SHOCKPub Date : 2026-08-04DOI: 10.1097/SHK.0000000000002921
Junhyuk Seo, Namkee Oh, Gee Young Suh, Chae-Man Lim, Won Chul Cha, Ryoung-Eun Ko
{"title":"Phenotyping Sepsis at Emergency Department Presentation Using Early Clinical Data: A Multicenter Cohort Study.","authors":"Junhyuk Seo, Namkee Oh, Gee Young Suh, Chae-Man Lim, Won Chul Cha, Ryoung-Eun Ko","doi":"10.1097/SHK.0000000000002921","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002921","url":null,"abstract":"<p><strong>Background: </strong>Sepsis is heterogeneous, and early emergency department (ED) management is constrained by limited information and dynamic clinical trajectories.</p><p><strong>Methods: </strong>Using the nationwide Korean Sepsis Alliance (KSA) registry, we applied k-means clustering to nine routine ED variables (demographics, vital signs, Clinical Frailty Scale, mental status, lactate). The model was developed in KSA 3 (2019-2021) and tested for temporal reproducibility in the independent KSA 5 cohort (2022-2023). Phenotypes were compared on 7-day mortality, early sepsis-bundle compliance, and SOFA trajectories; stability was assessed by bootstrap resampling and alternative clustering. One-hour vasopressor non-compliance was decomposed into criterion-not-met versus delivered-with-delay.</p><p><strong>Results: </strong>Six phenotypes were identified in 9,430 patients and reproduced in 7,184 (mortality-rank ρ = 1.00; calibration drift, O/E 0.83-1.32). Seven-day mortality ranged 6.7%-31.8%. Extreme-severity phenotypes (A, F, E) were bootstrap-robust (Jaccard 0.65-0.91), whereas intermediate phenotypes (B, D) were less stable (0.21-0.47), consistent with a continuous severity spectrum. Non-compliance composition separated phenotypes that severity scores rank together: predominantly criterion-not-met (appropriate withholding) in low-acuity phenotype C versus delivered-with-delay in high-acuity phenotype E. Phenotypes B and F, matched on presenting physiology and mortality but differing in frailty and mental status, still differed in composition (criterion-not-met 49.6% vs 28.3%; p < 0.001). SOFA trajectories were highest in phenotype E.</p><p><strong>Conclusions: </strong>ED-presentation phenotyping using routine variables identifies six cross-sectional signatures along the sepsis severity spectrum rather than definitive subtypes. Decomposing bundle non-compliance shows that it combines appropriate withholding and urgency-associated delay in phenotype-dependent proportions, a distinction one-dimensional severity scores cannot make, relevant to phenotype-stratified resuscitation warranting prospective evaluation.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148702075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2026-04-03DOI: 10.1097/SHK.0000000000002853
Tyler J Rolland, Sumbule Zahra, Luke A Graser, Daniel Cucinotta, Rebeccah Young, Brian R Weil
{"title":"Mesenchymal Stem Cell-Derived Extracellular Vesicles Mitigate Immune Cell Activation in an in Vitro Model of Postresuscitation Inflammation.","authors":"Tyler J Rolland, Sumbule Zahra, Luke A Graser, Daniel Cucinotta, Rebeccah Young, Brian R Weil","doi":"10.1097/SHK.0000000000002853","DOIUrl":"10.1097/SHK.0000000000002853","url":null,"abstract":"<p><strong>Background: </strong>Systemic inflammation is a key component of postcardiac arrest syndrome (PCAS) and contributes to significant morbidity and mortality after resuscitation from sudden cardiac arrest. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as promising immunomodulatory agents in various inflammatory conditions, including ischemia-reperfusion injury (IRI). We investigated the therapeutic potential of MSC-EVs in porcine peripheral blood mononuclear cells (PBMCs) stimulated with lipopolysaccharide (LPS) or mitochondrial DNA (mtDNA) to model immune cell activation relevant to PCAS.</p><p><strong>Methods: </strong>Transcriptomic profiling was performed on PBMCs from swine at baseline and 4 hours after resuscitation from cardiac arrest and compared with ex vivo mtDNA-stimulated PBMCs to establish mtDNA as a PCAS-relevant pro-inflammatory stimulus. PBMCs from healthy pigs were then stimulated with 1 μg/mL mtDNA + transfection reagent or 5 μM LPS and treated with escalating concentrations of MSC-EVs. Flow cytometry, quantitative PCR, ELISA, and reactive oxygen/nitrogen species measurements were performed to assess PBMC activation.</p><p><strong>Results: </strong>Transcriptomic profiling identified overlapping differentially expressed genes and convergent enrichment of cytosolic DNA-sensing/antiviral response pathways and cytokine/chemokine signaling programs in mtDNA-stimulated PBMCs and PBMCs collected from swine with PCAS. In mtDNA-stimulated PBMCs, MSC-EVs attenuated dendritic cell activation, reduced inflammatory cytokine gene expression and release, and decreased reactive oxygen/nitrogen species production in a concentration-dependent manner. MSC-EVs also produced concentration-dependent reductions in LPS-induced granulocyte activation and expression of IFNα, IL-1β, and TNFα.