SHOCK最新文献

{"title":"Impaired fatty liver regeneration post-major resection: a mitochondrial problem.","authors":"Tyler P Robinson, Tewfik Hamidi, Yanlin Jiang, Xiaoling Jin, Robson Francisco Carvalho, Sarah Santiloni Cury, Rafael Ribeiro Correia, Adrian M Baris, Andris Kronbergs, Teresa A Zimmers, Leonidas G Koniaris","doi":"10.1097/SHK.0000000000002713","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002713","url":null,"abstract":"<p><p>Fatty liver disease is associated with a markedly increased risk of liver dysfunction and death after major hepatectomy. We previously demonstrated impaired hepatocyte proliferation, delayed liver regeneration, and increased mortality in post-hepatectomy murine fatty liver. However, the underlying mechanism(s) remains unclear. In this study, we sought to define the mechanisms underlying fatty liver regenerative failure following resection. The hepatic transcriptome was analyzed after 70% or 80% hepatectomy in lean, and diet-induced obese (DIO) mice. A gene array analysis was conducted. Human liver samples with lean and fatty livers were evaluated in a similar manner. Gene ontology (GO) and KEGG pathways were analyzed. Principal component analysis showed striking differences between lean and DIO livers at baseline and following graded hepatectomy, suggesting fundamental underlying differences in DIO livers. At baseline, DIO livers demonstrated an upregulation of mitochondrial-related processes. Post-hepatectomy, however, these processes were downregulated. PPARγ signaling, which activates mitochondrial biogenesis, was significantly downregulated. Essential mitochondrial functions such as citrate cycle, oxidative phosphorylation, and fatty acid degradation were significantly decreased in the DIO liver after resection, demonstrating an inability to accommodate the increased mitochondrial energy demands associated with the regenerative response. Examination of human fatty livers revealed similar changes in baseline mitochondrial function. Using an unbiased analytic approach, fatty liver demonstrates an inability of mitochondrial-related processes to adapt to increased hepatocellular energetic demands following resection. Future therapies to improve post-hepatectomy mitochondrial function should improve post-resection outcomes in fatty liver patients.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150678","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":"Abnormal Platelet-to-Lymphocyte Ratio is Associated with Poor Outcomes in Pediatric Sepsis.","authors":"Carine S Abi Gerges, Courtney M Rowan, Francis Pike, Daniel T Cater","doi":"10.1097/SHK.0000000000002681","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002681","url":null,"abstract":"<p><strong>Objective: </strong>Sepsis remains a major cause of morbidity and mortality in children, necessitating an early risk assessment to prevent delayed treatment and achieve optimal outcomes. This study investigated the association between systemic immune-inflammatory indices and clinical outcomes in children with sepsis.</p><p><strong>Design: </strong>Single-center, retrospective cohort study.</p><p><strong>Setting: </strong>Pediatric intensive Care Unit (PICU) of a tertiary care children's hospital from 2015 to 2023.</p><p><strong>Patients: </strong>Children aged 0-18 years admitted with sepsis. Patients were excluded if they lacked a complete blood count with differential on admission.</p><p><strong>Results: </strong>420 patients were included. The platelet-to-lymphocyte ratio (PLR) was associated with higher mortality [HR:1.001 (1.000-1.002), p:0.032]. Incorporating PLR into the Pediatric Index of Mortality (PIM) score improved the model discrimination for mortality (AUROC 0.705 vs. 0.774; AUPRC 0.202 vs 0.257). Similarly, adding PLR to the PRISM-III improved AUROC from 0.648 to 0.697. High PLR was also associated with higher odds of requiring intubation (OR 2.42, p:0.005) and extracorporeal membrane oxygenation (OR 4.74, p:0.002) and with decreased sub distribution hazard of extubation, ICU discharge, and hospital discharge alive at 28 days (SHR: 0.89, 0.72, and 0.76 respectively; all p < 0.005).</p><p><strong>Conclusions: </strong>High PLR at admission was independently associated with worse clinical outcomes in pediatric patients with sepsis. Adding PLR to PIM and PRISM III enhanced the predictive performance. PLR is a simple and readily available index that may improve early risk stratification in this high-risk population.