scholarly journals COVID-19, COPD, and AECOPD: Immunological, Epidemiological, and Clinical Aspects

2021 ◽  
Vol 7 ◽  
Author(s):  
Francesca Polverino ◽  
Farrah Kheradmand
Keyword(s):  
Cigarette Smoke ◽  
Clinical Features ◽  
Respiratory Infections ◽  
Severe Disease ◽  
Epidemiological Data ◽  
Clinical Aspects ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Obstructive Pulmonary Disease ◽  
Ultimate Cause

The newly identified severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) causes several heterogeneous clinical conditions collectively known as Coronavirus disease-19 (COVID-19). Older patients with significant cardiovascular conditions and chronic obstructive pulmonary disease (COPD) are predisposed to a more severe disease complicated with acute respiratory distress syndrome (ARDS), which is associated with high morbidity and mortality. COPD is associated with increased susceptibility to respiratory infections, and viruses are among the top causes of acute exacerbations of COPD (AECOPD). Thus, COVID-19 could represent the ultimate cause of AECOPD. This review will examine the pathobiological processes underlying SARS-CoV-2 infection, including the effects of cigarette smoke and COPD on the immune system and vascular endothelium, and the known effects of cigarette smoke on the onset and progression of COVID-19. We will also review the epidemiological data on COVID-19 prevalence and outcome in patients with COPD and analyze the pathobiological and clinical features of SARS-CoV-2 infection in the context of other known viral causes of AECOPD. Overall, SARS-CoV-2 shares common pathobiological and clinical features with other viral agents responsible for increased morbidity, thus representing a novel cause of AECOPD with the potential for a more long-term adverse impact. Longitudinal studies aimed at COPD patients surviving COVID-19 are needed to identify therapeutic targets for SARS-CoV2 and prevent the disease's burden in this vulnerable population.

Chrysene accelerates the proceeding of chronic obstructive pulmonary disease with the aggravation of inflammation and apoptosis in cigarette smoke exposed mice

2020 ◽  
pp. 096032712097934
Author(s):  
Yuan Gao ◽  
Xinjia Zhou ◽  
Yan Zhou ◽  
Wei Zhang ◽  
Li Zhao
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Molecular Mechanisms ◽  
Smooth Muscle Actin ◽  
Lavage Fluid ◽  
Living Environment ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Obstructive Pulmonary Disease

Chrysene, one of the basic polycyclic aromatic hydrocarbons (PAHs), has been reported to make damages to human health and living environment. Chronic obstructive pulmonary disease (COPD) is a progressive disorder with high morbidity and mortality. To investigate the role of chrysene in the development of COPD, male C57BL/6 mice were exposed to the cigarette smoke (CS) followed with the administration of chrysene. Morphological analyses indicated that chrysene caused earlier and severer pathological changes in CS-exposed mice. Besides, CS-exposed mice with chrysene treatment showed obvious collagen deposition, elevated α-smooth muscle actin (α-SMA) expression and reduced E-cadherin abundance at earlier stage, which suggested the acceleration and aggravation of pulmonary fibrosis. Moreover, quantification of leukocytes and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues implied that chrysene significantly exacerbated the proceeding of inflammation in CS-exposed mice. Furthermore, significantly increased apoptotic rates, augmented expressions of apoptotic related proteins and highly expressed TRPV1 were determined in CS-exposed mice with chrysene treatment, which indicated the association between COPD pathogenesis and TRPV1 channel. In summary, our findings elucidate that chrysene accelerates the development of COPD in a murine model with new molecular mechanisms.

Hospitalizations Due to Cirrhosis: Clinical Aspects in a Large Cohort of Italian Patients and Cost Analysis Report

2017 ◽  
Vol 35 (5) ◽  
pp. 433-438 ◽  
Author(s):  
Marco Di Pascoli ◽  
Elena Ceranto ◽  
Paolo De Nardi ◽  
Daniele Donato ◽  
Angelo Gatta ◽  
...  
Keyword(s):  
Cost Analysis ◽  
Economic Impact ◽  
Large Population ◽  
Clinical Aspects ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Obstructive Pulmonary Disease ◽  
Epidemiological Analysis ◽  
Duration Of Hospitalization ◽  
Upper Gastrointestinal

