinical outcomes in patients with septic cardiomyopathy, becoming variables that impact clinical outcomes. Positive bacteremia ( = 0.031, OR = 5.084), SOFA score ( = 0.021, OR = 1.304), and sestrin2 protein ( =  0.039, OR = 0.897) were revealed to have independent influences in predicting clinical mortality outcome in septic cardiomyopathy using multivariate binary logistic regression.

CONCLUSION

High serum sestrin2 levels clearly distinguish septic shock patients from healthy controls, whereas low serum sestrin2 levels are related with cardiac dysfunction to some extent but are not an independent influence factor for septic cardiomyopathy. Low serum sestrin2 levels were shown to be useful in predicting clinical outcome in patients with septic cardiomyopathy.

摘要

背景

为了确定血清 sestrin2 蛋白水平变化在脓毒性休克患者脓毒性心肌病发展中的临床意义。

方法

采用 ELISA 法测定 67 例对照者和 188 例脓毒性休克患者的血清 sestrin2 浓度。进一步采用经胸超声心动图,根据是否发生心肌病将脓毒性休克患者分为两组,并分析两组间各指标的差异。观察血清 sestrin2 水平、去甲肾上腺素用量和 NTproBNP 水平的关系。采用多变量二项逻辑回归确定与脓毒性心肌病发展相关的影响因素及脓毒性心肌病临床预后的预测因子。

结果

通过测量 LVEF 评估左心室收缩功能,发现研究中的 188 例脓毒性休克患者中有 61 例(32.4%)符合脓毒性心肌病的诊断标准。(1)血清 sestrin2 蛋白水平在脓毒性休克与健康对照组之间有显著差异(<0.01)。(2)与无脓毒性心肌病组相比,合并脓毒性心肌病组的血清 sestrin2 蛋白水平较低(<0.05),收缩压较低(<0.05),血浆 NTproBNP 水平较高(<0.01),去甲肾上腺素用量较大(<0.01)。血清 sestrin2 蛋白水平与 NTproBNP 和去甲肾上腺素剂量呈负相关。然而,二项逻辑回归分析显示,这些因素均不是脓毒性休克的独立预测因子。(3)年龄、乳酸水平、SOFA 评分、阳性菌血症和 sestrin2 蛋白在脓毒性心肌病患者的临床结局中有显著差异,成为影响临床结局的变量。阳性菌血症(=0.031,OR=5.084)、SOFA 评分(=0.021,OR=1.304)和 sestrin2 蛋白(=0.039,OR=0.897)在多变量二项逻辑回归中显示对脓毒性心肌病临床死亡率有独立影响。

结论

高血清 sestrin2 水平可明显区分脓毒性休克患者与健康对照者,而低血清 sestrin2 水平与心功能不全有一定关系,但不是脓毒性心肌病的独立影响因素。低血清 sestrin2 水平有助于预测脓毒性心肌病患者的临床预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/e4dc7269671e/DM2022-1390373.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/65c9afc54c4e/DM2022-1390373.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/eddfc5584bfd/DM2022-1390373.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/73d63f38638e/DM2022-1390373.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/9c7e1e4fec35/DM2022-1390373.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/e4dc7269671e/DM2022-1390373.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/65c9afc54c4e/DM2022-1390373.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/eddfc5584bfd/DM2022-1390373.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/73d63f38638e/DM2022-1390373.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/9c7e1e4fec35/DM2022-1390373.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa4/9458382/e4dc7269671e/DM2022-1390373.005.jpg

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