RETRACTED: Do Plasma Levels of Circulating Soluble Adhesion Molecules Differ Between Surviving and Nonsurviving Critically III Patients?

Boldt, Joachim; Wollbrück, Matthias; Kuhn, D.; Linke, L C; Hempelmann, G.

doi:10.1378/chest.107.3.787

Cited by 69 publications

(47 citation statements)

References 25 publications

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“…This is characterized by local and systemic release of cytokines and other inflammatory mediators, including hepatic acute phase proteins, arachidonic acid metabolites, complement components, reactive species (oxygen and nitrogen), proteolytic enzymes, and neuroendocrine signals (23,47,63). For example, elevated circulating levels of IL-1, IL-6, IL-8, IL-10, TNF, soluble TNF receptor, and sICAM have all been shown to correlate with injury severity, organ failure, and mortality in multiply injured trauma patients (5,6,15,26,29,39,43,48). The upregulation of leukocyte adhesion molecules, endothelial cell damage, and the resulting influx of inflammatory cells into damaged tissues all indicate that a profound inflammatory process occurs after severe tissue trauma.…”

Section: Discussionmentioning

confidence: 99%

Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4

Levy¹,

Prince²,

Yang³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Extensive soft tissue injury and bone fracture are significant contributors to the initial systemic inflammatory response in multiply injured patients. Systemic inflammation can lead to organ dysfunction remote from the site of traumatic injury. The mechanisms underlying the recognition of peripheral injury and the subsequent activation of the immune response are unknown. Toll-like receptors (TLRs) recognize microbial products but also may recognize danger signals released from damaged tissues. Here we report that peripheral tissue trauma initiates systemic inflammation and remote organ dysfunction. Moreover, this systemic response to a sterile local injury requires toll-like receptor 4 (TLR4). Compared with wild-type (C3H/HeOuJ) mice, TLR4 mutant (C3H/HeJ) mice demonstrated reduced systemic and hepatic inflammatory responses to bilateral femur fracture. Trauma-induced nuclear factor (NF)-κB activation in the liver required functional TLR4 signaling. CD14−/− mice failed to demonstrate protection from fracture-induced systemic inflammation and hepatocellular injury. Therefore, our results also argue against a contribution of intestine-derived LPS to this process. These findings identify a critical role for TLR4 in the rapid recognition and response pathway to severe traumatic injury. Application of these findings in an evolutionary context suggests that multicellular organisms have evolved to use the same pattern recognition receptor for surviving traumatic and infectious challenges.

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Section: Discussionmentioning

confidence: 99%

Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4

Levy¹,

Prince²,

Yang³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…First, higher levels of circulating E-selectin and ICAM-1 are found in critically ill patients as compared with healthy individuals (4,(16)(17)(18)(19)(20). Furthermore, E-selectin and ICAM-1 levels further rise or remain persistently elevated in patients with multiple organ dysfunction and in nonsurvivors as compared with survivors (16,17,19,21). Especially ICAM-1 appeared to independently predict subsequent development of multiple organ failure and/or death (17,19,20).…”

Section: Figurementioning

confidence: 99%

Intensive insulin therapy protects the endothelium of critically ill patients

Langouche

Vanhorebeek²,

Vlasselaers³

et al. 2005

Journal of Clinical Investigation

425

245

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The vascular endothelium controls vasomotor tone and microvascular flow and regulates trafficking of nutrients and biologically active molecules. When endothelial activation is excessive, compromised microcirculation and subsequent cellular hypoxia contribute to the risk of organ failure. We hypothesized that strict blood glucose control with insulin during critical illness protects the endothelium, mediating prevention of organ failure and death. In this preplanned subanalysis of a large, randomized controlled study, intensive insulin therapy lowered circulating levels of ICAM-1 and tended to reduce E-selectin levels in patients with prolonged critical illness, which reflects reduced endothelial activation. This effect was not brought about by altered levels of endothelial stimuli, such as cytokines or VEGF, or by upregulation of eNOS. In contrast, prevention of hyperglycemia by intensive insulin therapy suppressed iNOS gene expression in postmortem liver and skeletal muscle, possibly in part via reduced NF-κB activation, and lowered the elevated circulating NO levels in both survivors and nonsurvivors. These effects on the endothelium statistically explained a significant part of the improved patient outcome with intensive insulin therapy. In conclusion, maintaining normoglycemia with intensive insulin therapy during critical illness protects the endothelium, likely in part via inhibition of excessive iNOS-induced NO release, and thereby contributes to prevention of organ failure and death.

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“…Elevated adhesion molecules have also been reported in patients with systemic inflammatory response syndrome, sepsis, and multiple organ failure (16)(17)(18)(19). These clinic syndromes and LCOS are inseparable parameters especially in critically ill patients.…”

Section: Discussionmentioning

confidence: 99%

Prognostic significance of sICAM-1 and sVCAM-1 Molecules for cardiac surgery in pediatric patients with pulmonary hypertension

Yıldırım¹,

Güzelmeriç²,

Oner³

et al. 2014

Anadolu Kardiyol Derg

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Objective: To investigate preoperative and postoperative blood levels of soluble intercellular and vascular cell adhesion molecules (sICAM-1, sVCAM-1) in patients with and without pulmonary hypertension (PAH) due to congenital heart disease and left to right (L-R) shunt and to determine whether these molecules can be used as reliable prognostic markers of endothelial activity to predict surgical outcomes. Methods: In this observational prospective cohort study; 42 patients, operated for L-R shunt were divided into three groups. Group 1: L-R shunt without PAH, Group 2: L-R shunt with PAH, Group 3: L-R shunt with PAH and postoperative low cardiac output syndrome (LCOS). Their sICAM-1 and sVCAM-1 levels were measured preoperatively (sICAM-0, sVCAM-0) and on the first (sICAM-1, sVCAM-1) and fifth postoperative days (sICAM-2, sVCAM-2).ROC curve for various cut-off levels of sICAM-0, sVCAM-0 in differentiating PAH patients with and without LCOS. Results: In Group 3, sICAM-0 and sVCAM-2 levels were higher than Group 1 and 2. The ROC curve demonstrated a significant association between sICAM-0 in patients with L-R shunt and PAH (Group 2 and 3) and the development of LCOS (area under the curve: 0.98, p<0.01 and 0.97, p<0.01, respectively). At a sICAM-0 concentration >359 ng/mL, there was a sensitivity of 90% and specificity of 95% for identification of LCOS in patients with L-R shunt and PAH (AUC: 0.98, 95% CI: 0.95-1.02, p<0.01). Conclusion: High preoperative sICAM-1 molecule may be used to predict postoperative dichotomous outcome in patients with PAH associated with L-R shunt. (Anadolu Kardiyol Derg 2014; 14: 274-9)

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RETRACTED: Do Plasma Levels of Circulating Soluble Adhesion Molecules Differ Between Surviving and Nonsurviving Critically III Patients?

Cited by 69 publications

References 25 publications

Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4

Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4

Intensive insulin therapy protects the endothelium of critically ill patients

Prognostic significance of sICAM-1 and sVCAM-1 Molecules for cardiac surgery in pediatric patients with pulmonary hypertension

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