Purpose The present study aimed to investigate the prevalence and associated factors of suboptimal daily peak inspiratory flow (PIF) and technical misuse of three commonly used dry powder inhalers (DPIs) in outpatients with stable chronic airway diseases. Patients and Methods Included in this study were 85 outpatients with stable asthma, chronic obstructive pulmonary disease (COPD), or asthma-COPD Overlap (ACO) and had previously used any of Turbuhaler ® (TUR), Diskus ® (DIS), HandiHaler ® (HAN) between December 2018 and September 2019. The patient’s daily PIF against the resistance of a specific DPI and operation technique was investigated by two pharmacists by using In-Check DIAL G16 and a checklist. Results Of the 85 patients, the proportion of patients with a suboptimal daily PIF and technical misuse was 38.8% and 65.9%, respectively. In logistic regression, we observed that the factors that increase the risk for suboptimal daily PIF were age (OR=1.06) and combination with respiratory diseases (OR = 6.59). The factor that decreases the risk for misuse was the higher education level (OR =0.63). Conclusion Even if patients have received training at the time of initial prescription, the standardization of the use of DPIs by patients in our center was still unoptimistic. Age and combined with respiratory diseases were associated with suboptimal PIF. Higher education level decreased the incidence of technique misuse.
Background: Chronic obstructive pulmonary disease (COPD) is characterized by pulmonary and systemic inflammatory processes, and exacerbation of COPD represents a critical moment in the progression of COPD. Several biomarkers of inflammation have been proposed to have a predictive function in acute exacerbation. However, their use is still limited in routine clinical practice. The purpose of our study is to explore the prognostic efficacy of novel inflammatory hemogram indexes in the exacerbation among stable COPD patients.Method: A total of 275 stable COPD patients from the Shanghai COPD Investigation Comorbidity Program were analyzed in our study. Blood examinations, especially ratio indexes like platelet–lymphocyte ratio (PLR), platelet × neutrophil/lymphocyte ratio [systemic immune-inflammation index (SII)], and monocyte × neutrophil/lymphocyte ratio [systemic inflammation response index (SIRI)], lung function test, CT scans, and questionnaires were performed at baseline and routine follow-ups. Clinical characteristics and information of exacerbations were collected every 6 months. The relationship between hemogram indexes and diverse degrees of exacerbation was assessed by logistic regression. The receiver operating characteristic (ROC) curve and area under the curve (AUC) were used to evaluate the ability of hemogram indexes to predict exacerbation of COPD. Furthermore, the discrimination and accuracy of combined indexes were measured by ROC and calibration curve.Result: There was a significant positive correlation between PLR levels and total exacerbation of COPD patients in a stable stage in a year. Also, the predictive ability of PLR exceeded any other ratio indexes, with an AUC of 0.66. SII and SIRI ranked second only to PLR, with an AUC of 0.64. When combining PLR with other indexes (sex, COPD year, and St. George's Respiratory Questionnaire scores), they were considered as the most suitable panel of index to predict total exacerbation. Based on the result of the ROC curve and calibration curve, the combination shows optimal discrimination and accuracy to predict exacerbation events in COPD patients.Conclusion: The hemogram indexes PLR, SII, and SIRI were associated with COPD exacerbation. Moreover, the prediction capacity of exacerbation was significantly elevated after combining inflammatory hemogram index PLR with other indexes, which will make it a promisingly simple and effective marker to predict exacerbation in patients with stable COPD.
Background: Asthma is one of the most common noninfectious chronic diseases characterized by type II in ammation. This study aimed to investigate the effects of molecular hydrogen on the pathogenesis of asthma.Methods: OVA sensitized asthma mouse model was established and hydrogen/oxygen mixture was used to treat asthmatic mice. Serum and BALF cytokines were measured with speci c ELISA assays. Ecadherin and ZO-1 were detected by immunohistochemical staining and expression of caspase 3 and 9, NF-kB, IL-33 and ST2 was assessed by quantitative real-time PCR, western blot and / or immuno uorescence. IL-33 promoter activity was analyzed by dual-luciferase assay. ILC2 population was assayed by ow cytometry and differentially expressed miRNAs were detected using miRNA array.Results: Serum and BALF levels of IL-33 and other alarmin and type II cytokines were greatly increased by OVA and inhibited by H 2 in asthmatic mice. The expression of NF-kB (p65) and ST2 was upregulated by OVA and suppressed by H 2 . ILC2 population was markedly increased in OVA-induced asthmatic mice, and such increase was inhibited by H 2 . E-cadherin and ZO-1 levels in airway tissues of asthmatic mice were signi cantly lower than that of control mice, and the reduction was recovered by H 2 treatment. H 2 alleviated HDM induced apoptosis of 16HBE cells, upregulation of IL-33 and ST2, and elevation of IL-33 promoter activity. A group of miRNAs differentially expressed in HDM and HDM+H 2 treated 16HBE cells were identi ed.Conclusions: These data demonstrated that H2 is e cient in suppressing allergen-induced asthma and could be developed as a therapeutic method for asthma and other conditions of type II in ammation.
