ABSTRACT
ObjectiveTo investigate the predictive factors for third-generation cephalosporin-resistant spontaneous bacterial peritonitis (SBP). MethodsA retrospective analysis was performed for the clinical data of 206 patients with liver cirrhosis who were hospitalized in the Ninth Hospital of Nanchang from January 2010 to December 2018, and all patients had SBP with positive bacteria based on ascites culture. According to drug susceptibility results, the patients were divided into third-generation cephalosporin-resistant SBP group (101 patients with third-generation cephalosporin-resistant pathogenic bacteria in ascites) and control group (105 patients with pathogenic bacteria sensitive to third-generation cephalosporin). Electronic medical records were reviewed to collect related information. The t-test was used for comparison of normally distributed continuous data between groups, and the Mann-Whitney U test was used for comparison of data with skewed distribution between groups. The chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. A dichotomous logistic regression analysis was used for multivariate analysis, and the Forward: LR method was used for the screening of independent variables. ResultsThere was a significant difference in the composition of pathogenic bacteria between the two groups (P＜0.001). The univariate analysis showed that a history of broad-spectrum antibiotic exposure in the past three months (χ2=12.351, P＜0001), non-first-time onset of SBP (χ2=14.427, P＜0.001), blood creatinine (χ2=-2.537, P=0.011), and blood bicarbonate (χ2=-4.592, P＜0.001) were candidate predictive factors with statistical significance between the two groups, and further multivariate analysis showed that a history of broad-spectrum antibiotic exposure in the past three months (odds ratio ［OR］=2.376, 95% confidence interval ［CI］: 1.009-5.598, P=0.048), non-first-time onset of SBP (OR=2.841, 95%CI: 1.133-7.122, P=0.026), and blood bicarbonate (OR=0.892, 95%CI: 0.818-0.973, P=0.010) had an independent predictive value for third-generation cephalosporin-resistant SBP. ConclusionA history of broad-spectrum antibiotic exposure in the past three months, non-first-time onset of SBP, and a low level of blood bicarbonate are independent predictive factors for third-generation cephalosporin-resistant SBP, and third-generation cephalosporins should be used with caution in SBP patients with these features.
ABSTRACT
Objective To study the effect of ursolic acid (UA) intervention on hepatocyte apoptosis induced by TGF-β1 and its potential mechanism.Methods Primary hepatocytes were extracted from healthy SD rats by in situ perfusion,cultured for 12-24h,then randomly divided into the following groups:blank control group,UA control group (UA 25μmol/L),TGF-β1 group (TGF-β1 2.5ng/ml),UA intervention group (UA 25μmol/L and TGF-β1 2.5ng/ml),DPI intervention group (DPI 0.5μmol/L and TGF-β1 2.5ng/ml).Each group was treated with drugs for corresponding time and their proliferation and apoptosis were detected by flow cytometry,the expression of CD95 (Fas) mRNA was analyzed by RT-qPCR,the expression of protein CD95 and membrane translocation of NADPH oxidase (NOX) subunit p47Phox were analyzed by Western blotting,and the reactive oxygen species (ROS) generation in primary hepatocytes was analyzed with reactive oxygen detection kit.Results UA intervention at 30min before TGF-β1 stimulating hepatocytes markedly reduced hepatocyte apoptosis (63.97 ± 3.19 vs 80.53 ± 1.56,P＜0.01) and promoted hepatocyte proliferation (18.67 ± 1.60 vs 10.83 ± 2.03,P＜0.01).UA intervention notably down-regulated the expressions of CD95 mRNA and protein (1.28 ± 0.15 vs 2.40 ± 0.25,P＜0.01;1.05 ± 0.15 vs 1.37 ± 0.18,P＜0.05),restrained membrane translocation of p47phox (1.13 ± 0.12 vs 1.76 ± 0.22,P＜0.01),and decreased ROS level in primary hepatocytes induced by TGF-β1 (2.12 ± 0.45 vs 3.23 ± 0.53,P＜0.01).Conclusion The mechanism of UA inhibiting hepatocyte apoptosis induced by TGF-β1 is likely to be that UA intervention reduced hepatocyte apoptosis by inhibiting NOX activation and decrease generation of ROS so as to down-regulate expression of CD95 in hepatocytes.