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脓毒症休克患者中,髓系细胞表面持续高表达的可溶性触发受体1及单核细胞人类白细胞抗原DR表达降低与医院感染相关。

Persistently Elevated Soluble Triggering Receptor Expressed on Myeloid Cells 1 and Decreased Monocyte Human Leucocyte Antigen DR Expression Are Associated With Nosocomial Infections in Septic Shock Patients.

作者信息

Venet Matthieu, Bidar Frank, Derive Marc, Delwarde Benjamin, Monard Céline, Hengy Baptiste, Jolly Lucie, Rimmelé Thomas, Lukaszewicz Anne-Claire, Monneret Guillaume, Venet Fabienne

机构信息

Hospices Civils de Lyon, Edouard Herriot Hospital, Anesthesia and Critical Care Medicine Department, Lyon, France.

Inotrem SA, Vandoeuvre-les-Nancy, France.

出版信息

Crit Care Explor. 2023 Feb 24;5(3):e0869. doi: 10.1097/CCE.0000000000000869. eCollection 2023 Mar.

DOI:10.1097/CCE.0000000000000869
PMID:36861044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9970267/
Abstract

UNLABELLED

Sepsis-acquired immunosuppression may play a major role in patients' prognosis through increased risk of secondary infections. Triggering receptor expressed on myeloid cells 1 (TREM-1) is an innate immune receptor involved in cellular activation. Its soluble form (sTREM-1) has been described as a robust marker of mortality in sepsis. The objective of this study was to evaluate its association with the occurrence of nosocomial infections alone or in combination with human leucocyte antigen-DR on monocytes (mHLA-DR).

DESIGN

Observational study.

SETTING

University Hospital in France.

PATIENTS

One hundred sixteen adult septic shock patients as a post hoc study from the IMMUNOSEPSIS cohort (NCT04067674).

INTERVENTIONS

None.

MEASUREMENTS AND MAIN RESULTS

Plasma sTREM-1 and monocyte HLA-DR were measured at day 1 or 2 (D1/D2), D3/D4, and D6/D8 after admission. Associations with nosocomial infection were evaluated through multivariable analyses. At D6/D8, both markers were combined, and association with increased risk of nosocomial infection was evaluated in the subgroup of patients with most deregulated markers in a multivariable analysis with death as a competing risk. Significantly decreased mHLA-DR at D6/D8 and increased sTREM-1 concentrations were measured at all time points in nonsurvivors compared with survivors. Decreased mHLA-DR at D6/D8 was significantly associated with increased risk of secondary infections after adjustment for clinical parameters with a subdistribution hazard ratio of 3.61 (95% CI, 1.39-9.34; = 0.008). At D6/D8, patients with persistently high sTREM-1 and decreased mHLA-DR presented with a significantly increased risk of infection (60%) compared with other patients (15.7%). This association remained significant in the multivariable model (subdistribution hazard ratio [95% CI], 4.65 [1.98-10.9]; < 0.001).

CONCLUSIONS

In addition to its prognostic interest on mortality, sTREM-1, when combined with mHLA-DR, may help to better identify immunosuppressed patients at risk of nosocomial infections.

摘要

未标注

脓毒症获得性免疫抑制可能通过增加继发感染风险在患者预后中起主要作用。髓系细胞触发受体1(TREM-1)是一种参与细胞活化的固有免疫受体。其可溶性形式(sTREM-1)已被描述为脓毒症死亡率的可靠标志物。本研究的目的是评估其单独或与单核细胞上的人类白细胞抗原-DR(mHLA-DR)联合与医院感染发生的相关性。

设计

观察性研究。

地点

法国大学医院。

患者

116例成年脓毒性休克患者,作为免疫脓毒症队列(NCT04067674)的事后研究。

干预措施

无。

测量和主要结果

入院后第1天或第2天(D1/D2)、D3/D4和D6/D8测量血浆sTREM-1和单核细胞HLA-DR。通过多变量分析评估与医院感染的相关性。在D6/D8时,将两种标志物结合起来,在以死亡为竞争风险的多变量分析中,在标志物失调最严重的患者亚组中评估与医院感染风险增加的相关性。与幸存者相比,非幸存者在所有时间点均检测到D6/D8时mHLA-DR显著降低,sTREM-1浓度升高。在调整临床参数后,D6/D8时mHLA-DR降低与继发感染风险增加显著相关,亚分布风险比为3.61(95%CI,1.39-9.34;P = 0.008)。在D6/D8时,与其他患者(15.7%)相比,sTREM-1持续升高且mHLA-DR降低的患者感染风险显著增加(60%)。在多变量模型中,这种相关性仍然显著(亚分布风险比[95%CI],4.65[1.98-10.9];P < 0.001)。

结论

除了对死亡率具有预后意义外,sTREM-1与mHLA-DR联合使用时,可能有助于更好地识别有医院感染风险的免疫抑制患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/dd3d17711fb4/cc9-5-e0869-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/211414f6b1cd/cc9-5-e0869-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/25a8443b71b3/cc9-5-e0869-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/dd3d17711fb4/cc9-5-e0869-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/211414f6b1cd/cc9-5-e0869-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/25a8443b71b3/cc9-5-e0869-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a45f/9970267/dd3d17711fb4/cc9-5-e0869-g003.jpg

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