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150709","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":"Astrocytes in Sepsis-Associated Encephalopathy: Pivotal Roles in Dual Pathogenesis and Therapeutic Perspectives.","authors":"Jiatian Cui, Jianfeng Liu, Yan Cui, Keliang Xie","doi":"10.1097/SHK.0000000000002709","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002709","url":null,"abstract":"<p><p>Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction secondary to the systemic inflammatory response in sepsis. Clinically characterized by impaired cognition and altered consciousness, SAE contributes to poor patient prognosis. Astrocytes, one of the predominant glial cells in the central nervous system (CNS), are essential for maintaining CNS homeostasis. Mounting evidence highlights their critical involvement in SAE pathogenesis, driving increasing research interest. This review explores the mechanistic roles of astrocytes in SAE and identifies related therapeutic targets. We categorize astrocytic involvement in SAE into: (1) Mediation of neuroinflammation initiation and progression; (2) Impairment of antioxidant defenses; (3) Dual roles in blood-brain barrier integrity (protection and disruption); (4) Modulation of energy metabolism; (5) Modulation of neurotransmitter metabolism; (6) Regulation of water and ion homeostasis; (7) Modulation of synaptic plasticity. Furthermore, we systematically review current astrocyte-targeted therapeutic strategies for SAE and elucidate their underlying mechanisms, offering insights for developing future targeted interventions.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081435","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":"Suppressive effects of lovastatin on OGD/hemin-induced inflammation and ferroptosis in brain microvascular endothelial cells through the METTL3/HDAC6 cascade.","authors":"Xiaolong Wang, Liangsheng Peng, Li Han, Yuanzhao Tuo, Huahui Chen, Xuemin Wang, Lixiong Xue, Xinmin Ding","doi":"10.1097/SHK.0000000000002688","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002688","url":null,"abstract":"<p><strong>Background: </strong>Intracerebral hemorrhage (ICH) induces dysfunction in brain microvascular endothelial cells (BMVECs), thereby contributing to secondary brain injuries. Emerging evidence implicates METTL3 and HDAC6 as critical mediators of inflammation and ferroptosis that contribute to post-ICH neurological impairment. Lovastatin exhibits anti-inflammatory, anti-oxidative, and neuroprotective properties. This study elucidated the therapeutic potential of lovastatin in attenuating BMVEC injury following ICH, while investigating the mechanistic involvement of METTL3 and HDAC6 in this protective process.</p><p><strong>Methods: </strong>The cell damage model following ICH was generated by stimulating human BMVECs with oxygen and glucose deprivation (OGD) and hemin (OGD/H). Cell impairment was assessed by detecting permeability. Cell viability, migration, tube formation, and apoptosis were evaluated by CCK-8, transwell, tube formation, and flow cytometry analyses, respectively. TNF-α and IL-6 levels were detected by ELISA. Cell ferroptosis was analyzed by assessing related factor expression. Methylated RNA immunoprecipitation (MeRIP), RIP, quantitative PCR, and actinomycin D treatment assays were used to test the METTL3/histone deacetylase 6 (HDAC6) relationship.</p><p><strong>Results: </strong>Lovastatin protected BMVECs from OGD/H-evoked dysfunction. Moreover, lovastatin relieved OGD/H-evoked oxidative stress, inflammation, and ferroptosis in BMVECs. Mechanistically, the potential docking poses of lovastatin with METTL3 were predicted, and METTL3 stabilized HDAC6 mRNA through mRNA m6A modification. Lovastatin reduced METTL3 and HDAC6 levels in OGD/H-stimulated human BMVECs, and lovastatin decreased HDAC6 expression by downregulating METTL3. Furthermore, lovastatin alleviated OGD/H-induced BMVEC impairment, inflammation and ferroptosis by the METTL3/HDAC6 cascade.</p><p><strong>Conclusion: </strong>Our study demonstrates that lovastatin suppresses OGD/H-induced inflammation and ferroptosis in human BMVECs through the potential METTL3/HDAC6 cascade, providing novel evidence for the neuroprotective role of lovastatin.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081474","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":"Artificial oxygen carriers: lessons from hemoglobin-based oxygen carrier clinical trials and current development efforts.","authors":"Youmna Abdelghany, Matthew B Amdahl, Qinzi Xu, Mark T Gladwin, Jesus Tejero, Jason J Rose","doi":"10.1097/SHK.0000000000002716","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002716","url":null,"abstract":"<p><p>The clinical benefit of blood transfusion is undeniable, and yet reliance on donated blood products has several shortcomings. These include risks of supply shortages due to reliance on volunteer donors, short storage life, and potential infectious disease transmission. Immune response complications to