ObjectivesTo systematically review the prognostic value of plasma soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) level in predicting 28-day mortality in sepsis.MethodsPubMed, The Cochrane Library, EMbase, Web of Science, CBM, CNKI, VIP and WanFang Data databases were electronically searched to collect studies about the prognostic value of plasma sTREM-1 in early 28-day mortality in sepsis from inception to April 16th, 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using Stata 14.0 software.ResultsA total of 13 studies involving 1 115 patients were included. The results of meta-analysis showed that the sensitivity and specificity were 79% and 77%, respectively. The positive likelihood ratio and the negative likelihood ratio were 3.4 and 0.28, respectively. The diagnostic ratio was 12. The overall area under the summary receiver operator characteristic (SROC) curve was 0.80.ConclusionsCurrent evidence shows that plasma sTREM-1, as a single index, may play a prognostic role in the early 28-day mortality of sepsis in patients. Due to limited quality and quantity of the included studies, more high quality studies are needed to verify the above conclusion.
Ｂｙ ｐｅｒｆｕｓｉｎｇ ｌｉｖｅｒｓ ｆｒｏｍ Ｗｉｓｔａｒ ｒａｔｓ ｒｅｎｄｅｒｅｄ ｓｅｐｓｉｓ ｗｉｔｈ ａｃｕｔｅ ｏｂｓｔｒｕｃｔｉｖｅ ｃｈｏｌａｎｇｉｔｉｓ（ＡＯＣ）ｉｎ ｖｉｔｒｏ ｉｎ ａ ｎｏｎｒｅｃｉｒｃｕｌａｔｉｎｇ ｍｏｄｅ，ｗｅ ｍｅａｓｕｒｅｄ ｔｈｅ ｒａｔｅｓ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｅｓｉｓ ｆｒｏｍ ｓａｔｕｒａｔｉｎｇ ｃｏｎｃｅｎｔｒａｔｉｏｎ ｏｆ ｌａｃｔａｔｅ （５ ｍｍｏｌ／L) ｐｌｕｓ ｐｙｒｕｖａｔｅ （０５ ｍｍｏｌ／Ｌ） ａｎｄ ｔｈｅ ｒｅｓｐｏｎｓｅ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｅｓｉｓ ｔｏ ｇｌｕｃａｇｏｎ ａｎｄ ｅｐｉｎｅｐｈｒｉｎｅ．Ｗｅ ａｌｓｏ ｓｔｕｄｉｅｄ ｔｈｅ ＡＯＣ ｉｎｄｕｃｅｄ ａｌｔｅｒａｔｉｏｎｓ ｉｎ ｔｈｅ ｍｉｌｉｅｕ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｉｃ （ｇｌｕｃａｇｏｎ，ｅｐｉｎｅｐｈｒｉｎｅ ａｎｄ ｃｏｒｔｉｓｏｌ） ａｎｄ ｃｏｎｔｅｒｒｅｇｕｌａｔｏｒｙ （ｉｎｓｕｌｉｎ） ｈｏｒｍｏｎｅｓ．Ｔｈｅ ｒｅｓｕｌｔｓ ｓｈｏｗｅｄ ｔｈｅ ｒａｔｅ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｅｓｉｓ ｏｆ ＡＯＣ ２４ ｈ．ｇｒｏｕｐ ｗａｓ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｒｅｄｕｃｅｄ ａｎｄ ｔｈｉｓ ｒｅｄｕｃｔｉｏｎ ｃｏｕｌｄ ｂｅ ｃｏｍｐｅｎｓａｔｅｄ ｂｙ ｉｎｃｒｅａｓｅｓ ｏｆ ｇｌｕｃｏｓｅ ｐｒｅｃｕｒｓｏｒｓ，ｅｓｐｅｃｉａｌｌｙ ｌａｃｔａｔｅ ａｎｄ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｉｃ ｈｏｒｍｏｎｅｓ ｔｏ ａ ｓｅｒｕｍ ｇｌｕｃｏｓｅ ｌｅｖｅｌ ａｓ ｍｕｃｈ ａｓ ２．５ ｔｉｍｅｓ ｔｈｅ ｎｏｒｍａｌ ｗｈｉｃｈ ｉｓ ｎｅｅｄｅｄ ｉｎ ｓｔｒｅｓｓ ｒｅａｃｔｉｏｎ．Ｔｈｅ ｒａｔｅ ｏｆ ｇｌｕｃｏｎｅｏｇｅｎｅｓｉｓ ｏｆ ＡＯＣ ４８ ｈ．ｗａｓ ｆｕｒｔｈｅｒ ｄｅｃｒｅａｓｅｄ ａｎｄ ｔｈｉｓ ｄｅｃｒｅａｓｅ ｃｏｕｌｄ ｎｏｔ ｂｅ ｃｏｍｐｅｎｓａｔｅｄ ｐｒｏｂａｂｌｙ ａｓ ａ ｒｅｓｕｌｔ ｏｆ ｓｅｖｅｒｅ ｄａｍａｇｅ ｔｏ ｈｅｐａｔｏｃｙｔｅｓ． Ｔｈｅ ｒｅｓｕｌｔｓ ｉｎｄｉｃａｔｅ ｔｈａｔ ｔｈｅ ｒｅｄｕｃｅｄ ｇｌｕｃｏｓｅ ｍｅｔａｂｏｌｉｃ ｒｅｓｐｏｎｓｅ ｄｕｅ ｔｏ ＡＯＣ ｍａｙ ｐｌａｙ ａｎ ｉｍｐｏｒｔａｎｔ ｒｏｌｅ ｉｎ ｔｈｅ ｄｅｖｅｌｏｐｍｅｎｔ ｏｆ ｃｈｏｌａｎｇｉｔｉｓｉｎｄｕｃｅｄ ｄｙｓｆｕｎｃｔｉｏｎ ｏｆ ｍｕｌｔｉｐｌｅ ｏｒｇａｎｓ．
