Objective To evaluate the efficiency and associated factors of noninvasive positive pressure ventilation( NPPV) in the treatment of acute lung injury( ALI) and acute respiratory distress syndrome( ARDS) .Methods Twenty-eight patients who fulfilled the criteria for ALI/ARDS were enrolled in the study. The patients were randomized to receive either noninvasive positive pressure ventilation( NPPV group) or oxygen therapy through a Venturi mask( control group) . All patients were closely observed and evaluated during observation period in order to determine if the patients meet the preset intubation criteria and the associated risk factors. Results The success rate in avoiding intubation in the NPPV group was 66. 7%( 10/15) , which was significantly lower than that in the control group ( 33. 3% vs. 86. 4% , P = 0. 009) . However, there was no significant difference in the mortality between two groups( 7. 7% vs.27. 3% , P =0. 300) . The incidence rates of pulmonary bacteria infection and multiple organ damage were significantly lower in the NPPV success subgroup as compared with the NPPV failure group( 2 /10 vs. 4/5, P =0. 01;1 /10 vs. 3/5, P = 0. 03) . Correlation analysis showed that failure of NPPV was significantly associated with pulmonary bacterial infection and multiple organ damage( r=0. 58, P lt;0. 05; r =0. 53, P lt;0. 05) . Logistic stepwise regression analysis showed that pulmonary bacterial infection was an independent risk factor associated with failure of NPPV( r2 =0. 33, P =0. 024) . In the success subgroup, respiratory rate significantly decreased( 29 ±4 breaths /min vs. 33 ±5 breaths /min, P lt; 0. 05) and PaO2 /FiO2 significantly increased ( 191 ±63 mmHg vs. 147 ±55 mmHg, P lt;0. 05) at the time of 24 hours after NPPV treatment as compared with baseline. There were no significant change after NPPV treatment in heart rate, APACHEⅡ score, pH and PaCO2 ( all P gt;0. 05) . On the other hand in the failure subgroup, after 24 hours NPPV treatment, respiratory rate significantly increased( 40 ±3 breaths /min vs. 33 ±3 breaths /min, P lt;0. 05) and PaO2 /FiO2 showed a tendency to decline( 98 ±16 mmHg vs. 123 ±34 mmHg, P gt; 0. 05) . Conclusions In selected patients, NPPV is an effective and safe intervention for ALI/ARDS with improvement of pulmonary oxygenation and decrease of intubation rate. The results of current study support the use of NPPV in ALI/ARDS as the firstline choice of early intervention with mechanical ventilation.
ObjectiveTo explore the value of procalcitonin-to-albumin (PAR) in patients with acute respiratory distress syndrome (ARDS).MethodsA retrospective study was carried on patients diagnosed with ARDS from December 2016 to March 2018. The receiver-operating characteristics (ROC) curve was used to identify the cutoff value of PAR. The association of PAR and 28-day mortality was evaluated using univariate and multivariable Cox regression.ResultsIn the final analysis, there were a total of 255 patients included. Of whom 164 (64.3%) was male, 91 (35.7%) was female and the mean age was 52.1±14.5 years old. The 28-day mortality of all the patients was 32.9% (n=84). ROC curve revealed that the cutoff value of PAR was 0.039 (specificity: 0.714, sensitivity: 0.702) and area under the curve was 0.793 (95%CI: 0.735 - 0.850, P<0.001). The following variables were considered for multivariable adjustment: age, body mass index, pneumonia, aspiration, sepsis, surgery, PaO2/FiO2, red blood cell counts and PAR (P<0.01 in univariate analysis). After multivariable analysis, only age (HR: 1.033, 95%CI: 1.009 - 1.059, P=0.008), PaO2/FiO2 (HR: 0.992, 95%CI: 0.985 - 1.000, P=0.044) and PAR (HR: 4.899, 95%CI: 2.148 - 11.174, P<0.001) remained independently associated with 28-day mortality (P<0.05).ConclusionHigh PAR predicts a poor outcome in ARDS patients, therefore it appears to be a prognostic biomarker of outcomes in patients with ARDS.
Objective To explore the pathogenesis of acute respiratory disease syndrome (ARDS) by bioinformatics analysis of neutrophil gene expression profile in order to find new therapeutic targets. Methods The gene expression chips include ARDS patients and healthy volunteers were screened from the Gene Expression Omnibus (GEO) database. The differentially expressed genes were carried out through GEO2R, OmicsBean, STRING, and Cytoscape, then enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) pathways was conducted to investigate the biological processes involved in ARDS via DAVID website. Results Bioinformatics analysis showed 86 differential genes achieved through the GEO2R website. Eighty-one genes were included in the STRING website for protein interaction analysis. The results of the interaction were further analyzed by Cytoscape software to obtain 11 hub genes: AHSP, ALAS2, CD177, CLEC4D, EPB42, GPR84, HBD, HVCN1, KLF1, SLC4A1, and STOM. GO analysis showed that the differential gene was enriched in the cellular component, especially the integrity of the plasma membrane. KEGG analysis showed that multiple pathways especially the cytokine receptor pathway involved in the pathogenesis of ARDS. Conclusions A variety of genes and pathways have been involved in the pathogenesis of ARDS. Eleven hub genes are screened, which may be involved in the pathogenesis of ARDS and can be used in subsequent studies.
