Trial reportCritical care (London, England)2005
Time course of endothelial damage in septic shock: prediction of outcome.
Trial report in Critical care (London, England), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Time course of angiopoietin-2 release during experimental human endotoxemia and sepsis.Critical care (London, England) · 2009Trial
- Invention and characterization of a systemically administered, attenuated and killed bacteria-based multiple immune receptor agonist for anti-tumor immunotherapy.Frontiers in immunology · 2024Article
- Protective Effect of Sirtuin 3 on CLP-Induced Endothelial Dysfunction of Early Sepsis by Inhibiting NF-κB and NLRP3 Signaling Pathways.Inflammation · 2021Article
- Role of the Nucleotide-Binding Domain-Like Receptor Protein 3 Inflammasome in the Endothelial Dysfunction of Early Sepsis.Inflammation · 2020Article
- Gene Expression of Protein Tyrosine Phosphatase 1B and Endoplasmic Reticulum Stress During Septic Shock.Frontiers in medicine · 2019Article
- The influence of esmolol on right ventricular function in early experimental endotoxic shock.Physiological reports · 2018Article
- Time Response of Oxidative/Nitrosative Stress and Inflammation in LPS-Induced Endotoxaemia-A Comparative Study of Mice and Rats.International journal of molecular sciences · 2017Article
- Microcirculatory dysfunction and tissue oxygenation in critical illness.Acta anaesthesiologica Scandinavica · 2015Review
- Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture.Critical care (London, England) · 2014Article
- Neutrophils from critically ill septic patients mediate profound loss of endothelial barrier integrity.Critical care (London, England) · 2013Article
- Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro.BMC research notes · 2011Article
- Elevated sICAM-1 levels in patients with hemorrhagic fever with renal syndrome caused by Hantaan virus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010Article
- Interleukin-8 as a stratification tool for interventional trials involving pediatric septic shock.American journal of respiratory and critical care medicine · 2008Article
- Year in review 2005: Critical Care - resource management.Critical care (London, England) · 2006Article
- Dose-related effects of dexmedetomidine on sepsis-initiated lung injury in rats.Brazilian journal of anesthesiology (Elsevier)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEndothelial damage accounts greatly for the high mortality in septic shock. Higher expression of mediators (IL-6, IL-8, soluble intercellular adhesion molecule 1 [sICAM-1], soluble endothelial-linked adhesion molecule 1 [sELAM-1]) have been described for non-survivors in comparison with survivors. We investigated the predictive value of the mediators IL-6, IL-8, sELAM-1 and sICAM-1 and their time course in intensive care unit patients who developed septic shock with respect to outcome. MATERIALS AND
methodsWe measured serum levels of IL-6, IL-8, sELAM-1 and sICAM-1 in 40 intensive care unit patients who developed septic shock. Measurements were performed until death or until resolution of septic shock. Clinical and laboratory data were also recorded.
resultsAfter 48 hours the levels of sELAM-1 and sICAM-1 increased in non-survivors and decreased in survivors. sELAM-1 was predictive for outcome on the third day (P = 0.02) and the fourth day (P = 0.02) after diagnosis of septic shock. This difference in the time course between survivors and non-survivors occurred 7 days before death of the patients (median, 10 days). sICAM-1 levels increased significantly in non-survivors over the study period (P < 0.001). sELAM-1 (P = 0.04), IL-6 (P = 0.04) and IL-8 (P = 0.008) were significantly higher in non-survivors over the whole study period. The age and norepinephrine dose >0.5 mug/kg/min were significantly different between the groups.
conclusionsELAM-1 showed a markedly opposing course after 48 hours of septic shock. This adhesion molecule may be a useful early predictor of disease severity in the course of septic shock after early initial treatment of the patients, and might suggest considering endothelial-restoring therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.