Two-year survival after scheduled extubation in patients with pneumonia or ARDS: a prospective observational study.

PURPOSE: To report two-year survival after scheduled extubation in patients with pneumonia or acute respiratory distress syndrome (ARDS). METHODS: This was a prospective observational study performed in a respiratory ICU of a teaching hospital. Pneumonia or ARDS patients who successfully completed a spontaneous breathing trial were enrolled. Data were collected before extubation. Patients were followed up to two years by phone every 3 months. RESULTS: A total of 230 patients were enrolled in final analysis. One-, 3-, 6-, 12-, and 24-month survival was 77.4%, 63.8%, 61.3%, 57.8%, and 47.8%, respectively. Cox regression shows that Charlson comorbidity index (hazard ratio: 1.20, 95% confidence interval: 1.10-1.32), APACHE II score before extubation (1.11, 1.05-1.17), cough peak flow before extubation (0.993, 0.986-0.999), and extubation failure (3.96, 2.51-6.24) were associated with two-year mortality. To predict death within two years, the area under the curve of receiver operating characteristic was 0.79 tested by Charlson comorbidity index, 0.75 tested by APACHE II score, and 0.75 tested by cough peak flow. Two-year survival was 31% and 77% in patients with Charlson comorbidity index ≥ 1 and < 1, 28% and 62% in patients with APACHE II score ≥ 12 and < 12, and 64% and 17% in patients with cough peak flow > 58 and ≤ 58 L/min, respectively. CONCLUSIONS: Comorbidity, disease severity, weak cough and extubation failure were associated with increased two-year mortality in pneumonia or ARDS patients who experienced scheduled extubation. It provides objective information to caregivers to improve decision-making process during hospitalization and post discharge.

Lower geriatric nutritional risk index is associated with a higher risk of all-cause mortality in patients with chronic obstructive pulmonary disease: a cohort study from the National Health and Nutrition Examination Survey 2013-2018.

OBJECT: Malnutrition negatively affects patients with chronic obstructive pulmonary disease (COPD). This study aimed to explore the potential association between malnutrition, as defined by the Geriatric Nutritional Risk Index (GNRI), and all-cause mortality in patients with COPD using the National Health and Nutrition Examination Survey (NHANES). METHOD: The data of 579 adults with COPD during NHANES 2013-2018 were analysed. Each patient was assigned to one of the two groups according to GNRI values: normal nutritional status (GNRI>98) and malnutrition status (GNRI≤98). Survival curves and Cox regressions were applied to evaluate the association between nutritional status and mortality. RESULTS: Overall, the mean age was 63.4±0.5 years, and 53.9% of the patients were women. The prevalence of malnutrition was 6.6%, and the Kaplan-Meier curves for all-cause mortality according to nutritional status showed that malnutrition was associated with a higher incidence of all-cause mortality. The Cox regression analysis found that in the unadjusted model, the HR was 2.30 (95% CI 1.24 to 4.27, p=0.01). In the fully adjusted model, the adjusted HR was 2.47 (95% CI 1.36 to 4.5, p=0.003). Furthermore, subgroup analysis revealed that the risk of death due to malnutrition increased more than threefold in the low education and cancer subgroups. CONCLUSION: A low GNRI was an independent risk factor for all-cause mortality in patients with COPD.

Cigarette smoke extract alters the cell cycle via the phospholipid transfer protein/transforming growth factor-ß1/CyclinD1/CDK4 pathway.

This study was aimed to investigate the effect of phospholipid transfer protein (PLTP) on cigarette smoke extract (CSE)-induced alteration of the cell cycle and the possible mechanism. Male Wistar rats and the rat alveolar epithelial cell line (RLE-6TN) were exposed to normal air or different concentrations of CSE. Then PLTP siRNA was transfected into cells and an inhibitor of transforming growth factor-ß1 (TGF-ß1) was administered prior to CSE exposure. Histological changes and cell cycle stage were recorded, as were the expression levels of PLTP, TGF-ß1, CyclinD1 and CDK4. Resulting morphological changes included diffuse interstitial substance incrassation and elevated alveolar rupturing. Flow cytometry analysis revealed an increase in the number of cells in the G1 phase in a time- and dose-related manner. Both PLTP and TGF-ß1 were up-regulated at protein and mRNA levels, whereas CyclinD1 and CDK4 expression was down-regulated after CSE exposure. Furthermore, PLTP siRNA significantly suppressed CSE-induced TGF-ß1 expression, resulting in up-regulation of CyclinD1 and CDK4, but the TGF-ß1 inhibitor was not able to abrogate CSE-induced PLTP over-expression. In conclusion, PLTP may operate upstream of the TGF-ß1/CyclinD1/CDK4 pathway and may mediate the CSE-induced G1 arrest in RLE-6TN cells. Our work provides some new insight into the relation between PLTP and cell cycle progression.