Objective To explore the role of renin-angiotensin system( RAS) in acute lung injury( ALI) /acute respiratory dysfunction syndrome( ARDS) by using amouse cecal ligation and puncture ( CLP)model.Methods The ALI/ARDS animal models were assessed bymeasuring blood gas, wet/dry lung weight ratio( W/D) , and lung tissue histology 18 hours after CLP operation. After the ALI/ARDS models was successfully established, immunohistochemistry, western blotting and radioimmunity were used to investigate the changes of several key enzymes of RAS, such as ACE, ACE2 and Ang Ⅱ. In addition, two groups of animals received a separate intraperitoneal injection of angiotensin-converting enzyme ( ACE) inhibitor captopril or recombinant mouse ACE2 ( rmACE2) after CLP, then the changes of RAS in ALI/ARDS modelswere observed. Results The extensive lung injuries can be observed in the lung tissues from CLP-treated animals 18 hours after operation. The CLP-induced ALI/ARDS led to an increase in the wet/dry weight ratio of the lung tissues, and a decrease in the PaO2 /FiO2 [ ( 194. 3 ±23. 9) mm Hg vs ( 346. 7 ±20. 5) mm Hg,P lt;0. 01] . Immunohistochemistry and western blotting tests of the lung tissues from CLP-treated animals showed a decrease in the ACE2 protein level. However, in both the CLP and sham mice there were no significant differences between the two groups. CLP markedly increased Ang Ⅱ level in lungs and plasma of mice, and RAS drugs significantly impacted the Ang Ⅱ levels of mice. Compared with the CLP group,captopril or rmACE2 led to a decrease of the Ang Ⅱ level in mice [ Lung: ( 1. 58 ±0. 16) fmol /mg,( 1. 65 ±0. 21) fmol /mg vs ( 2. 38 ±0. 41) fmol /mg; Plasma: ( 178. 04 ±17. 87) fmol /mL, ( 153. 74 ±10. 24) fmol /mL vs ( 213. 38 ± 25. 44) fmol /mL] . Conclusions RAS activation is one of the characteristics of CLP-induced ALI/ARDS in mice models. ACE and ACE2 in RAS have a different role in the regulation of AngⅡ synthesis, while ACE has a positive effect in generating AngⅡ, and ACE2 shows a negative effect.
Objective To investigate the effect of microRNA-22-3p (miR-22-3p) on the inflammation of human pulmonary microvascular endothelial cells (HPMEC) induced by lipopolysaccharide (LPS) by regulating the HMGB1/NLRP3 pathway. Methods miRNA microarray was taken from peripheral blood of patients with acute respiratory distress syndrome (ARDS) caused by abdominal infection and healthy controls for analysis, and the target miRNA was selected. miRNA mimics, inhibitor and their negative controls were transfected in HPMECs which were stimulated with LPS. Real time fluorescent quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect the mRNA and protein levels of high mobility group box-1 protein (HMGB1) and nucleotide binding oligomerization segment like receptor family 3 (NLRP3). RT-qPCR and enzyme linked immunosorbent assay were used to detect the levels of inflammatory factors in the cells and supernatant. Results miRNA microarray showed that miR-22-3p was down-regulated in the plasma of patients with ARDS. Compared with the negative control group, after miR-22-3p over-expression, the protein and mRNA levels of HMGB1 and NLRP3 decreased significantly. Similarly, the level of cleaved-caspase-1 decreased significantly. At the same time, interleukin (IL)-6, IL-8 and IL-1β mRNA level in cytoplasm and supernatant were down-regulated by miR-22-3p mimics. After transfected with miR-22-3p inhibitor, the expression levels of HMGB1, NLRP3, caspase-1 protein and inflammatory factors were significantly up-regulated. Conclusion miR-22-3p is significantly downregulated in peripheral blood of ARDS patients caused by abdominal infection, which can inhibit the expression of HMGB1 and NLRP3 and its downstream inflammatory response in HPMECs.