Objective To investigate the effects of simvastatin on lung tissue in septic rats by observing the protein expression of nuclear factor kappa B ( NF-κB) and pathologic changes in lung tissue at different time points. Methods 90 healthy male Sprague-Dawley rats were randomly divided into three groups ( n =30 in each group) . All the rats received administration by caudal vein and capacity volume is 2 mL. The rats in the control group were treated with saline ( 2 mL) . The rats in the LPS group were treated with LPS ( 5 mg/kg ) . The rats in the simvastatin group were treated with LPS ( 5 mg/kg) and simvastatin ( 20 mg/kg) . Six rats in each group were killed randomly at 2, 4, 6, and 12 hours after the injection, and the right middle lobe of lung was taken out. Pathological changes of lung tissue wee investigated under light microscope. The expression of NF-κB in lung tissue was determined by immunohistochemistry ( IHC) method. Results Microscopic studies showed that there were not pathological changes in the lung tissue of rats in the control group. While in the LPS group, the alveolar spaces were narrowed and the alveolar wall were thickened. Furthermore, severe interstitial edema of lung and proliferation of epithelial cells were observed. In the simvastatin group, the degree of the infiltration of leukocytes and the lung interstitial edema were less severe than those in the simvastatin group. In the control group, the expression of NF-κB protein in most of lung tissue was negative. In the LPS group, the expression of NF-κB protein was detected at 2h, andreached the peak at 6h, then decreased at 12h. In the Simvastatin group, the NF-κB expression was significantly lower than that in the LPS group at all time points ( P lt; 0. 01) . Conclusion Simvastatin can ameliorate pathological lesions and decrease expression of NF-κB in lung tissue of septic rats.
Objective To investigate the pathological characteristics of hepatic energy metabolism changes due to biliary sepsis. Methods The hepatic mitochondrial respiratory function and content of ATP was dynamically measured in the self controlled rabbit model of biliary sepsis.Results The mitochondrial S3, respiration control rate (RCR) and phosphorus/oxygen (P/O) were significantly dropping in the infective hepatic lobe 12 hrs after operation with S4 increasing markedly, and the oxidative phosphorylation was uncoupled from 48 hrs after operation onward. The hepatic mitochondrial RCR showed early ascending and then dropping in the non-infective hepatic lobe. The content of ATP and mitochondrial respiratory activity decreased synchronously in both hepatic lobes. Conclusion The hepatic energy metabolic failure was induced in the early stage by biliary sepsis. This is probably the pathological basis of biliary sepsis that is highly critical and always lead to MOF following acute liver function failure.