</p><p><strong>Conclusions: </strong>MSC-EVs exert immunomodulatory effects against mtDNA- and LPS-mediated PBMC activation, supporting further investigation as a cell-free therapeutic strategy to target immune activation in PCAS and other acute inflammatory conditions.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"538-549"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147729782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2025-12-26DOI: 10.1097/SHK.0000000000002763
Xiaowei Zhou, Liyong Zou, Haoyue Deng, Yu Zhu, Jie Zhang, Qinghui Li, Shijie Zhou, Liangming Liu, Li Wang, Tao Li
{"title":"Pirinixic Acid Protects Against Hemorrhagic Shock by Regulating Neutrophil-Associated Key Genes.","authors":"Xiaowei Zhou, Liyong Zou, Haoyue Deng, Yu Zhu, Jie Zhang, Qinghui Li, Shijie Zhou, Liangming Liu, Li Wang, Tao Li","doi":"10.1097/SHK.0000000000002763","DOIUrl":"10.1097/SHK.0000000000002763","url":null,"abstract":"<p><strong>Background: </strong>The uncontrolled inflammatory cascade triggered by hemorrhagic shock (HS) can exacerbate tissue damage and organ dysfunction. Neutrophils, as the most abundant type of leukocytes, are key mediators of the innate immune response in the early stages of injury. There is a lack of suitable treatments targeting neutrophils in HS.</p><p><strong>Methods: </strong>We used machine learning algorithms to identify neutrophil-associated key genes in patients with HS and assessed the diagnostic efficacy of these genes. Weighted gene co-expression network analysis and consensus clustering analysis were performed based on the key genes to explore their role in HS. Finally, we predicted the binding of key genes to drug candidates using molecular docking and observed the effects of drug candidates and the expression of key genes in animals with HS.</p><p><strong>Results: </strong>We screened for key genes with good diagnostic efficacy (ARG1, F2RL1, MPP1, RHOG, UPP1) that activate JAK-STAT3 signaling and apoptotic signaling, leading to poor prognosis. Pirinixic acid screened by the Comparative Toxicogenomics Database has good affinity with key genes, and it can significantly restore the level of inflammatory factors and coagulation function in HS rats, protect the function of vital organs, and prolong the survival time. It was confirmed that pirinixic acid may improve neutrophil immunity disorders by acting on MPP1, RHOG, and F2RL1, and thus protect against HS.</p><p><strong>Conclusions: </strong>The protective effect of pirinixic acid against HS-induced immune dysregulation is closely associated with the neutrophil genes MPP1, RHOG, and F2RL1.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"560-574"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2026-03-20DOI: 10.1097/SHK.0000000000002725
Sergio M Navarro, Riley J Thompson, Taleen A MacArthur, Grant M Spears, Kent R Bailey, Dong Chen, Rajiv Pruthi, Donald H Jenkins, Jing-Fei Dong, Rosemary A Kozar, Myung S Park
{"title":"Assessment of Novel Platform of Thrombin Generation to Predict Venous Thromboembolism Early After Traumatic Injury: A Prospective Cohort Study.","authors":"Sergio M Navarro, Riley J Thompson, Taleen A MacArthur, Grant M Spears, Kent R Bailey, Dong Chen, Rajiv Pruthi, Donald H Jenkins, Jing-Fei Dong, Rosemary A Kozar, Myung S Park","doi":"10.1097/SHK.0000000000002725","DOIUrl":"10.1097/SHK.0000000000002725","url":null,"abstract":"<p><strong>Introduction: </strong>Calibrated automated thrombogram assay parameters have been shown to assess hypercoagulation state and, therefore, may independently predict posttrauma, symptomatic venous thromboembolism (VTE). Yet, calibrated automated thrombogram lacks high throughput and standardization, limiting diagnostic potential. This study analyzed thrombin generation (TG) profiles in trauma patients using a high-throughput assay, processing up to 10 samples at once, providing batch testing capabilities. We hypothesized that trauma patients who developed VTE would show distinct TG profiles compared with those who did not.</p><p><strong>Methods: </strong>Trauma patients presenting to a Level I Trauma Center had samples collected within 12 hours postinjury prospectively. Follow-up was conducted to 90 days, time to symptomatic VTE diagnosis or death, confirmed via autopsy or imaging. TG profiles were measured from the ST Genesia assay. Data were presented as median (interquartile ranges) or n (%), with the Wilcoxon rank-sum or chi-squared test. Associations between TG parameters and clinical risk factors were assessed using Spearman correlation analysis or the Wilcoxon rank-sum test.