ABSTRACT
Objective:To explore the predictive value of Red Blood Cell Distribution Width (RDW) in predicting the prognosis of patients with Extracorporeal Membrane Oxygenation (ECMO).Methods:The clinical data of patients undergoing ECMO admitted to Intensive Care Unit of Sichuan Provincial People’s Hospital from January 2015 to January 2020 were retrospectively analyzed. Patients were divided into the survival group and death group according to the prognosis during ICU hospitalization. The patients' basic data , acute physiology and chronic health score system Ⅱ (APACHE Ⅱ), RDW and activated partial thromboplastin time (APTT) at 72 hours after treatment with ECMO were compared between the two groups. Univariate and Logistic regression multivariate analyses were used to analyze the prognostic factors of patients with ECMO, predictive models and death warning scores were established. The receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic efficacy of RDW and death warning scores for the prognosis of patients with ECMO.Results:A total of 71 patients with ECMO who met the inclusion criteria were included, including 38 patients in the death group and 33 patients in the survival group. The age, APACHE-Ⅱscore, 72 h RDW and 72 h APTT in the death group were higher than those in the survival group. Respectively, the hospitalization time of ICU in the death group was significantly lower than that in the survival group ( P< 0.05). Logistic regression analysis showed that APACHE-Ⅱscore ( OR=1.117, P=0.047)、72 h RDW( OR=1.102, P=0.029) and 72 h APTT ( OR=1.049, P=0.029) were independent risk factors for death in patients with ECMO. ROC curve analysis showed that the area under ROC curve (AUC) of the APACHE-Ⅱ, score 、72 h RDW and 72 h APTT were 0.691, 0.691 and 0.632( P<0.05), Respectively, the combined AUC was 0.764, the sensitivity was 0.526, and the specificity was 0.909. The death warning score of patients with ECMO was established according to the Predictive model , which is less than 2 points with low risk of death and more than 2 points with high risk of death. The area under the ROC curve of death warning score is 0.8, the sensitivity is 0.607 and the specificity is 0.923. Conclusions:The RDW at 72 hours after treatment with ECMO has a good value in predicting the prognosis of patients with ECMO. Besides, a greater predictive value for the prognosis of patients with ECMO by combining 72 hours RDW, 72 hours APTT with APACHE-Ⅱscore than that of any separate indicator.
ABSTRACT
Objective To clarify the role of FLT3 signaling-dependent pulmonary conventional dendritic cells (cDCs) in the pathogenesis of lipopolysaccharide (LPS)-induced acute lung injury (ALI),and as well as the modulation effects of cDCs in vivo on the inflammatory responses to acute lung injury.Methods Thirty C57BL/6 male mice were divided into normal control group,LPS group,FLT3L pretreatment group,lestaurtinib,(a high efficient and specific blocker in FLT3 signal pathway) pretreatment group and vehicle (DMSD) control group.FLT3L and lestaurtinib were administrated subcutaneously for 5 days.Murine model of ALI was subsequently established by intra-tracheal application of LPS and lung specimens were harvested 6 h or 24 h later.The accumulation and maturation of pulmonary cDCs were assessed by flow cytometry.IL-6 and TNF-α were quantified to evaluate lung inflammation.Lung injury was estimated by lung wet weight/body weight ratio (LWW/BW) and histopathological assessment.Lung myeloperoxidase (MPO) activity was measured to evaluate neutrophil infiltration.Transcription factors Tbet/GATA-3 mRNA ratio was determined to estimate balance of Th1/Th2 response.IFN-γ and IL-4 were quantified to evaluate Th1-specific and Th2-specific cytokine production respectively.Results The accumulation and maturation of pulmonary cDCs peaked at 6h after LPS challenge.FLT3L pretreatment significantly stimulated the accumulation and maturation of pulmonary cDCs (P ＜ 0.05),leading to markedly deterioration of LWW/BW and lung histopathological changes.Meanwhile lung MPO activity and T-bet/GATA-3 mRNA ratio were elevated (P ＜ 0.05).Furthermore,the production of IL-6,TNF-α and IFN-γwas markedly increased by FLT3L pretreatment (P ＜ 0.05).In contrast,lestaurtinib pretreatment markedly inhibited the accumulation and maturation of pulmonary cDCs (P ＜ 0.05),leading to significant improvement of LWW/BW and lung histopathological changes.Meanwhile lung MPO activity and T-bet/ GATA-3 mRNA ratio were decreased (P ＜ 0.05).Furthermore lestaurtinib efficiently suppressed the production of IL-6,TNF-α and IFN-γ (P ＜ 0.05).Conclusion This study thus demonstrated that FLT3 signaling-dependent pulmonary cDCs could control the initiation of acute lung inflammation response to LPS-induced ALI through the regulation of neutrophil infiltration and balance of Thl/Th2 response.
