Efficacy of treatment with N-acetylcysteine inhalation for AECOPD: A propensity-score-matched cohort study.

INTRODUCTION: N-acetylcysteine (NAC) prevents acute exacerbations of chronic obstructive pulmonary disease (AECOPD). However, the value of NAC inhalation in the treatment of patients with AECOPD is still poorly understood. The study was conducted to evaluate the efficacy of NAC inhalation in AECOPD patients requiring hospitalization. METHODS: In this single institutional, retrospective cohort study, all patients with AECOPD requiring hospitalization between January 2021 and January 2022 were included. Patients were divided into NAC group and Non-NAC group according to whether being treated with NAC inhalation and were matched using the propensity score. The primary outcome was a composite of progression to ventilation requirement, in-hospital mortality and readmission for AECOPD within 30 days. The effect on the mean hospitalized days, blood gas indexes and the incidence rate of adverse drug events were compared between the two groups. RESULTS: Ninety-six patients in the NAC group were matched with 96 patients in the Non-NAC group. The differences in the primary composite end point (NAC group vs Non-NAC group, 5.2% vs 16.7%; P = 0.011) were significant. The median time to discharge was shorter in the NAC group (8.3 vs. 9.1 days, P = 0.030). The NAC group presented a larger increase in partial pressure of arterial oxygen (Pa O2 ) and a higher ratio of self-reported symptomatic improvement from admission to day 5. There was no definite difference between the two groups in the frequency of adverse event. CONCLUSION: NAC inhalation is associated with an improved clinical outcome. A further study should be conducted to confirm the clinical usefulness of NAC inhalation in AECOPD patients.

Bacterial co-infection raises in-hospital mortality of COVID-19 patients: a retrospective study.

Background: We aim to explore whether the bacterial co-infection with COVID-19 will raise the in-hospital mortality. Methods: COVID-19 patients' information were collected for analysis in our retrospective study. Neutrophil count and procalcitonin (PCT) were used to estimate whether there was a suspected bacterial co-infection. Results: The main baselines between the suspected bacterial infection (SBI) and no evidence of bacterial infection (NBI) groups were no significant differences. In SBI group, patients required more therapies than NBI group. There was significantly higher in-hospital mortality (26% vs.9%, P < 0.001) between SBI and NBI groups in overall population. And in each subgroup based on pneumonia inflammation index (PII), it also showed higher in-hospital mortality of COVID-19 patients with bacterial co-infection. With logistic regression models, it showed that bacterial co-infection was associated with significantly higher in-hospital mortality in overall population (OR 1.694, 95% CI 1.179-2.434, p = 0.004) and mild subgroup (OR 2.374, 95% CI 1.249-4.514, p = 0.008). The rate of bacterial co-infection in overall population was 51%. At the same time, it showed a significantly higher rate of bacterial co-infection in critical subgroup than severe subgroup (63% vs. 49%, p = 0.003), and than that in moderate subgroup (63% vs. 48%, p = 0.002) based on clinical classification. It showed a significantly higher rates of bacterial co-infection in severe subgroup than moderate subgroup (66% vs. 49%, p = 0.001) based on PII. The result showed that the risk factor associated with significantly higher in-hospital mortality was PII (OR 1.018, 95%CI 1.012 to 1.024, P < 0.001) with logistic regression models. Interpretation: Bacterial co-infection estimated by Neutrophil count and procalcitonin significantly raises in-hospital mortality of COVID-19 patients in overall population in our study. Its impact is more significant in mild and moderate PII subgroups. PII based on CT imaging combined with neutrophil count and PCT is beneficial for accurate differentiation of bacterial co-infection of COVID-19.

Meta-Analysis of Atezolizumab vs Docetaxel in Non-Small Cell Lung Cancer Treatment Outcomes.

Objective: We aimed to investigate the clinical efficacy of atezolizumab and docetaxel in the treatment of non-small cell lung cancer (NSCLC) via meta-analysis and systematic review. Methods: Publications were searched from China National Knowledge Infrastructure (CNKI), Chongqing Vipers Chinese Science and Technology Journal database (VIP), Wanfang database, PubMed database, Embase database, Cochrane Library and Web of Science. Randomized controlled trials (RCTs) of atezolizumab and docetaxel in the treatment of patients with NSCLC were collected. The retrieval period was from the establishment of the database to November 2021 and updated on 22 April 2023. According to the inclusion and exclusion criteria, the included studies were screened and quality evaluated. Meta-analysis was performed using RevMan 5.4.3 (Cochrane Training, Summertown, Oxford UK) software. Results: A total of 6 RCTs were included in our analysis, including 6348 patients with NSCLC. Our results showed that the atezolizumab group had significantly longer overall survival (OS) than the docetaxel group (hazard ratio [HR] = 0.77; 95% CI, 0.73-0.81); P < .00001). In terms of progression-free survival (PFS) and objective response rate (ORR), the atezolizumab group was not significantly superior to the docetaxel group (HR = 0.96; 95% CI, 0.90-1.02; P = .20), (relative ratio [RR] = 1.10, 95% CI, 0.95-1.26; P = .20). In terms of treatment-related adverse events (TRAEs), after treatment, the number of patients with TRAEs in the atezolizumab group was significantly lower than in the docetaxel group (RR = 0.65; 95% CI, 0.54-0.79; P < .00001). Conclusion: Compared with docetaxel, atezolizumab can significantly prolong OS in patients with NSCLC and reduce the occurrence of TRAEs, but there is no advantage in PFS or ORR remission rate. Due to some limitations in case numbers and quality of included studies, multicenter, large sample, high-quality RCTs are still needed for further validation.

Cisplatin induces expression of drug resistance-related genes through c-jun N-terminal kinase pathway in human lung cancer cells.

PURPOSE: Change of multidrug resistance-related genes (e.g., lung resistance protein, LRP) and overexpression of anti-apoptotic genes (Bcl-2, Bcl-Xl, XIAP, Survivin) are responsible for cisplatin resistance. In our study, we investigated the mechanism by which cisplatin induces LRP, Bcl-2, Bcl-xL, XIAP, and Survivin expression in human lung adenocarcinoma A549 cells and human H446 small cell lung cancer cells at mRNA and protein levels. METHODS: In our study, cell proliferation was assessed with CCK-8 assays, and cell apoptosis was assessed with flow cytometric analysis and Annexin-V/PI staining. qPCR was used to complete RNA experiments. Protein expression was assessed with Western blotting. RESULTS: Cisplatin increased Bcl-2, LRP, and Survivin expression, but decreased Bcl-xL and XIAP expression in a dose-dependent manner. Preincubation with JNK-specific inhibitor, SP600125, significantly inhibited these genes' expression at mRNA and protein levels, enhanced chemosensitivity of lung cancer cells to cisplatin, and promoted cisplatin-induced apoptosis. CONCLUSION: Our data suggest that the JNK signaling pathway plays an important role in cisplatin resistance. Lung resistance protein (LRP) and anti-apoptotic genes (Bcl-2, Bcl-Xl, XIAP, Survivin) are involved in the process. The results reminded us of a novel therapy target for lung cancer treatment.