Development and validation of a nomogram for predicting in-hospital mortality of intensive care unit patients with liver cirrhosis

BACKGROUND Liver cirrhosis patients admitted to intensive care unit(ICU)have a high mortality rate.AIM To establish and validate a nomogram for predicting in-hospital mortality of ICU patients with liver cirrhosis.METHODS We extracted demographic,etiological,vital sign,laboratory test,comorbidity,complication,treatment,and severity score data of liver cirrhosis patients from the Medical Information Mart for Intensive Care IV(MIMIC-IV)and electronic ICU(eICU)collaborative research database(eICU-CRD).Predictor selection and model building were based on the MIMIC-IV dataset.The variables selected through least absolute shrinkage and selection operator analysis were further screened through multivariate regression analysis to obtain final predictors.The final predictors were included in the multivariate logistic regression model,which was used to construct a nomogram.Finally,we conducted external validation using the eICU-CRD.The area under the receiver operating characteristic curve(AUC),decision curve,and calibration curve were used to assess the efficacy of the models.RESULTS Risk factors,including the mean respiratory rate,mean systolic blood pressure,mean heart rate,white blood cells,international normalized ratio,total bilirubin,age,invasive ventilation,vasopressor use,maximum stage of acute kidney injury,and sequential organ failure assessment score,were included in the multivariate logistic regression.The model achieved AUCs of 0.864 and 0.808 in the MIMIC-IV and eICU-CRD databases,respectively.The calibration curve also confirmed the predictive ability of the model,while the decision curve confirmed its clinical value.CONCLUSION The nomogram has high accuracy in predicting in-hospital mortality.Improving the included predictors may help improve the prognosis of patients.

Criteria-specific long-term survival prediction model for hepatocellular carcinoma patients after liver transplantation

AIM: To establish a model to predict long-term survival of hepatocellular carcinoma (HCC) patients after liver transplantation (MHCAT).

Study on anti-inflammatory mechanism and effects of Flemingia Roxb.exAit extract intervene acute gouty arthritis in rats

Objective:To investigate the effect and anti-inflammatory mechanism the effect of Flemingia Roxb.exAit extract on acute gouty arthritis.Methods:Sixty SD rats were randomly divided into 6 groups by weight,control and model group,(100、150、200 mg/kg)of Flemingia Roxb.exAit extract group and colchicine group.The rats of each group were given by intragastric for 7 days of continuous administration,meanwhile,there were given 0.9%NaCl solution instead as control and model group.The acute gouty arthritis model was constructed through right ankle joint cavity injection of sodium urate crystal solutionon day 5 after 1 h,but rats in the negative control group were injected with 0.9%NaCl solution into the articular cavity of the right foot.The general condition of rats and the degree of joint swelling,and the gait was observed after constructed model.To detected the joint fluid IL-1β、TNF-α、IL-6 indicators,and the expression of NLRP3,Caspase-1 protein in ankle joint tissue for 2 hours after the last administration.Results:Groups of Flemingia Roxb.exAit extract could markedly reduce the joint swelling on acute gouty arthritis rat model,improve gait in a dose-dependent manner,high dose group of Flemingia Roxb.exAit extract did particularly well(Pjoint swelling<0.01;Pgait<0.05),close to the therapeutic effect colchicine group.Further mechanism studies show that the joint fluid IL-1β、TNF-α、IL-6 level was reduced by Flemingia Roxb.exAit extract group,the expressions of NLRP3、Caspase-1 protein of Flemingia Roxb.exAit extract group was decreased observbly than model group,but the most obvious is that high dose group as well as colchicine group(PNALP3<0.01;PCaspase-1<0.01).Conclusion:Flemingia Roxb.exAit extract has the effect of treating acute gouty arthritis and its mechanism may be related toinhibiting NLRP3 inflammasome activation and inhibiting inflammatory response.