With the growth of offshore activities, the incidence rates of seawater drowning (SWD) induced acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) increase significantly higher than before. Pulmonary interstitial edema, alveolar septum fracture, red blood cells, and inflammatory cells infiltration can be seen under light microscope in the pathologic changes of lungs. The major clinical manifestations are continual hyoxemia and acidosis, which lead to a severe condition, a high death rate, and a poor treatment effect. Bone marrow mesenchymal stem cells are capable of self-renewal, multilineage differentiation and injured lung-homing, which are induced to differentiate into alveolar epithelial cells and pulmonary vascular endothelial cells for tissues repairing. This may be a new way to treat SWD-ALI and SW-ARDS.
ObjectiveTo investigate the clinical characteristics and contribution factors in severe coronavirus disease 2019 (COVID-19).MethodsThe clinical symptoms, laboratory findings, radiologic data, treatment strategies, and outcomes of 110 COVID-19 patients were retrospectively analyzed in these hospitals from Jan 20, 2020 to Feb 28, 2020. All patients were confirmed by fluorescence reverse transcription polymerase chain reaction. They were classified into a non-severe group and a severe group based on their symptoms, laboratory and radiologic findings. All patients were given antivirus, oxygen therapy, and support treatments. The severe patients received high-flow oxygen therapy, non-invasive mechanical ventilation, invasive mechanical ventilation or extracorporeal membrane oxygenation. The outcomes of patients were followed up until March 15, 2020. Contribution factors of severe patients were summarized from these clinical data.ResultsThe median age was 50 years old, including 66 males (60.0%) and 44 females (40.0%). Among them, 45 cases (40.9%) had underlying diseases, and 108 cases (98.2%) had different degrees of fever. The common clinical manifestations were cough (80.0%, 88/110), expectoration (33.6%, 37/110), fatigue (50.0%, 55/110), and chest tightness (41.8%, 46/110). Based on classification criteria, 78 (70.9%) non-severe patients and 32 (29.1%) severe patients were identified. Significant difference of the following parameters was found between two groups (P<0.05): age was 47 (45, 50) years vs. 55 (50, 59) years (Z=–2.493); proportion of patients with underlying diseases was 27 (34.6%) vs. 18 (56.3%) (χ2=4.393); lymphocyte count was 1.2 (0.9, 1.5)×109/L vs. 0.6 (0.4, 0.7)×109/L (Z=–7.26); C reactive protein (CRP) was 16.2 (6.5, 24.0) mg/L vs. 45.3 (21.8, 69.4) mg/L (Z=–4.894); prothrombin time (PT) was 15 (12, 19) seconds vs. 18 (17, 19) seconds (Z=–2.532); D-dimer was 0.67 (0.51, 0.82) mg/L vs. 0.98 (0.80, 1.57) mg/L (Z=–5.06); erythrocyte sedimentation rate (ESR) was 38.0 (20.8, 59.3) mm/1 h vs. 75.5 (39.8, 96.8) mm/1 h (Z=–3.851); lactate dehydrogenase (LDH) was 218.0 (175.0, 252.3) U/L vs. 325.0 (276.5, 413.5) U/L (Z=–5.539); neutrophil count was 3.1 (2.1, 4.5)×109/L vs. 5.5 (3.7, 9.1)×109/L (Z=–4.077). Multivariable logistic analysis showed that there was positive correlation in elevated LDH, CRP, PT, and neutrophil count with the severity of the disease. Currently, 107 patients were discharged and 3 patients died. Total mortality was 2.7%.ConclusionsOld age, underlying diseases, low lymphocyte count, elevated CPR, high D-dimer and ESR are relevant to the severity of COVID-19. LDH, CPR, PT and neutrophil count are independent risk factors for the prognosis of COVID-19.
Acute respiratory distress syndrome (ARDS) is a serious threat to human life and health disease, with acute onset and high mortality. The current diagnosis of the disease depends on blood gas analysis results, while calculating the oxygenation index. However, blood gas analysis is an invasive operation, and can’t continuously monitor the development of the disease. In response to the above problems, in this study, we proposed a new algorithm for identifying the severity of ARDS disease. Based on a variety of non-invasive physiological parameters of patients, combined with feature selection techniques, this paper sorts the importance of various physiological parameters. The cross-validation technique was used to evaluate the identification performance. The classification results of four supervised learning algorithms using neural network, logistic regression, AdaBoost and Bagging were compared under different feature subsets. The optimal feature subset and classification algorithm are comprehensively selected by the sensitivity, specificity, accuracy and area under curve (AUC) of different algorithms under different feature subsets. We use four supervised learning algorithms to distinguish the severity of ARDS (P/F ≤ 300). The performance of the algorithm is evaluated according to AUC. When AdaBoost uses 20 features, AUC = 0.832 1, the accuracy is 74.82%, and the optimal AUC is obtained. The performance of the algorithm is evaluated according to the number of features. When using 2 features, Bagging has AUC = 0.819 4 and the accuracy is 73.01%. Compared with traditional methods, this method has the advantage of continuously monitoring the development of patients with ARDS and providing medical staff with auxiliary diagnosis suggestions.