123 research outputs found

    La NIV nel paziente con insufficienza respiratoria cronica, la gestione domiciliare - Competenza specialistica nelle patologie pneumologiche pure

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    Questo capitolo ha lo scopo di revisionare la letteratura in merito ai meccanismi dell’insufficienza respiratoria cronica e gli effetti fisiologici e l’efficacia della ventilazione meccanica non invasiva nei pazienti affetti da BPCO in fase di stabilità clinica, cercando di dare indicazioni sulla selezione dei pazienti che potrebbero maggiormente beneficiare di questo trattamento

    Acute exacerbations of chronic obstructive pulmonary disease provide a unique opportunity to take care of patients

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    Exacerbation of chronic obstructive pulmonary disease (ECOPD) identifies the acute phase of COPD. The COPD patient is often frail and elderly with concomitant chronic diseases. This requires the physician not only looks at specific symptoms or organs, but to consider the patient in all his or her complexity. \ua9Copyright B. Begh\ue9 et al., 2013 Licensee PAGEPress

    We Have to Learn to Do Without Knowing Enough: Anti-Eosinophilic Treatments for Severe Asthma

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    Interleukin.5 (IL.5) is the main eosinophilic cytokine that promotes the differentiation, survival, and activation of eosinophils, which are the key inflammatory cells in severe eosinophilic asthma .Thus, it is no surprise that anti.IL.5 pathways have been explored for several years for their ability to reduce eosinophilic inflammation and thus to improve the treatment of this disease

    BPCO e altre malattie polmonari croniche

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    Introduction: Chronic obstructive pulmonary disease (COPD) is characterized by a relatively irreversible airflow limitation caused by chronic inflammation, in most cases tobacco-related. The impact of COPD on morbidity and mortality at the single-patient level depends upon the severity of COPD symptoms and the existence of other types of systemic and/or pulmonary disease, also known as co-morbid conditions. Materials and methods: This review examines the pulmonary diseases commonly associated with COPD, in terms of their prevalence, clinical features, pathogenic mechanisms, prognoses, and implications for management of COPD. Results: The incidence and prevalence of various pulmonary diseases are significantly increased in patients with COPD. These conditions include symptomatic bronchiectasis, combined pulmonary fibrosis and emphysema, lung cancer, sleep-related respiratory disorders, and pulmonary embolism. Some of these concomitant respiratory diseases have an independent negative impact on the prognosis of COPD patients, and their presence has important implications for treatment of these patients. Conclusions: Physicians treating patients with COPD need to be aware of these coexisting pulmonary diseases. All patients with COPD should be carefully evaluated to identify pulmonary comorbidities, since they not only influence the prognosis but also have an impact on disease management. The treatment of COPD is no longer restricted exclusively to inhaled therapy. The therapeutic approach to this disease is becoming increasingly multidimensional in view of the fact that successful management of comorbidities might positively affect the course of COPD itself. \ua9 2011 Elsevier Srl. All rights reserved

    Baseline exercise tolerance and perceived dyspnea to identify the ideal candidate to pulmonary rehabilitation: a risk chart in COPD patients.

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    Background The appropriate criteria for patient selection are still a key issue in the clinical management of patients referred to pulmonary rehabilitation (PR). Methods We retrospectively analyzed the records of a wide population of 1470 outpatient or inpatients with chronic obstructive pulmonary disease (COPD) referred to standard PR at two specialized Italian centers. Two models of multivariate logistic regression were developed to test the predictive powers of baseline exercise tolerance, namely the distance walked in 6 minutes (6MWD), and of baseline dyspnea on exertion, measured by the modified Medical Research Council scale (mMRC), versus the minimal clinically important difference (MCID) for the same outcomes. Results- (p<0.001) of predicting a MCID change. Compared to the category of individuals with mMRC 0-1point, all the other categories (2, 3, and 4) also showed a higher probability (p<0.001) of predicting a MCID change. The incorporation of baseline categories of 6MWD and mMRC in a risk chart showed that the percentage of patients reaching MCID in both variables increased as the baseline level of 6MWD decreased and of mMRC increased. Conclusion- This study demonstrates that lower levels of exercise tolerance and greater perceived dyspnea on exertion predict achieving clinically meaningful changes for both these treatment outcomes following PR. A specific risk chart that integrates these two variables may help clinicians to select ideal candidates and best responders to PR

    Marked alveolar apoptosis/proliferation imbalance in end-stage emphysema.