Background: Chronic obstructive pulmonary disease (COPD) often coexists with multiple comorbidities which may have a significant impact on acute exacerbations of patients. At present, what kind of comorbidities affects acute exacerbations and how comorbidities lead to poor prognosis are still controversial. The purpose of our study is to determine the impact of comorbidities on COPD exacerbation and establish an acute exacerbation risk assessment system related to comorbidities. Methods: A total of 742 COPD patients participated in the Shanghai COPD Investigation on Comorbidity Program (SCICP, ChiCTR2000030911). Finally, the baseline information of 415 participants and one-year follow-up data were involved in the analysis. We collected hemogram indices, pulmonary function tests and acute exacerbation of COPD with regular medical follow-up. Q-type cluster analysis was used to determine the clusters of participants. Receiver operating characteristic (ROC) analysis was constructed to assess the ability of indicators in predicting acute exacerbations. Results: Almost 65% of the population we investigated had at least one comorbidity. The distribution and incidence of comorbidities differed between exacerbation group and nonexacerbation group. Three comorbidity clusters were identified: (1) respiratory, metabolic, immune and psychologic disease (non-severe cases); (2) cardiovascular and neoplastic disease (severe cases); (3) less comorbidity. Different sub-phenotypes of COPD patients showed significant distinction in health status. Anxiety (OR=5.936, P=0.001), angina (OR=10.155, P=0.025) and hypertension (OR=3.142, P=0.001) were found to be independent risk factors of exacerbation in a year. The novel risk score containing BODEx and four diseases showed great prognostic value of COPD exacerbation in developing sample. Conclusion:Our study detailed the major interaction between comorbidities and exacerbation in COPD. Noteworthily, a novel risk score using comprehensive index -BODEx -and comorbidity parameters can identify patients at high risk of acute exacerbation.
Background: Asthma is one of the most common noninfectious chronic diseases characterized by type II inflammation. This study aimed to investigate the effects of molecular hydrogen on the pathogenesis of asthma.Methods: OVA sensitized asthma mouse model was established and hydrogen/oxygen mixture was used to treat asthmatic mice. Serum and BALF cytokines were measured with specific ELISA assays. E-cadherin and ZO-1 were detected by immunohistochemical staining and expression of caspase 3 and 9, NF-kB, IL-33 and ST2 was assessed by quantitative real-time PCR, western blot and / or immunofluorescence. IL-33 promoter activity was analyzed by dual-luciferase assay. ILC2 population was assayed by flow cytometry and differentially expressed miRNAs were detected using miRNA array. Results: Serum and BALF levels of IL-33 and other alarmin and type II cytokines were greatly increased by OVA and inhibited by H2 in asthmatic mice. The expression of NF-kB (p65) and ST2 was upregulated by OVA and suppressed by H2. ILC2 population was markedly increased in OVA-induced asthmatic mice, and such increase was inhibited by H2. E-cadherin and ZO-1 levels in airway tissues of asthmatic mice were significantly lower than that of control mice, and the reduction was recovered by H2 treatment. H2 alleviated HDM induced apoptosis of 16HBE cells, upregulation of IL-33 and ST2, and elevation of IL-33 promoter activity. A group of miRNAs differentially expressed in HDM and HDM+H2 treated 16HBE cells were identified. Conclusions: These data demonstrated that H2 is efficient in suppressing allergen-induced asthma and could be developed as a therapeutic method for asthma and other conditions of type II inflammation.
Background Chronic obstructive pulmonary disease (COPD) is closely related to the occurrence of lung cancer. Both diseases involve changes in the biological function and structure of bronchial epithelial cells. Recently, the role of exosomes in intercellular communication has attracted increasing attention from researchers. As an important molecule carried by exosomes, the role of exosomal miRNAs in diseases such as COPD and lung cancer has also been gradually confirmed. The aim of this study is to investigate the effect of exosomal miRNA derived from macrophages on the proliferation of bronchial epithelial cells. Results After co-culture with alveolar macrophages from COPD, the proliferative activity and migration capacity of 16HBE was significantly enhanced compared with those from healthy controls. Alveolar macrophages from COPD promoted the production of MUC5AC, MUC5B and MUC2 as well as TNF - α and IL-6 in 16HBE. MiR-380 was up-regulated miRNA in exosomes derived from alveolar macrophages through miRNA array analysis. Exosomal miR-380 enhanced the proliferation and migration of 16HBE, promoted the expression of mucins such as MUC5AC, MUC5B and MUC2 of 16HBE, but inhibited the expression of CFTR protein. The target gene of miR-380 was CFTR. The proliferative activity and migration ability of 16HBE was enhanced by blocking CFTR. Conclusions Alveolar macrophages from COPD can enhance the proliferation and migration of 16HBE and promote the expression of mucin and proinflammatory mediators such as IL-6 and TNF-α. Exosomal miR-380 derived from macrophages in COPD was significantly up-regulated. The enhancement of proliferation and migration may be related to the down regulation of CFTR by exosomes delivering miR-380 to bronchial epithelial cells, opening a new way for the therapy and prevention in COPD and its complication.
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