Immune profiles and clinical outcomes between sepsis patients with or without active cancer requiring admission to intensive care units

Fang, Wenfeng; Chen, Yu‐Mu; Lin, Chiung-Yu; Huang, Kuo‐Tung; Kao, Hsu-Ching; Fang, Ying-Tang; Huang, Chung‐Cheng; Chang, Ya‐Ting; Wang, Yi-His; Wang, Chin‐Chou

doi:10.1371/journal.pone.0179749

Cited by 19 publications

(17 citation statements)

References 48 publications

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“…The higher Charlson Comorbidity Index in the VAE group was due to the higher percentage of patients with cancer. As in our previous study, sepsis patients with underlying active cancer had higher baseline levels of plasma IL-10 9 . Although IL-10 levels were higher in the late VAE group than in the non-VAE group on day 1 and day 7, whether cancer patients were at risk of developing VAE for this reason needs further investigation.…”

Section: Discussionsupporting

confidence: 80%

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Risk factors and associated outcomes of ventilator-associated events developed in 28 days among sepsis patients admitted to intensive care unit

Fang

Huang

et al. 2020

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We hypothesized that Ventilator-Associated Event (VAE) within 28 days upon admission to medical intensive care units (ICUs) can be a predictor for poor outcomes in sepsis patients. We aimed to determine the risk factors and associated outcomes of VAE. A total of 453 consecutive mechanically ventilated (MV) sepsis patients were enrolled. Of them, 136 patients had immune profile study. Early VAE (< 7-day MV, n = 33) was associated with a higher mortality (90 days: 81.8% vs. 23.0% [non-VAE], P < 0.01), while late VAE (developed between 7 and 28 days, n = 85) was associated with longer MV day (43.8 days vs. 23.3 days [non-VAE], P < 0.05). The 90-day Kaplan-Meier survival curves showed three lines that separate the groups (non-VAE, early VAE, and late VAE). Cox regression models with time-varying coefficient covariates (adjusted for the number of days from intubation to VAE development) confirmed that VAE which occurred within 28 days upon admission to the medical ICUs can be associated with higher 90-day mortality. The risk factors for VAE development include impaired immune response (lower human leukocyte antigen D-related expression, higher interleukin-10 expression) and sepsis progression with elevated SOFA score (especially in coagulation sub-score). Ventilator-associated event (VAE) 1,2 was proposed to overcome the limitations of only focusing on ventilatorassociated pneumonia (VAP) 3 surveillance in mechanically ventilated (MV) patients in the context of surveying quality improvement. The limitations of previous VAP surveillance, which is proven to be neither sensitive nor specific 4 , hindered its application in quality improvement programs 5. Although VAE surveillance was a promising early warning tool for VAP prevention 6 , VAP prevention bundle compliance was not associated with a reduced risk of VAE 7. VAEs are defined as respiratory deterioration after a period of improved or stable gas exchange. The definition of VAE shifted the focus of surveillance from pneumonia to all conditions caused by mechanical ventilation including infectious or noninfectious conditions. The purpose was to expand the scope of surveillance to include multiple serious complications in ventilated patients, not just pneumonia, as well as to make surveillance more objective, efficient, and suitable for electronic implementation. Sepsis patients developed life-threatening organ dysfunctions (e.g., acute respiratory failure) caused by dysregulated host immune response to infection 8-10. An increase in sequential organ failure assessment (SOFA) score (including respiratory and other five sub-scores) has prognostic accuracy for in-hospital mortality in sepsis patients in the intensive care units (ICUs) 11. Since mechanical ventilator support and aggressive fluid resuscitation

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Section: Discussionsupporting

confidence: 80%

“…Plasma and peripheral blood mononuclear cell preparation, measurements of human leukocyte antigen D-related (HLA-DR) monocyte expression, and cytokine levels have been described in our previous studies 9 , 10 .…”

