Background A synergistic effect of combination therapy with favipiravir and oseltamivir has been reported in preclinical models of influenza. However, no data are available on the clinical effectiveness of combination therapy in severe influenza. Methods Data from 2 separate prospective studies of influenza adults were used to compare outcomes between combination and oseltamivir monotherapy. Outcomes included rate of clinical improvement (defined as a decrease of 2 categories on a 7-category ordinal scale) and viral RNA detectability over time. Subhazard ratios (sHRs) were estimated by the Fine and Gray model for competing risks. Results In total, 40 patients were treated with combination therapy and 128 with oseltamivir alone. Clinical improvement on day 14 in the combination group was higher than in the monotherapy group (62.5% vs 42.2%; P = .0247). The adjusted sHR for combination therapy was 2.06 (95% confidence interval, 1.30–3.26). The proportion of undetectable viral RNA at day 10 was higher in the combination group than the oseltamivir group (67.5% vs 21.9%; P < .01). No significant differences were observed in mortality or other outcomes. Conclusions Favipiravir and oseltamivir combination therapy may accelerate clinical recovery compared to oseltamivir monotherapy in severe influenza, and this strategy should be formally evaluated in a randomized controlled trial.
The aim of this study was to compare the clinical features of patients with avian influenza A (H7N9) and influenza A (H1N1) complicated by acute respiratory distress syndrome (ARDS).The clinical data of 18 cases of H7N9 and 26 cases of H1N1 with ARDS were collected and compared in the respiratory intensive care unit (RICU) of Fuzhou Pulmonary Hospital of Fujian from March 2014 to December 2016.Patients with H7N9 had a higher acute physiology and chronic health evaluation-II score (P < .05) and lung injury score (P < .05). The rates of coexisting diabetes mellitus, hyperpyrexia, and bloody sputum production were significantly higher in the H7N9 group than in the H1N1 group (P < .05). The H7N9 group had a longer duration of viral shedding from the onset of illness (P < .05) and from the initiation of antiviral therapy (P < .05) to a negative viral test result than the H1N1 group. Patients with H7N9 had higher rates of invasive mechanical ventilation; serious complications, including alimentary tract hemorrhage, pneumothorax or septum emphysema, hospital-acquired pneumonia (HAP) and multiple organ dysfunction syndrome (MODS); and hospital mortality (P < .05). At the 6th month of follow-up, the rates of bronchiectasia, reticular opacities, fibrous stripes, and patchy opacities on chest computed tomography (CT) were significantly higher in the H7N9 group than in the H1N1 group (P < .05). Based on multiple logistic regression analysis, H7N9 influenza viral infection was associated with a higher risk of the presence of severe ARDS than H1N1 influenza viral infection (odds ratio 8.29, 95% confidence interval [CI] 1.53–44.94; P < .05).Compared to patients with H1N1, patients with H7N9 complicated by ARDS had much more severe disease. During long-term follow-up, more changes in pulmonary fibrosis were observed in patients with H7N9 than in patients with H1N1 during the convalescent stage.
Background: Although cisplatin is an effective chemotherapeutic drug that is commonly used for non-small-cell lung cancer (NSCLC) treatment, the drug resistance usually occurs during the long-term use of it. It is urgent to develop strategies to reduce the resistance of NSCLC cells to cisplatin. Methods: Cisplatin-resistant NSCLC cell lines (PC9/R and A549/R) were acquired through long-term exposure of PC9 and A549 cells to cisplatin. QRT-PCR analysis was performed to compare the expression of miR-140 between routine NSCLC cells and cisplatin-resistant NSCLC cells. CCK-8 assay was used to evaluate the effect of miR-140 on the sensitivity of PC9/R and A549/R to cisplatin. Western blot assay and luciferase reporter assay were used to confirm the regulation of miR-140 on SIRT1. Western blot and flow cytometry analysis were performed to evaluate the effect of miR-140 on the apoptosis pathway induced by cisplatin. Results: PC9/R and A549/R exhibited obviously lower sensitivity compared to their parental PC9 and A549 cells, respectively. Furthermore, PC9/R and A549/R cells expressed significantly lower levels of miR-140 compared to their parental PC9 and A549 cells, respectively. However, transfection with miR-140 mimics significantly resensitized the PC9/R and A549/R to cisplatin-induced cytotoxicity. In the mechanism research, we confirmed that SIRT1 was overexpressed and was targeted by miR-140 in PC9/R and A549/R. Furthermore, overexpression of SIRT1 was responsible for the resistance to cisplatin in PC9/ R and A549/R cells. Transfection with miR-140 was able to inhibit the expression of SIRT1 and thus inhibited the SIRT1/ROS/JNK pathway. As a result, the PC9/R and A549/R cells restored the sensitivity to cisplatin-induced apoptosis. Conclusion: MiR-140 resensitizes cisplatin-resistant NSCLC cells to cisplatin treatment through the SIRT1/ROS/JNK pathway.
Hemophagocytic syndrome (HPS) is a life-threatening clinical syndrome that has various presentations, shows rapid progression and is associated with a high mortality. Clinical reports about pulmonary tuberculosis combined with respiratory failure accompanied by HPS are rare.HPS has no special clinical manifestations, and the main presentations include persistent fever, hepatosplenomegaly, hematocytopenia, and rash. In the Intensive Care Unit (ICU), the clinical manifestations of severe infection and secondary HPS overlap, thus there is often a delay in the diagnosis and treatment of HPS.HPS is not an independent disease but represents an excessive inflammatory response due to immune dysfunction induced by various causes such as infection and tumor.The 2 cases in this report show that tuberculosis-associated hemophagocytic syndrome is not easy to find, especially in ICU. There are few clinical reports of pulmonary tuberculosis combined with respiratory failure and HPS. Here, we describe 2 such clinical cases and review the relevant literature in order to deepen our understanding of this disease.
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