donated blood cannot be completely avoided, even despite significant advances in testing. Many of these limitations are exacerbated in low-income countries. For decades, cell-free hemoglobin-based blood substitutes have been developed and tested as potential substitutes for red blood cell transfusions. Early studies found that purified, native Hb exhibited significant safety risks, such as hypertension from excessive vasoconstriction and evidence of multiple organ toxicities. These effects are likely in part due to the reactive heme center, that will scavenge nitric oxide, generate reactive oxygen species, and may drive sterile inflammation. Numerous strategies have been explored to further modify hemoglobin in the hope of creating a safe and well-tolerated blood substitute. Despite some promising results in preliminary studies, large-scale clinical trials have continued to show elevated rates of adverse events and/or a failure to meet specified clinical endpoints. As a result, no hemoglobin-based oxygen carrier (HBOC) has obtained US FDA approval for clinical use. This review focuses on the history of hemoglobin-based oxygen carrier development, the lessons that have been learned from prior failures of HBOC programs, and the status of ongoing artificial oxygen carrier development efforts.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150730","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":"Association Between Geriatric Nutritional Risk Index and the Progression of Chronic Critical Illness and Short-term Prognosis in Sepsis Patients.","authors":"Chaowei Wang, Zhiyuan Zhang, Jiangui Wang, Chenghua Wang, Zixin Luo, Jianhua Li, Kang Zou, Qinglin Xu","doi":"10.1097/SHK.0000000000002711","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002711","url":null,"abstract":"<p><strong>Background: </strong>The impact of nutritional status on the advancement to chronic critical illness (CCI) in sepsis patients is not well understood. This study aimed to explore the connection between the nutritional risk index (GNRI) and the development of CCI.</p><p><strong>Methods: </strong>We performed a retrospective study utilizing data from 7,380 sepsis patients in the MIMIC-IV database. The patients were categorized into High GNRI (n = 3412) and Low GNRI (n = 3968) groups. CCI was defined as an ICU stay >14 days with persistent organ dysfunction. Statistical analyses included univariate and multivariate logistic regression, Cox regression, and curve fitting.</p><p><strong>Results: </strong>Among 7,380 patients (59.1% male, median age 66 years), the high GNRI group had lower body weight, albumin levels, and higher incidence of acute kidney injury. GNRI was a significant predictor of CCI progression (OR: 0.99, 95% CI: 0.98-0.99, p<0.001). After adjusting for confounders, the negative correlation remained (adjusted OR: 0.99, 95% CI: 0.98-1.00, p=0.002). A nonlinear relationship was observed, with an inflection point at GNRI 96.616. Subgroup analyses showed more pronounced protective effects in patients <65 years old and those without cancer, chronic kidney disease, or acute kidney injury. GNRI was also negatively associated with 28-day mortality (adjusted OR: 0.94, 95% CI: 0.93-0.96, p<0.001).</p><p><strong>Conclusion: </strong>GNRI is an independent predictor of CCI progression and 28-day mortality in sepsis patients. Early nutritional assessment and personalized interventions are crucial in critical care settings. Future research should validate these findings in diverse populations and explore targeted nutritional interventions.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150662","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":"Short Chain Fatty Acid Supplementation After Traumatic Brain Injury Attenuates Neurologic Injury Via the Gut-Brain-Microglia Axis.","authors":"Booker T Davis Iv, Hyebin Han, Mecca B A R Islam, Kacie Ford, Zhangying Chen, Hiam Abdala-Valencia, Stefan Greene, Craig Weiss, Daniele Procissi, Steven J Schwulst","doi":"10.1097/SHK.0000000000002706","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002706","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Traumatic brain injury (TBI) is an underrecognized public health threat. There are limited therapeutic options for TBI, and supportive care remains the mainstay of treatment. Our previously published data demonstrate that post-TBI fecal microbiome transplantation (FMT) can reverse TBI-induced depletion of commensal bacteria, preserve white matter connectivity and neurocognition, and decrease cortical volume loss in mice after TBI.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Hypothesis: &lt;/strong&gt;We hypothesized that post-TBI supplementation with Short Chain Fatty Acids (SCFAs), metabolites of commensal gut bacteria, would attenuate neurologic injury after TBI in mice.