Proton pump inhibitor use increases hepatic encephalopathy risk: A systematic review and meta-analysis.

BACKGROUND: Several studies have been conducted to explore the association between the use of proton pump inhibitors (PPIs) and hepatic encephalopathy (HE) risk in patients with liver cirrhosis. However, their results are controversial. AIM: To perform a systematic review and meta-analysis to evaluate the HE risk among PPI users. METHODS: A systematic search on PubMed, Web of Science, EMBase, and ScienceDirect databases was conducted up to December 31, 2018 for eligible studies involving PPI use and HE risk. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using the fixed or random effects model. Publication bias was evaluated using Begg's test, Egger's test, and trim-and-fill method. RESULTS: Seven studies with 4574 patients were included in the present meta-analysis. The meta-analysis results indicated a significant association between the PPI use and HE risk (OR = 1.50; 95%CI: 1.25-1.75) with low heterogeneity (I 2 = 14.2%, P = 0.321). Although publication bias existed when Egger's tests were used (P = 0.005), the trim-and-fill method verified the stability of the pooled result. Sensitivity analyses suggested that the results of this meta-analysis were robust. CONCLUSION: The current evidence indicates that PPI use increases HE risk in patients with liver cirrhosis. Further studies with a large data set and well-designed models are needed to validate our findings.

Arterial lactate in predicting mortality after paraquat poisoning: A meta-analysis.

OBJECTIVE: This study aimed to explore the effects of arterial lactate as a predictor of mortality in patients with paraquat (PQ) poisoning. METHODS: The databases PubMed, EMBase, Web of Science, ScienceDirect, Cochrane library, and studies published until 31 February 2018 were searched. The data were extracted to perform pooled analysis, heterogeneity testing, sensitivity analysis, publication bias analysis, and Fagan plot analysis. RESULTS: Pooled analysis showed that a high arterial lactate was significantly correlated with poor mortality (pooled odds ratio = 16.94, 95% confidence interval [CI]: 7.96-36.08, P < .001). The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 77% (95% CI: 0.69-0.84), 84% (95% CI: 0.74-0.90), 4.7 (95% CI: 2.9-7.8), 0.28 (95% CI: 0.20-0.39), and 17 (8-36), respectively. An area under the curve of 0.87 (95% CI: 0.83-0.89) means a high ability for prognostic detection. CONCLUSION: Our findings show that arterial lactate is an effective predictor of mortality in patients with PQ poisoning.

A retrospective analysis of leucocyte count as a strong predictor of survival for patients with acute paraquat poisoning.

The aim of this study is the identification of a reliable predictor of prognosis to optimize the treatment of acute paraquat (PQ) poisoning patients. We performed a retrospective analysis on 96 patients with acute PQ poisoning to evaluate leucocyte count as a predictor of 90-day survival. These patients were admitted to the emergency department from May 2012 to February 2017. Kaplan-Meier method was used to compare the 90-day survival. Cox proportional hazard models were utilized to estimate the hazard ratios (HR) and 95% confidence intervals (CI). Receiver operating characteristic (ROC) analysis was conducted to analyze the discriminatory potential of leucocyte with respect to 90-day survival. Result showed that leucocyte was significantly higher among nonsurvivors than that among survivors (p<0.001). Leukocyte was also an independent predictor of survival according to the multivariate Cox analysis (HR 1.103; 95%CI: 1.062-1.146; p<0.001). The area under the curve (AUC) for leucocyte (AUC 0.911; 95%CI: 0.855-0.966; p<0.001) showed a discriminatory potential similar to that of the plasma PQ concentration (AUC 0.961; 95%CI: 0.926-0.997; p<0.001) in predicting 90-day survival. The leucocyte count is a strong predictor of survival in patients with acute PQ poisoning.

Prolonged low-dose cyclophosphamide treatment after pulse therapy attenuates lung injury in rats with paraquat intoxication.

BACKGROUND/AIMS: This study tested the hypothesis that prolonged low-dose cyclophosphamide (CTX) treatment after pulse therapy attenuate paraquat (PQ)-induced lung injury in rats. METHODS: PQ (25 mg/kg) was administered intraperitoneally to induce PQ-intoxicated rat model. The rats were randomly divided into four groups: control group (1 mL/day saline solution for 14 days), PQ group (1 mL/day saline solution for 14 days after PQ exposure), pulse group (15 mg/kg/day CTX in 1 mL of saline solution for 2 days and subsequent 1 mL/day saline solution for 12 days), and prolonged low-dose group (15 mg/kg/day CTX in 1 mL of saline solution for 2 days and subsequent 1.5 mg/kg/day CTX in 1 mL of saline solution for 12 days). A 14-day follow-up was conducted to determine the survival rat, and lung hydroxyproline (HYP), wet-to-dry weight ratios (W/Dc) and histopathological changes were evaluated. RESULTS: Results showed similar survival rate (55% vs. 50%, p > 0.05) between prolonged low-dose and pulse groups. Lung W/Dc (4.94 ± 0.38 vs. 5.47 ± 0.28, p < 0.01), HYP (3.34 ± 0.29 µg/mg vs. 3.65 ± 0.19 µg/mg, p < 0.001), and fibrosis score (2.69 ± 0.84 vs. 3.13 ± 0.63, p < 0.05) were lower in prolonged low-dose group than those in the pulse group. CONCLUSION: These findings suggested prolonged low-dose CTX treatment after pulse therapy could attenuate PQ-induced lung injury in rats.