Objective To establish a short-term mortality risk scoring standard for sepsis-associated acute respiratory distress syndrome (sARDS) and provide a reference tool for clinicians to evaluate the severity of sARDS patients. Methods A retrospective cohort study was conducted on sARDS patients admitted to the adult intensive care unit (ICU) of the First Affiliated Hospital, Hengyang Medical School, University of South China from January 1, 2013 to August 31, 2020. They were divided into a death group and a survival group according to whether they died within 28 days after admission to ICU. Clinical data of the patients was collected within 24 hours admitted to ICU. Related risk factors for mortality within 28 days after admission to ICU were screened out through univariate logistic regression analysis. A risk prediction model for mortality within 28 days after admission to ICU was established by multivariate logistic regression analysis. The Hosmer-Lemeshow χ2 test and the area under the receiver operating characteristic (ROC) curve were used to evaluate the model’s goodness-fit and accuracy in predicting 28-day mortality of the sARDS patients, respectively. Finally, the clinical prognosis scoring criteria 28-day mortality of the sARDS patients were established according to the weight coefficients of each independent risk factor in the model. Results A total of 150 patients were recruited in this study. There were 67 patients in the survival group and 83 patients in the death group with a 28-day mortality rate of 55.3%. Four independent risk factors for 28-day mortality of the sARDS patients, including invasive mechanical ventilation, the number of dysfunctional organs≥3, serum lactic acid≥4.3 mmol/L and the severity of ARDS. A risk prediction model for mortality within 28 days of the sARDS patients was established. The area under the ROC curve and 95% confidence interval (CI), sensitivity and specificity of the risk prediction model for 28-day mortality for the sARDS patients were 0.896 (95%CI 0.846 - 0.945), 80.7% and 82.1%, respectively, while that for acute physiology and chronic health evaluation Ⅱ (APACHEⅡ) score were 0.865 (95%CI 0.805 - 0.925), 71.1% and 89.6%; for sequential organ failure assessment (SOFA) score were 0.841 (95%CI 0.7799 - 0.904), 68.7%, and 82.1%; for the prediction scores of lung injury were 0.855 (95%CI 0.789 - 0.921), 81.9% and 82.1%, respectively. It was indicated that the prediction accuracy of this risk prediction model of 28-day mortality maybe was better than that of APACHE-Ⅱ score, SOFA score and prediction score of lung injury. In addition, four risk factors were assigned as invasive mechanical ventilation (12 points), serum lactic acid≥4.3mmol /L (1 point), number of organs involved≥3 (3 points), and severity of ARDS (mild for 13 points, moderate for 26 points, severe for 39 points). Further more, the score of each patient was 13 - 55 points according to the scoring criteria, and the score grade was made according to the percentile method: 13 - 23 points for the low-risk group for 28-day mortality, 24 - 34 points for the medium-risk group for 28-day mortality, 35 - 45 points for the high-risk group for 28-day mortality, and over 45 points for the extremely high-risk group for 28-day mortality. According to the scoring criteria, the prognosis of the patients in this study was analyzed. The mortality probability of each group was 0.0% in the low-risk group, 13.8% in the medium-risk group, 51.9% in the high-risk group, and 89.7% in the extremely high-risk group, respectively. Conclusions The invasive mechanical ventilation, the number of involved organs≥3, serum lactic acid≥4.3 mmol /L and the severity of sARDS are independent risk factors for 28-day mortality of the sARDS patients. The scoring criteria may predict the risk of 28-day mortality for the sARDS patients.
Objective To investigate the protective mechanism of ulinastatin（UTI） in pulmonary microvascular endothelial cells （PMVECs） attacked by serum from the patients with severe sepsis. Methods PMVECs were cultured in vitro and randomly divided into 4 groups，ie. a normal group （culture medium with 10% fetal bovine serum，group N），a health group （culture medium with 10% healthy human serum，group H），a patient group （culture medium with 10% human septic shock serum，group S），and a ulinastatin group （culture medium with 1000 U/mL UTI and 10% human septic shock serum，group U）. The proliferation activity of PMVECs was measured by MTT expressed by optical density （OD）. The concentration of TNF-α in supernatant of culture medium was examined by ELISA at 0，1，2，4，6 hours. The expression of NF-κB was examined by immunohistochemistry at 1 hour. Results Compared with group N，the cell proliferation activity of group S decreased significantly，and the cell proliferation activity of group U decreased slightly at each time poi nt. Compared with group N，the cell proliferation activity of group S and group U at 1，4，6 hours were significant different （Plt;0.05 ）. Compared with group S，the cell proliferation activity of group U at 1，2，6 hours increased significantly （Plt;0.05）. Obviously positive expression of NF-κB in PMVECs could be seen in group S，a little positive expression in group S，and no expression in group N and group H. Compared with group N，the TNF-α levels of group S and group U increased significantly at each time point with significant differences （Plt;0.01）. Compared with group S，the TNF-α levels were significantly reduced at each time point in group U （Plt;0.01）. Conclusions UTI can reduce the release of TNF-α by inhibiting NF-κB activation，thus reduce PMVECs injury attacked by serum from severe sepsis patients.