</p><p><strong>Results: </strong>Two hundred and fifty-four trauma patients were analyzed [48.5 years (31.0, 62.0), 72.0% male]: 64 patients with VTE (25.2%) to 190 with non-VTE. VTE pts had a median time to VTE of 8 days, with 29 developing deep venous thrombosis, 24 with pulmonary embolism, and 11 with deep venous thrombosis/pulmonary embolism. No significant differences were found in age, sex, or body mass index; significantly more VTE patients underwent surgery and blood transfusions within 24 hours. TG profiles demonstrated accelerated TG in patients who developed VTE compared with non-VTE, with significant differences in peak height ( P = 0.001), time to peak ( P = 0.021), endogenous thrombin potential ( P < 0.001), and velocity index ( P = 0.001).</p><p><strong>Conclusion: </strong>TG profiles using ST Genesia can differentiate trauma patients at high risk of developing VTE. The platform suits clinical labs needing high throughput by providing batch testing capabilities.</p><p><strong>Study type: </strong>Prospective study with less than large effect and no negative criteria.</p><p><strong>Level of evidence: </strong>II.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"441-448"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13426469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2026-06-02DOI: 10.1097/SHK.0000000000002883
Nikolaos S Lotsios, Vasileios Issaris, Georgios Poupouzas, Charikleia S Vrettou, Chrysi Keskinidou, Matina Kardara, Kostas A Papavassiliou, Foteini Economidou, Stelios Kokkoris, Anastasia Kotanidou, Ioanna Dimopoulou, Alice G Vassiliou
{"title":"Temporal Aquaporin Expression Profiles in Immune Cell Subsets During Critical Illness.","authors":"Nikolaos S Lotsios, Vasileios Issaris, Georgios Poupouzas, Charikleia S Vrettou, Chrysi Keskinidou, Matina Kardara, Kostas A Papavassiliou, Foteini Economidou, Stelios Kokkoris, Anastasia Kotanidou, Ioanna Dimopoulou, Alice G Vassiliou","doi":"10.1097/SHK.0000000000002883","DOIUrl":"10.1097/SHK.0000000000002883","url":null,"abstract":"<p><p>Aquaporins (AQPs) are a family of water channel proteins with a significant role in immune cell function. Although AQPs have been studied in sepsis, their expression in critical illness remains underexplored. Our group aimed to examine the mRNA expression profile of AQP isoforms in polymorphonuclear leukocytes (PMNs) and peripheral blood mononuclear cells (PBMCs) of critically ill patients admitted to the intensive care unit (ICU). To this end, we designed a prospective, longitudinal, observational study performed in the ICU of \"Evangelismos\" General Hospital between February 2024 and October 2024. In total, 40 critically ill patients and 25 healthy controls were enrolled in the study. Blood samples were collected at four time points: upon ICU admission (24-48 hours), and at days 4 (D4), 8 (D8), and 14 (D14). Total RNA was extracted from PMNs and PBMCs, and RT-qPCR was performed to examine mRNA levels of AQPs 1, 2, 3, 4, 5, 7, and 9. Our results revealed downregulation of AQP isoforms, except AQP1, in PMNs, whereas PBMCs exhibited sustained upregulation of all AQPs except AQP3, which was downregulated. Our findings suggest that differential AQP expression in immune cell subsets may reflect adaptive immune responses during critical illness, providing insights into leukocyte function and potential therapeutic targets.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"367-376"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148164397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prognostic Impact and Risk Factors of Septic Cardiomyopathy in Patients with Septic Shock: An Observational Study.","authors":"Rui-Ming Xu, Da-Wei Wang, Lei Wang, Jian-Zhong Li, Yan-Yun He, Jing Zhang","doi":"10.1097/SHK.0000000000002782","DOIUrl":"10.1097/SHK.0000000000002782","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to identify risk factors associated with septic cardiomyopathy (SCM) in patients diagnosed with septic shock and to assess differences in clinical outcomes between those with septic shock alone and those with concomitant SCM.</p><p><strong>Methods: </strong>A retrospective observational study was conducted on 108 patients diagnosed with septic shock and admitted to Beijing Tongren Hospital, Capital Medical University, between December 2022 and July 2024. Patients were stratified into two groups based on the presence or absence of SCM: the non-SCM group (n = 90) and the SCM group (n = 18). Baseline characteristics, laboratory markers, cardiac function indices, and clinical outcomes were compared between the two groups. Multivariate logistic regression was employed to identify risk factors for SCM. Within the SCM group, outcomes were further analyzed according to survival status to assess the association between cardiac function recovery and mortality.