Prognostic value of neutrophil-to-monocyte/lymphocyte ratio for 28-day mortality in ICU sepsis patients: a retrospective cohort study.

Background: Sepsis is a life-threatening condition that requires rapid assessment to reduce mortality. This study investigates the relationship between the Neutrophil-to-Monocyte/Lymphocyte Ratio (NMLR) upon ICU admission and 28-day mortality in sepsis patients. Methods: A retrospective analysis was performed using clinical data from sepsis patients in the Medical Information Mart for Intensive Care IV (MIMIC-IV). Multivariate logistic regression, sensitivity analyses, and Restricted Cubic Spline (RCS) models were employed to explore the relationship between ICU admission NMLR and 28-day mortality. Kaplan-Meier method and inverse probability weighting (IPW) were used to adjust for confounders and estimate survival outcomes. Receiver operating characteristic (ROC) curve evaluating the predictive value of NLMR for 28-day mortality in ICU sepsis patients. Subgroup analyses considered factors like age, sex, race, comorbidities, and disease severity. Results: In total, 8,710 patients were included. Increased NMLR was associated with higher 28-day all-cause mortality, confirmed by multiple logistic regression models. In Model 3, after adjusting for confounders, each standard deviation increase in NMLR was associated with a 1.5% increase in 28-day mortality risk. Kaplan-Meier and IPW survival analyses showed higher 28-day all-cause mortality in patients with elevated NMLR levels at ICU admission compared to those with lower levels (p < 0.0001, p = 0.031). RCS models suggested a potential non-linear relationship between NMLR and 28-day mortality. ROC curve for the NMLR model, with an AUC of 0.658 (95% CI: 0.642-0.673). Sensitivity analyses confirmed the association even after excluding patients with myocardial infarction and severe liver disease. Conclusion: Elevated NMLR at ICU admission is significantly associated with increased 28-day all-cause mortality in sepsis patients, suggesting its potential as an early prognostic indicator for risk assessment and intervention.

Clinical characteristics and risk factors for symptomatic venous thromboembolism in hospitalized COVID-19 patients: A multicenter retrospective study.

BACKGROUND: High incidence of asymptomatic venous thromboembolism (VTE) has been observed in severe COVID-19 patients, but the characteristics of symptomatic VTE in general COVID-19 patients have not been described. OBJECTIVES: To comprehensively explore the prevalence and reliable risk prediction for VTE in COVID-19 patients. METHODS/RESULTS: This retrospective study enrolled all COVID-19 patients with a subsequent VTE in 16 centers in China from January 1 to March 31, 2020. A total of 2779 patients were confirmed with COVID-19. In comparison to 23,434 non-COVID-19 medical inpatients, the odds ratios (ORs) for developing symptomatic VTE in severe and non-severe hospitalized COVID-19 patients were 5.94 (95% confidence interval [CI] 3.91-10.09) and 2.79 (95% CI 1.43-5.60), respectively. When 104 VTE cases and 208 non-VTE cases were compared, pulmonary embolism cases had a higher rate for in-hospital death (OR 6.74, 95% CI 2.18-20.81). VTE developed at a median of 21 days (interquartile range 13.25-31) since onset. Independent factors for VTE were advancing age, cancer, longer interval from symptom onset to admission, lower fibrinogen and higher D-dimer on admission, and D-dimer increment (DI) ≥1.5-fold; of these, DI ≥1.5-fold had the most significant association (OR 14.18, 95% CI 6.25-32.18, p = 2.23 × 10-10 ). A novel model consisting of three simple coagulation variables (fibrinogen and D-dimer levels on admission, and DI ≥1.5-fold) showed good prediction for symptomatic VTE (area under the curve 0.865, 95% CI 0.822-0.907, sensitivity 0.930, specificity 0.710). CONCLUSIONS: There is an excess risk of VTE in hospitalized COVID-19 patients. This novel model can aid early identification of patients who are at high risk for VTE.

Chlorogenic acid protects against cholestatic liver injury in rats.

The aim of this study was to investigate the protective effect of chlorogenic acid (CA) on liver injury caused by bile duct ligation (BDL), as well as the potential mechanism. Permanent bile duct ligation induced liver injury was evaluated by liver index, liver function and pathological observation. Oral administration of CA for 3 weeks markedly attenuated liver swelling and fibrosis. Blood biochemistry results revealed that CA decreased alanine transaminase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, direct bilirubin and total bile acid. PCR analysis indicated that collagen I, collagen III, transforming growth factor and vascular endothelial growth factor mRNA were increased markedly by BDL treatment but these increases were suppressed by CA. Additionally, CA effectively alleviated the expression of α-smooth muscle actin induced by BDL. Taken together, our data indicate that CA can efficiently inhibit BDL-induced liver injury in rats, which is a candidate drug for preventing liver injury against cholestasis.