Background and Aim: Liver cirrhosis is characterized by high morbidity and mortality rates. This study was addressed to evaluate the epidemiological and economic impact of cirrhosis on hospitalizations in a large population in Italy. Methods: Epidemiological analysis was performed using hospital discharge sheets of 57,720 hospitalizations due to liver disease from 2006 to 2008, selected from the Veneto regional archive. In a sample of 100 randomly selected hospitalizations, a detailed cost analysis was performed and a comparison was made with sets of patients admitted for heart failure (HF) and chronic obstructive pulmonary disease (COPD). Results: Among patients with cirrhosis, ascites emerged as the most frequent cause of admission, followed by hepatic encephalopathy, hepatocellular carcinoma, and upper gastrointestinal bleeding. Encephalopathy and ascites were the complications with the highest rates of readmission. The detailed cost analysis of hospitalizations revealed that economic expenses in the set of patients admitted for cirrhosis were about 30% higher than those for patients admitted for HF or COPD, mainly due to the longer duration of hospitalization. Conclusions: Cirrhosis has a relevant epidemiological and economic impact on hospitalizations and preventive strategies for its clinical management are warranted.

scholarly journals Clinical features and prognostic analysis of patients with Aspergillus isolation during acute exacerbation of chronic obstructive pulmonary disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yu Gu ◽  
Xianping Ye ◽  
Yu Wang ◽  
Kunlu Shen ◽  
Jinjin Zhong ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Acute Exacerbation ◽  
Clinical Features ◽  
Antifungal Therapy ◽  
Cox Regression ◽  
Multivariable Analysis ◽  
Positive Culture ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Abstract Background Lower respiratory tract (LRT) specimen culture is widely performed for the identification of Aspergillus. We investigated the clinical features and prognosis of patients with Aspergillus isolation from LRT specimens during acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods This is a 6-year single-center, real-world study. 75 cases out of 1131 hospitalized AECOPD patients were positive for Aspergillus. These patients were carefully evaluated and finally diagnosed of pulmonary aspergillosis (PA, 60 cases, 80%) or colonization (15 cases, 20%). Comparisons of clinical data were performed between these two groups. A cox regression model was used to confirm prognostic factors of Aspergillus infection. Results The PA group had worse lung function and higher rates of systemic corticosteroid use and broad-spectrum antibiotic use before admission than the colonization group. The PA group had significantly higher in-hospital mortality and 180-day mortality than the colonization group (45% (27/60) vs. 0% (0/15), p = 0.001, and 52.5% (31/59) vs. 6.7% (1/15), p < 0.001, respectively). By multivariable analysis among Aspergillus infection patients, antifungal therapy (HR 0.383, 95% CI 0.163–0.899, p = 0.027) was associated with improved survival, whereas accumulated dose of systemic steroids > 700 mg (HR 2.452, 95% CI 1.134–5.300, p = 0.023) and respiratory failure at admission (HR 5.983, 95% CI 2.487–14.397, p < 0.001) were independently associated with increased mortality. Significant survival differential was observed among PA patients without antifungals and antifungals initiated before and after Aspergillus positive culture (p = 0.001). Conclusions Aspergillus isolation in hospitalized AECOPD patients largely indicated PA. AECOPD patients with PA had worse prognosis than those with Aspergillus colonization. Empirical antifungal therapy is warranted to improve the prognosis for Aspergillus infection.

scholarly journals Comparison of clinical features and outcomes in COVID-19 and influenza pneumonia patients requiring intensive care unit admission

Infection ◽  
2021 ◽  
Author(s):  
A. Oliva ◽  
G. Ceccarelli ◽  
C. Borrazzo ◽  
M. Ridolfi ◽  
G. D.’Ettorre ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Clinical Features ◽  
Multivariable Analysis ◽  
Invasive Pulmonary Aspergillosis ◽  
Lower Percentage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Single Centre Study ◽  
Male Sex

Abstract Background Little is known in distinguishing clinical features and outcomes between coronavirus disease-19 (COVID-19) and influenza (FLU). Materials/methods Retrospective, single-centre study including patients with COVID-19 or FLU pneumonia admitted to the Intensive care Unit (ICU) of Policlinico Umberto I (Rome). Aims were: (1) to assess clinical features and differences of patients with COVID-19 and FLU, (2) to identify clinical and/or laboratory factors associated with FLU or COVID-19 and (3) to evaluate 30-day mortality, bacterial superinfections, thrombotic events and invasive pulmonary aspergillosis (IPA) in patients with FLU versus COVID-19. Results Overall, 74 patients were included (19, 25.7%, FLU and 55, 74.3%, COVID-19), median age 67 years (58–76). COVID-19 patients were more male (p = 0.013), with a lower percentage of COPD (Chronic Obstructive Pulmonary Disease) and chronic kidney disease (CKD) (p = 0.001 and p = 0.037, respectively) than FLU. SOFA score was higher (p = 0.020) and lymphocytes were significantly lower in FLU than in COVID-19 [395.5 vs 770.0 cells/mmc, p = 0.005]. At multivariable analysis, male sex (OR 6.1, p < 0.002), age > 65 years (OR 2.4, p = 0.024) and lymphocyte count > 725 cells/mmc at ICU admission (OR 5.1, p = 0.024) were significantly associated with COVID-19, whereas CKD and COPD were associated with FLU (OR 0.1 and OR 0.16, p = 0.020 and p < 0.001, respectively). No differences in mortality, bacterial superinfections and thrombotic events were observed, whereas IPA was mostly associated with FLU (31.5% vs 3.6%, p = 0.0029). Conclusions In critically ill patients, male sex, age > 65 years and lymphocytes > 725 cells/mmc are related to COVID-19. FLU is associated with a significantly higher risk of IPA than COVID-19.

