Association between lactate dehydrogenase and ventilator-associated pneumonia risk: an analysis of the MIMIC database 2001-2019.

BACKGROUND: Serum lactate dehydrogenase (LDH) is a nonspecific inflammatory biomarker and has been reported to be associated with pneumonia prognosis. This study aimed to evaluate the relationship between LDH levels and ventilator-associated pneumonia (VAP) risk in intensive care unit (ICU) patients. METHODS: This retrospective cohort study used data from the Multiparameter Intelligent Monitoring in Intensive Care database from 2001 to 2019. ICU patients aged ≥ 18 years and receiving mechanical ventilation were included. LDH levels were analyzed as continuous and categorical variables (< 210, 210-279, 279-390, > 390 IU/L), respectively. Restricted cubic spline (RCS) curves and quartiles were used to categorize LDH levels. Logistic regression and linear regression were utilized to assess the relationship of LDH levels with VAP risk and duration of mechanical ventilation, respectively. RESULTS: A total of 9,164 patients were enrolled, of which 646 (7.05%) patients developed VAP. High levels of LDH increased the risk of VAP [odds ratio (OR) = 1.15, 95% confidence interval (CI): 1.06-1.24] and LDH levels were positively correlated with the duration of mechanical ventilation [ß = 4.49, 95%CI: (3.42, 5.56)]. Moreover, patients with LDH levels of 279-390 IU/L (OR = 1.38, 95%CI: 1.08-1.76) and > 390 IU/L (OR = 1.50, 95%CI: 1.18-1.90) had a higher risk of VAP than patients with LDH levels < 210 IU/L. Patients with LDH levels of 279-390 IU/L [ß = 3.84, 95%CI: (0.86, 6.82)] and > 390 IU/L [ß = 11.22, 95%CI: (8.21, 14.22)] (vs. <210 IU/L) had a longer duration of mechanical ventilation. CONCLUSION: Elevated serum LDH levels were related to a higher risk of VAP and longer duration of mechanical ventilation and may be useful for monitoring VAP risk.

Therapeutic effects of human umbilical cord mesenchymal stem cell on sepsis-associated encephalopathy in mice by regulating PI3K/AKT pathway.

Sepsis-associated encephalopathy is a common brain diseases, presenting severe diffuse brain dysfunction. The umbilical cord mesenchymal stem cells have been reported to have protective role for treating diseases, while its role in sepsis-associated encephalopathy remained elusive. This brief report investigated the therapeutic effect of umbilical cord mesenchymal stem cells on sepsis-associated encephalopathy in mice model and uncovering the underlying mechanism. The sepsis-associated encephalopathy mice were injected with 3 mg/kg lipopolysaccharide. An enzyme-linked immunosorbent assay was carried out to determine the production of inflammatory cytokines. Morris water maze test was used to evaluate mice's neurological dysfunction. Cell apoptosis and tissue injury of the cerebral cortex were assessed using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and HE staining. Evans Blue leakage detection was used to examine the blood-brain barrier integrity. The protein levels were determined using Western blot. Results showed that the productions of inflammatory cytokines including interleukin 6 (IL-6), interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α), and high mobility group box protein 1 (HMGB1) and activated NF-κB were increased in sepsis-associated encephalopathy mice, which were decreased by umbilical cord mesenchymal stem cells treatment. Besides, umbilical cord mesenchymal stem cells inhibited lipopolysaccharide-induced cell apoptosis and neuron injury of the cerebral cortex in sepsis-associated encephalopathy mice. Moreover, cognitive dysfunction was observed in sepsis-associated encephalopathy mice, which was alleviated by umbilical cord mesenchymal stem cells. Furthermore, umbilical cord mesenchymal stem cells activated PI3K/AKT signaling pathway. In conclusion, umbilical cord mesenchymal stem cells alleviated inflammation, cell apoptosis and neuron injury of the cerebral cortex, and cognitive dysfunction in sepsis-associated encephalopathy animal model in a PI3K/AKT dependent pathway, making them to be a promising therapeutic strategy for treating sepsis-associated encephalopathy.

Intravenous thiamine for septic shock: A meta-analysis of randomized controlled trials.

INTRODUCTION: The efficacy of intravenous thiamine to treat septic shock remains controversial. We conduct a systematic review and meta-analysis to explore the impact of intravenous thiamine on treatment efficacy of septic shock. METHODS: We have searched PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through June 2020 and included randomized controlled trials (RCTs) assessing the effect of intravenous thiamine on septic shock. This meta-analysis was performed using the random-effect model. RESULTS: Four RCTs were included in the meta-analysis. Overall, compared with control group in patients with septic shock, intravenous thiamine revealed no substantial impact on mortality (odd ratio [OR] = 0.87; 95% confidence interval [CI) = 0.62 to 1.21; P = 0.40), lactate change (standard mean difference [SMD] = 0.04; 95% CI = -0.28 to 0.35; P = 0.82), Sequential Organ Failure Assessment (SOFA) change (SMD = 0.02; 95% CI = -0.18 to 0.21; P = 0.87), intensive care unit (ICU) stay (SMD = -0.02; 95% CI = -0.33 to 0.30; P = 0.90) or renal replacement therapy (OR = 0.47; 95% CI = 0.07 to 3.15; P = 0.43). CONCLUSIONS: Intravenous thiamine showed no benefit over placebo in treating patients with septic shock.