Section: Methodsmentioning

confidence: 99%

Risk factors and associated outcomes of ventilator-associated events developed in 28 days among sepsis patients admitted to intensive care unit

Fang

Huang

et al. 2020

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“…We are actively studying the effect of co-morbidity on the outcomes of patients with sepsis, although it is out of the scope of this study. Our previous study revealed that among patients admitted to the ICU with sepsis, those with underlying active cancer had higher baseline levels of plasma IL-10, higher trend of G-CSF and higher mortality rate than those without active cancer 30 . Our ventilator dependence risk score could help predict who will need prolonged mechanical ventilation.…”

Section: Discussionmentioning

confidence: 94%

Ventilator Dependence Risk Score for the Prediction of Prolonged Mechanical Ventilation in Patients Who Survive Sepsis/Septic Shock with Respiratory Failure

Chang

Huang

Chen

et al. 2018

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We intended to develop a scoring system to predict mechanical ventilator dependence in patients who survive sepsis/septic shock with respiratory failure. This study evaluated 251 adult patients in medical intensive care units (ICUs) between August 2013 to October 2015, who had survived for over 21 days and received aggressive treatment. The risk factors for ventilator dependence were determined. We then constructed a ventilator dependence (VD) risk score using the identified risk factors. The ventilator dependence risk score was calculated as the sum of the following four variables after being adjusted by proportion to the beta coefficient. We assigned a history of previous stroke, a score of one point, platelet count less than 150,000/μL a score of one point, pH value less than 7.35 a score of two points, and the fraction of inspired oxygen on admission day 7 over 39% as two points. The area under the curve in the derivation group was 0.725 (p < 0.001). We then applied the VD risk score for validation on 175 patients. The area under the curve in the validation group was 0.658 (p = 0.001). VD risk score could be applied to predict prolonged mechanical ventilation in patients who survive sepsis/septic shock.

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“…We used LPS-induced inflammation in macrophages as an in vitro model of sepsis. Sepsis is a life-threatening condition, and is one of the leading causes of mortality worldwide; patients’ outcomes are dependent on their immune response [ 49 , 50 ]. Despite the efforts of medical professionals, antibiotic administration within 1 h from the time of diagnosis can be difficult [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression

et al. 2018

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BackgroundSepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection, and is primarily characterized by an uncontrolled systemic inflammatory response. In the present study, we developed an effective adjunct therapy mediated by a novel mechanism, to attenuate overt inflammation. LPS-treated macrophages were adopted as an in vitro model of endotoxin-induced inflammation during sepsis. Experiments were carried out using primary mouse peritoneal macrophages and the murine macrophage cell line RAW264.7, to elucidate the mechanisms by which HDAC2 modulates endotoxin-induced inflammation.ResultsResults revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation. Thus, HDAC2 plays an important role in immune defense by regulating the expression of inflammatory genes via the c-Jun/PAI-1 pathway. During LPS-induced inflammation, overexpression of HDAC2 was found to inhibit PAI-1, TNF, and MIP-2 expression. Following LPS stimulation, HDAC2 knockdown increased nuclear translocation and DNA binding of c-Jun to the PAI-1 gene promoter, thereby activating PAI-1 gene transcription. Furthermore, inhibition of PAI-1 by TM5275 alone or in combination with theophylline notably suppressed TNF and MIP-2 expression.ConclusionHDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.

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Immune profiles and clinical outcomes between sepsis patients with or without active cancer requiring admission to intensive care units

Cited by 19 publications

References 48 publications

Risk factors and associated outcomes of ventilator-associated events developed in 28 days among sepsis patients admitted to intensive care unit

Risk factors and associated outcomes of ventilator-associated events developed in 28 days among sepsis patients admitted to intensive care unit

Ventilator Dependence Risk Score for the Prediction of Prolonged Mechanical Ventilation in Patients Who Survive Sepsis/Septic Shock with Respiratory Failure

Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression

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