scholarly journals Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Daisuke Morichika ◽  
Akihiko Taniguchi ◽  
Naohiro Oda ◽  
Utako Fujii ◽  
Satoru Senoo ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Intratracheal Instillation ◽  
Inflammatory Cells ◽  
Cigarette Smoke Extract ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Porcine Pancreas ◽  
Obstructive Pulmonary Disease ◽  
Quantitative Morphometry ◽  
Cytokines And Chemokines

Abstract Background IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33−/− mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33−/− mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33−/− and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33−/− mice than WT mice. IL-33−/− mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD.

scholarly journals FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Liu ◽  
Jiawei Xu ◽  
Tian Liu ◽  
Jinxiang Wu ◽  
Jiping Zhao ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Airway Remodeling ◽  
Critical Factor ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Impaired Lung Function

Abstract Background Cigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulation, airway inflammation and remodeling. Methods Serum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1± mice and FSTL1flox/+ mice were exposed to room air or chronic CS. Additionally, 3-methyladenine (3-MA), an inhibitor of autophagy, was applied in CS-exposed WT mice. The lung tissues and serum from patients and murine models were tested for FSTL1 and autophagy-associated protein expression by ELISA, western blotting and immunohistochemical. Autophagosome were observed using electron microscope technology. LTB4, IL-8 and TNF-α in bronchoalveolar lavage fluid of mice were examined using ELISA. Airway remodeling and lung function were also assessed. Results Both FSTL1 and autophagy biomarkers increased in COPD patients and CS-exposed WT mice. Autophagy activation was upregulated in CS-exposed mice accompanied by airway remodeling and airway inflammation. FSTL1± mice showed a lower level of CS-induced autophagy compared with the control mice. FSTL1± mice can also resist CS-induced inflammatory response, airway remodeling and impaired lung function. CS-exposed WT mice with 3-MA pretreatment have a similar manifestation with CS-exposed FSTL1± mice. Conclusions FSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke-induced COPD.

scholarly journals Profile of patients admitted in a pulmonology ward and developing Clostridium difficile enterocolitis

Pneumologia ◽  
2019 ◽  
Vol 68 (1) ◽  
pp. 31-36
Author(s):  
Ioana Cojocaru ◽  
Livia Luculescu ◽  
Daniela Negoescu ◽  
Irina Strâmbu
Keyword(s):  
Clostridium Difficile ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Respiratory Infections ◽  
Demographic Data ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Male Predominance ◽  
Number Of Patients ◽  
Lower Intestine

Abstract Clostridium difficile is an anaerobic bacterium than can colonise the lower intestine and cause enterocolitis in susceptible patients. Clostridium difficile infection (CDI) is typically a nosocomial infection, favoured by treatment with antibiotics (especially with broad-spectrum drugs), proton pump inhibitors, but also comorbidities, old age and prolonged hospitalisation. Based on the observation that in the past years, the frequency of nosocomial CDI has increased in the Institute of Pulmonology, Bucharest, this retrospective observational study aimed to analyse the characteristics of admitted patients who develop CDI, in order to identify possible particular features and risk factors. Accordingly, medical files from 80 patients admitted from January 2015 to August 2017 were analysed for demographic data, respiratory diagnosis, comorbidities, blood tests, treatments prescribed, time of CDI onset, evolution and outcome. The number of patients studied was 29 in 2015, 16 in 2016 and 35 in 2017, with slight male predominance. Totally, 54 patients (67.5%) had tuberculosis (pulmonary or pleural), 12 had lung cancer, five had respiratory infections, two had chronic obstructive pulmonary disease and seven had other diseases. All patients but nine were receiving antibiotics: tuberculosis drugs, cephalosporins, fluoroquinolones and beta-lactams. About half of the patients received proton pump inhibitors. Most patients had several comorbidities. Mean time since admittance to onset of diarrhoea was 20 days. CDI was treated with metronidazole or vancomycin. The evolution was favourable in 90% of patients, but eight patients (10%) died This study highlights a high frequency of CDI in patients treated for tuberculosis. Due to insufficient data, no epidemiological consideration could be made. Further studies are needed to assess the relationship among tuberculosis, tuberculosis treatment and CDI.

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