ABSTRACT
Objective To evaluate the effect of sucralfate and acid-suppressive drugs on preventing ventilator-associated pneumonia (VAP) in mechanically ventilated patients.Methods All randomized controlled trials (RCTs),which studied the effect of sucralfate and acid-suppressive drugs on the incidence of VAP in mechanically ventilated patients,were searched from PubMed,Embase and the Cochrane Library during January 1966 to March 2013 via manual and computer retrieval.All related data were extracted.Meta analysis was conducted using the statistical software RevMan 5.2 and the quality of the RCTs was strictly evaluated with the methods recommended by the Cochrane Collaboration.Results A total of 15 RCTs involving 1315 patients in the sucralfate group and 1568 patients in the acid-suppressive drug group were included in this study.The incidence of VAP was significantly reduced in the sucralfate group (RR =0.81,95％ CI 0.7-0.95,P =0.008),while no difference was found between the two groups in the incidence of stress-related gastrointestinal bleeding (RR =0.96,95％ CI 0.59-1.58,P =0.88).No statistical difference was found in the days on ventilator,duration of ICU stay and ICU mortality in the two groups (all P values ＞ 0.05).Conclusion In patients with mechanical ventilation,sucralfate could decrease the incidence of VAP,while has no such effect on the stress-related gastrointestinal bleeding,the days on ventilator,duration of ICU stay and ICU mortality.
ABSTRACT
Objective To investigate the accumulation and maturation status of pulmonary conventional dendritic cells (cDCs) in the early phase of acute lung injury (ALI),and to explore the way of the inflammatory responses and lung injury modulated by cDCs in vivo.MethodsMale C57BL/6 mice were randomly ( random number) divided into the normal control group,6 h-ALI group and 24 h-ALI group.Murine model of ALI was made by intra-tracheal administration of lipopolysaccharide (LPS) and lung specimens were taken 6 h or 24 h later.The accumulation and maturation status of pulmonary cDCs were assessed by flow cytometry.IL-6 and TNF-α were quantified to evaluate the lung inflammation.Transcription factors T-bet/GATA-3 mRNA ratio was determined to estimate the balance between Th1/Th2 responses.IFN-γand IL-4 were quantified to evaluate Thl-specific and Th2-specific cytokine production respectively.Lung injury was estimated by lung wet weight/body weight ratio (LWW/BW) and histopathological assessment.Comparison between groups was performed using one -way ANOVA.ResultsCompared with normal control group,LPS challenge resulted in higher level of IL-6 and TNF-α,increased LWW/BW ratio and significant histopathological changes (P ＜0.01 ).The accumulation and maturation of pulmonary cDCs in 6 h-ALI group were significantly increased after LPS challenge (P ＜0.01 ),while the accumulation and maturation of pulmonary cDCs in 24 h-ALI group were significantly lower than that in 6 h-ALI group ( P ＜0.01 ).Compared with normal control group,the expression of T-bet mRNA in 24 h-ALI group was markedly enhanced ( P ＜ 0.01 ) and the production of IFN-γ was increased as well ( P ＜ 0.01 ).ConclusionsThe accumulation and maturation of pulmonary cDCs peaked within 24 h after LPS challenge,pulmonary cDCs may initiate and amplify acute lung inflammation of ALI by enhancing the Th1 immune response and ensuing cytokine production.