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;14-week-old male C57BL/6 mice (n=52) underwent TBI via a controlled cortical impact vs. sham injury. Post-TBI, each group was treated with the SCFAs acetate, butyrate, and propionate vs. molar equivalent sodium chloride vehicle via free access to drinking water for four weeks post-TBI. The stool was collected three days pre-and sixty days post-TBI to assess the gut microbial community structure via 16s ribosomal RNA gene amplicon sequencing. Neurocognitive testing was performed with open-field and zero-maze testing. Ventricular volume and white matter connectivity were measured with 3D, contrast-enhanced MRI. Lastly, the transcriptional response of microglia was assessed with single-cell RNA sequencing (scRNAseq).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;SCFA supplementation decreased TBI-induced microbial loss, attenuated ventricular volume loss, preserved white matter connectivity, and altered the transcriptional profile of microglia after TBI. Post-TBI SCFA supplementation preserved the abundance of the butyrate-producing taxa Firmicutes, Clostridia, Ruminoccacaceae, and Peptoccacaceae (p=0.01). SCFA also reduced the TBI-induced increase in Clostridiales and Bacteroidales compared to the salt vehicle group (p=0.05). We also observed the preservation of non-TBI murine anxiety-like behavior in SCFA-treated TBI mice compared to vehicle-treated TBI mice in zero-maze (152.3 ± 101.8 cm vs. 147.5 ± 60.0 cm, p=0.006). These results were recapitulated with open field testing (11.7 ± 3%-time in the center in SCFA-treated TBI mice vs. 15.0 ± 6% %-time in the center of the field in vehicle-treated mice; p=0.002). Lastly, we observed upregulation of transcripts for the neuroprotective heat shock family of proteins and downregulation of neurodegeneration-associated transcripts, indicating an overall neuroprotective phenotype in microglia after SCFA supplementation post-TBI.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;We hypothesized that SCFA supplementation would attenuate neurologic injury after TBI in mice. SCFA supplementation attenuated neurocognitive deficits, reduced cortical volume loss, preserved white matter connectivity, and decreased neuroinflammation. These benefits may result from the direct replacement of SCFAs. However, there may also be secondary mechanisms rel","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081500","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":"Methylene blue in cardiogenic shock and cardiac arrest: A systematic review.","authors":"Riley J Batchelor, Millie Watkins, Jason E Bloom, Malanka Lankaputhra, Derek P Chew, Aiden Burrell, Andrew Taylor, Dion Stub, David M Kaye","doi":"10.1097/SHK.0000000000002700","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002700","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiogenic shock and cardiac arrest are associated with high risk of mortality despite advances in resuscitation techniques and supportive care. A growing body of evidence implicates a systemic inflammatory response syndrome (SIRS) in the pathogenesis of post-arrest vasoplegia and end-organ injury. Methylene blue (MB), a nitric oxide pathway inhibitor, has shown efficacy in vasoplegic and septic shock, yet its role in cardiogenic shock or cardiac arrest is not well established.</p><p><strong>Methods: </strong>We conducted a systematic review of peer-reviewed studies examining methylene blue in cardiogenic shock or cardiac arrest. Electronic databases MEDLINE, EMBASE, CENTRAL, Scopus, and Web of Science were searched in March 2025. Preclinical randomised trials and clinical studies in adult humans or animal models were included.</p><p><strong>Results: </strong>Out of 676 screened records, seven studies met inclusion criteria: six preclinical randomised animal studies and one retrospective human cohort study. Early porcine studies using electrically induced ventricular fibrillation and continuous MB infusion during CPR demonstrated improved survival, haemodynamic profile, and neurologic outcomes. In contrast, more recent, well conducted bolus-only studies using infarct-induced models reported minimal or no benefit associated with MB administration. The single human study lacked a comparator group and provided limited cardiogenic shock-specific outcome data.</p><p><strong>Conclusions: </strong>This systematic review highlights the lack of data available for MB in cardiogenic shock and cardiac arrest, especially in humans. There was a potential therapeutic signal for methylene blue in some animal models of cardiogenic shock and cardiac arrest. Prospective studies with clinically relevant models of cardiac injury are warranted to determine whether MB can improve outcomes in this high-risk population.