</p><p><strong>Results: </strong>The incidence of SCM among patients with septic shock was 16.67%. Compared with the non-SCM group, the SCM group showed a significantly higher prevalence of urinary tract infections and a history of diabetes mellitus ( P < 0.05). Higher scores were observed for the Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment scales, along with increased levels of admission-day troponin I, interleukin-1 (IL-1), tumor necrosis factor-α, maximum lactic acid (LACmax), maximum brain natriuretic peptide, and peak troponin I ( P < 0.05). In contrast, mean arterial pressure at admission, minimum left ventricular ejection fraction (LVEF), and end-point LVEF (LVEFend%) were significantly lower in this group ( P < 0.05). Multivariate logistic regression identified elevated IL-1 levels (odds ratio [OR] = 1.14), higher APACHE II scores (OR = 1.13), and increased LACmax (OR = 1.47) as risk factors for SCM ( P < 0.05). The presence of SCM was associated with significantly higher in-hospital mortality and increased healthcare costs ( P < 0.05). Among patients with SCM, recovery of LVEF and cardiac output was correlated with improved survival outcomes.</p><p><strong>Conclusions: </strong>Elevated IL-1 levels, increased peak lactic acid concentration, and higher APACHE II scores were associated with the development of SCM in patients with septic shock. SCM was further associated with increased mortality and greater healthcare resource utilization. Restoration of cardiac function, particularly improvements in LVEF and cardiac output, was correlated with improved prognosis and may serve as a valuable indicator of clinical outcomes.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"340-347"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146158287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2026-06-26DOI: 10.1097/SHK.0000000000002881
Matthew Montoya Rush, Mark H Hoofnagle, Grace M Niziolek, Sarbani Ghosh, Philip C Spinella, Grant V Bochicchio, Isaiah R Turnbull
{"title":"Early STAT3 Activation and Delayed STAT5 Dominance Define the Acute Leukocyte Signaling Response to Trauma and May Correlate with Clinical Outcomes.","authors":"Matthew Montoya Rush, Mark H Hoofnagle, Grace M Niziolek, Sarbani Ghosh, Philip C Spinella, Grant V Bochicchio, Isaiah R Turnbull","doi":"10.1097/SHK.0000000000002881","DOIUrl":"10.1097/SHK.0000000000002881","url":null,"abstract":"<p><p>Major trauma dysregulates the immune system, leaving injured patients at increased risk of infection. Despite extensive research to define the effect of trauma on the immune system, there are no effective interventions to restore immune function in injured patients. We previously used single-cell phosphoproteomics to identify pathways for immunomodulation in COVID-19 induced critical illness. We hypothesized that trauma would also be associated with definable changes in leukocyte signaling, providing therapeutic targets. To test this hypothesis, we used mass cytometry to assess signaling phosphoproteins and associated surface markers at single-cell resolution in a cohort of critically injured patients. We find that injury causes an acute increase in STAT3 signaling across leukocyte populations, followed by a shift from STAT3 to STAT5 predominance in T cells over the first 72 hours after injury. We used computational clustering to identify subpopulations of T cells and found that injury causes an increase in activated CD4 memory T cells. We assessed the relationship between phosphoprotein levels and clinical outcomes and identified significant correlations between early phospho-STAT3 levels in T cells, monocytes, and neutrophils and clinical outcomes, including ICU and hospital length of stay. These data demonstrate that severe injury is associated with cell-type-specific changes in the signaling phosphoproteome in circulating leukocytes, which may underlie clinical outcomes from injury.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"385-394"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148332368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification and Validation of Key Genes Related to Arginine Methylation Modification in Sepsis Using Transcriptome Combined with Mendelian Randomization Analysis.","authors":"Peng Huang, Meifeng Wang, Weihong Hong, Jinyuan Kang, Yuyang Li, Ying Li, Xiao Lin","doi":"10.1097/SHK.0000000000002741","DOIUrl":"10.1097/SHK.0000000000002741","url":null,"abstract":"<p><strong>Background: </strong>Patients with sepsis often exhibit a decrease in lymphatic numbers, which can be facilitated by protein arginine methyltransferase (PRMT). However, it is unclear how PRMT contributes to lymphopenia in sepsis.