Patients with mild paraquat poisoning treated with prolonged low-dose methylprednisolone have better lung function: A retrospective analysis.

Lung dysfunction is an important characteristic of injury induced by paraquat (PQ). This study aimed to evaluate the effects of prolonged low-dose methylprednisolone (MP) treatment on lung function in patients with mild PQ poisoning. We analyzed the results of lung function testing in all patients with mild PQ poisoning admitted to Cangzhou Central Hospital between January 2012 and August 2017. Patients were grouped according to short-term treatment (3 mg/kg/day MP for 3 days) or prolonged treatment (3 mg/kg/day MP for 3 days, followed by dosage reduction by half every 3 days, with treatment terminated when a dosage of 0.375 mg/kg/day was reached). Lung function was evaluated at 2 to 3 months after PQ exposure. The forced expiratory volume in 1 second (85.72 ±â€Š4.93% vs 78.41 ±â€Š4.58%; P < .001), forced vital capacity (81.98 ±â€Š4.93% vs 77.85 ±â€Š4.37%; P < .001), and diffusing capacity (84.27 ±â€Š5.16% vs 76.21 ±â€Š3.71%; P < .001) in the prolonged low-dose MP group were improved compared with those in the short-term MP group. Patients with mild PQ poisoning treated with prolonged low-dose MP had better lung function 2 to 3 months after PQ poisoning.

HuR induces inflammatory responses in HUVECs and murine sepsis via binding to HMGB1.

The aim of the present study was to explore the roles of human antigen R (HuR) in sepsis. Reverse transcription­quantitative polymerase chain reaction and western blot analyses demonstrated that overexpression of HuR increased the expression of high­mobility group box 1 (HMGB1) in human umbilical vein endothelial cells (HUVECs). HMGB1 was investigated as a potential target of HuR through bioinformatics and RNA­immunoprecipitation assays. Furthermore, treatment with HuR small interfering (si)RNA suppressed the lipopolysaccharide (LPS)­mediated release of HMGB1 and reduced HMGB1­mediated hyperpermeability and leukocyte migration in HUVECs and in septic mice. In addition, HuR­siRNA injection reduced cecal ligation and puncture (CLP)­induced HMGB1 release, reduced production of interleukin 6 and lowered mortality rates. Notably, the promotive effects of HuR overexpression on the inflammatory response were attenuated when HUVECs were co­treated with HMGB1 short hairpin RNA. Therefore, the present results indicated that the ectopic expression of HuR may induce inflammatory responses and thus sepsis by activating the HMGB1 signaling pathway.

[Effect of a stabilization device for maintaining the balance of a CPR performer during ambulance transportation on quality of CPR in out-of-hospital cardiac arrest: a prospective randomized controlled trial].

OBJECTIVE: To investigate the effect of a stabilization device for maintaining the balance of a cardiopulmonary resuscitation (CPR) performer during ambulance transportation on quality of CPR in out-of-hospital cardiac arrest (OHCA). METHODS: A prospective randomized controlled trial was performed. 167 OHCA patients with cardiac arrest (CA) time < 10 minutes admitted to Cangzhou Central Hospital from October 2014 to January 2017 were enrolled, and divided into armed stabilization device group (n = 86) and unarmed stabilization device group (n = 81) by random number table. Restoration of spontaneous circulation (ROSC) rate, 24-hour survival rate and survival rate of discharge were evaluated. RESULTS: Compared with unarmed stabilization device group, ROSC rate (29.1% vs. 9.9%, χ2 = 9.691, P = 0.002), 24-hour survival rate (20.9% vs. 6.2%, χ2 = 7.649, P = 0.006) and survival rate of discharge (12.8% vs. 3.7%, χ2 = 4.485, P = 0.035) were significant increased in armed stabilization device group. CONCLUSIONS: CPR with stabilization device during ambulance transport could effectively ensure quality of CPR and improve prognosis in OHCA. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-IPR-14005337.

Prolonged methylprednisolone therapy after the pulse treatment for patients with moderate-to-severe paraquat poisoning: A retrospective analysis.

This retrospective study aims to evaluate the effect of prolonged methylprednisolone (MP) therapy on the mortality of patients with moderate-to-severe paraquat (PQ) poisoning after the pulse treatment.We performed a retrospective analysis of patients with acute moderate-to-severe PQ poisoning that were admitted to the emergency department from May 2012 to August 2016. Out of 138 patients, 60 were treated with pulse treatment (15 mg kg day MP for 3 days) and 78 were treated with prolonged MP therapy after pulse treatment (15 mg kg day MP for 3 days; afterward, the dosage was reduced in half every 2 days, and the MP therapy was terminated until 0.47 mg kg day). Kaplan-Meier method was used to compare the mortality between the 2 groups. Cox proportional hazard models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI).The mortality of the prolonged MP therapy after pulse treatment group was lower than that of the pulse group (47.4% vs 63.3%; log-rank tests, P  =  .003). According to the multivariate Cox analysis, the prolonged MP therapy after pulse treatment was significantly associated with a lower mortality risk (HR: 0.31, 95% CI: 0.19-0.52, P < .001) compared with the pulse group. In addition, the prolonged MP therapy after pulse treatment caused more incidences of leucopenia than the pulse treatment alone (25.6% vs 11.7%, P  =  .04).The prolonged MP therapy after pulse treatment can reduce the mortality of moderate-to-severe PQ poisoning patients.