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081496","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":"Endothelial Activation and Stress Index Elevation Associated with Adverse Prognosis in Sepsis-associated acute kidney injury Patients: Validation Based on Two Critical Care Cohorts.","authors":"Zhiyuan Zhang, Chaowei Wang, Jiangui Wang, Zixin Luo, Kang Zou, Qinglin Xu","doi":"10.1097/SHK.0000000000002715","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002715","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-associated acute kidney injury (SA-AKI) is a prevalent complication in critical care settings with high mortality. Early identification of high-risk patients is crucial. The Endothelial Activation Stress Index (EASIX) has been studied in other conditions but not in SA-AKI. This study evaluates EASIX's association with short-term mortality in SA-AKI patients.</p><p><strong>Methods: </strong>In this retrospective cohort study, data from 12,267 SA-AKI patients in MIMIC-IV were analyzed. EASIX was categorized using curve fitting and inflection point analysis. Propensity score matching (PSM), overlap weighting (OW), pair algorithm (PA), and inverse probability of treatment weight (IPTW) ensured data balance. Cox models, Kaplan-Meier analysis, subgroup analyses, ROC Curves and E-value assessments were used to examine the relationship between EASIX and outcomes. Furthermore, we validated these findings using the eICU database.</p><p><strong>Results: </strong>A non-linear association between EASIX and 28-day mortality was found, with an inflection point at 10.83. PSM balanced covariates. Kaplan-Meier analysis showed significantly lower survival in the high EASIX group (P < 0.001 pre-PSM, P = 0.002 post-PSM). Post-PSM, the high EASIX group had higher 28-day mortality (42.9% vs. 32.9%), in-hospital mortality (40.5% vs. 30.8%), and ICU mortality (29.6% vs. 20.4%; all P < 0.001). Multivariable regression and weighting methods (IPTW, PA, OW) confirmed the increased mortality risk. Subgroup and E-value analyses further validated these findings. ROC analysis yielded an AUC for 28-day mortality, outperforming SOFA and other traditional covariates. External validation in the eICU database confirmed similar performance.</p><p><strong>Conclusion: </strong>EASIX is a reliable prognostic indicator for short-term mortality in SA-AKI patients. Elevated EASIX levels are associated with increased mortality risk. Future research should explore its clinical utility in risk stratification for SA-AKI.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150639","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":"Re-increases in C-reactive protein in patients with sepsis are associated with the development of persistent inflammation, immunosuppression, and catabolism syndrome.","authors":"Takuma Kishimoto, Naoto Mizumura, Jun Matsubayashi, Kazunori Fujino, Yasuyuki Tsujita, Naoto Shiomi","doi":"10.1097/SHK.0000000000002705","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002705","url":null,"abstract":"<p><strong>Background: </strong>Multiple insults, such as infection and trauma, can induce the features of persistent inflammation, immunosuppression, and catabolism syndrome (PICS) in animal models.</p><p><strong>Methods: </strong>We performed a retrospective cohort study to investigate the relationship between multiple insults and the development of PICS in patients with sepsis. The study was conducted on 282 intensive care unit patients with sepsis (Sepsis-3 criteria) hospitalized for ≥15 days. The number and sizes of C-reactive protein (CRP) re-increases during the first 14 days were measured to represent multiple insults. PICS development was assessed between days 15 and 28.</p><p><strong>Results: </strong>Patients in the PICS group (n=145) had significantly larger numbers of CRP re-increases and size of the largest CRP re-increase than the non-PICS group (n=137) (2 vs. 1, P<0.001; and 3.3 vs. 1.3 mg/dL, P<0.001; respectively). Multivariable conditional logistic regression analysis showed that both the number of CRP re-increases and the size of the largest CRP re-increase were significantly associated with PICS development (adjusted odds ratio [95% confidence interval], 1.57 [1.12-2.21], P=0.009; and 1.10 [1.02-1.19], P=0.012; respectively).</p><p><strong>Conclusion: </strong>These findings suggest that CRP re-increases within the 14 days following intensive care unit admission are significantly associated with the development of PICS in patients with sepsis within 15-28 days.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150712","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}