</p><p><strong>Methods: </strong>This study employed the sepsis-related datasets (GSE65682 and GSE134347) and nine PRMT genes. First, we intersected the differentially expressed genes with the weighted gene co-expression network analysis module genes to identify differentially expressed PRMT-related genes. Thereafter, candidate key genes were obtained after Mendelian randomization analysis and machine learning screening. Eventually, we subjected key genes identified by expression analysis and receiver operating characteristic curves to gene set enrichment analysis, immune infiltration analysis, immune checkpoint analysis, molecular docking, regulatory networks construction, and nomogram development.</p><p><strong>Results: </strong>We first intersected 4,246 differentially expressed genes with 1,884 PRMT scoring module genes to obtain 969 differentially expressed PRMT-related genes. Further Mendelian randomization analysis and machine learning jointly identified five candidate genes ( CRLF3 , ELAC2 , PBX2 , MCTP2 , and EMB ). Among these, ELAC2 , PBX2 , MCTP2 , and EMB demonstrated consistent expression trends, with the area under the curve values of the receiver operating characteristic curve exceeding 0.7 in GSE65682 and GSE134347. Therefore, they were defined as key PRMT-related genes. The gene set enrichment analysis showed enrichment in cytoplasmic translation ( ELAC2 , MCTP2 ), noncoding RNA metabolism ( EMB ), and metabolic processes ( PBX2 ). The immune infiltration analysis revealed a significant correlation between PBX2 and neutrophils, as well as between ELAC2 / MCTP2 / EMB with activated natural killer cells, CD8+ T cells.</p><p><strong>Conclusion: </strong>In this study, ELAC2 , PBX2 , MCTP2 , and EMB were identified as key genes related to PRMT for sepsis, which provided a theoretical basis for the study of sepsis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"424-440"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SHOCKPub Date : 2026-08-01Epub Date: 2025-09-23DOI: 10.1097/SHK.0000000000002710
Xiaofang Xu, Fang Hu, Zhaocai Zhang
{"title":"Nutritional Status-Based Model for Predicting Low-Lactate Shock: A Retrospective Cohort Study.","authors":"Xiaofang Xu, Fang Hu, Zhaocai Zhang","doi":"10.1097/SHK.0000000000002710","DOIUrl":"10.1097/SHK.0000000000002710","url":null,"abstract":"<p><strong>Background: </strong>Although Sepsis-3.0 defines septic shock as hypotension with serum lactate levels >2.0 mmol/L, this criterion may miss low-lactate shock: a clinically significant phenotype characterized by hypotension but without elevated lactate levels. The epidemiological characteristics and prognostic significance of low-lactate shock remain unclear, highlighting a critical gap in current shock management models.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of 3,134 patients with shock admitted to a tertiary care medical institution from January 2015 to March 2022. We used propensity score matching (1:2 ratio) to control for confounding factors, aiming to determine the prevalence of low-lactate shock (lactate ≤ 2.0 mmol/L), identify risk factors through multivariable logistic regression, and validate the predictive model [Nutritional Risk Screening-2002-Acute Physiology and Chronic Health Evaluation-Triglycerides-Total Bilirubin (NRS-APACHE II-TG-TBIL)] using receiver operating characteristic analysis.</p><p><strong>Results: </strong>The 28-day mortality rate was slightly lower in the low-lactate shock group compared with the high-lactate group [25.4% (94/369) vs. 35.8% (990/2,765), respectively]. The age, Nutritional Risk Screening-2002 (NRS-2002) score, and venous thromboembolism risk score were significantly lower in the low-lactate shock group than in the high-lactate shock group ( P < 0.05). No statistically significant differences were observed in gender distribution ( P = 0.092). Multivariable analysis identified four independent predictors of low-lactate shock: NRS-2002 [odds ratio (OR) = 0.570, P < 0.001], Acute Physiology and Chronic Health Evaluation II (APACHE II) (OR = 0.869, P < 0.001), triglycerides (OR = 0.772, P = 0.035), and total bilirubin (OR = 0.993, P = 0.002). The composite NRS-APACHE II-TG-TBIL model showed excellent discrimination (area under curve = 0.800, P < 0.001) with balanced sensitivity (72.6%) and specificity (73.5%).</p><p><strong>Conclusions: </strong>Low-lactate shock carries substantial mortality risk (25.4%). The validated NRS-APACHE II-TG-TBIL model (area under curve = 0.800) provides an effective tool for early detection, addressing critical diagnostic gaps in shock management.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":"323-332"},"PeriodicalIF":2.7,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145131905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}