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    BACKGROUND: Apoptosis has recently been proposed to contribute to the pathogenesis of emphysema. METHODS: In order to establish if cell fate plays a role even in end-stage disease we studied 16 lungs (9 smoking-associated and 7 alpha1antitrypsin (AAT)-deficiency emphysema) from patients who had undergone lung transplantations. Six unused donor lungs served as controls. Apoptosis was evaluated by TUNEL analysis, single-stranded DNA laddering, electron microscopy and cell proliferation by an immunohistochemical method (MIB1). The role of the transforming growth factor (TGF)-beta1 pathway was also investigated and correlated with epithelial cell turnover and with the severity of inflammatory cell infiltrate. RESULTS: The apoptotic index (AI) was significantly higher in emphysematous lungs compared to the control group (p < or = 0.01), particularly if only lungs with AAT-deficiency emphysema were considered (p < or = 0.01 vs p = 0.09). The proliferation index was similar in patients and controls (1.9 +/- 2.2 vs 1.7 +/- 1.1). An increased number of T lymphocytes was observed in AAT-deficiency lungs than smoking-related cases (p < or = 0.05). TGF-beta1 expression in the alveolar wall was higher in patients with smoking-associated emphysema than in cases with AAT-deficiency emphysema (p < or = 0.05). A positive correlation between TGF-betaRII and AI was observed only in the control group (p < or = 0.005, r2 = 0.8). A negative correlation was found between the TGF-beta pathway (particularly TGF-betaRII) and T lymphocytes infiltrate in smoking-related cases (p < or = 0.05, r2 = 0.99) CONCLUSION: Our findings suggest that apoptosis of alveolar epithelial cells plays an important role even in end-stage emphysema particularly in AAT-deficiency disease. The TGFbeta-1 pathway does not seem to directly influence epithelial turnover in end-stage disease. Inflammatory cytokine different from TGF-beta1 may differently orchestrate cell fate in AAT and smoking-related emphysema types

    [Pathology of chronic obstructive pulmonary disease]

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    Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder of the lung characterized by poorly reversible airflow limitation. It is not a unique disease entity but rather a complex of conditions which include emphysema, chronic bronchitis and, sometimes, asthma. Moreover, COPD is a progressive disease often associated with exacerbations. Cigarette smoking, which is the most important risk factor for the development of COPD, induces pathological changes involving lung parenchyma, peripheral airways and central airways. Since lung parenchyma and peripheral airways are the sites responsible for airflow limitation and central airways are the main site of mucus hypersecretion, pathological changes in these compartments may be relevant in the development of COPD

    Effects of anti-IL5 biological treatments on blood IgE levels in severe asthmatic patients: A real-life multicentre study (BIONIGE)

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    Background: Mepolizumab and benralizumab are clinically effective biological treatments for severe eosinophilic asthmatic patients by hampering eosinophilic inflammation. The effects of these compound on the immunoglobulin (Ig)E T2 component are virtually unknown. Objectives: To evaluate the change in total IgE levels at 4&nbsp;±&nbsp;2&nbsp;months after initiation of the mepolizumab (primary outcome) or benralizumab. When available, the changes of blood inflammatory cell counts, lung function and asthma control test (ACT) were also assessed and correlated with changes in total IgE levels. Methods: Observational, retrospective, multicentre, cohort study. Severe eosinophilic atopic asthmatic patients treated with mepolizumab or benralizumab were included in the analysis. Results: Three-month treatment (on average) with mepolizumab (n&nbsp;=&nbsp;104) or benralizumab (n&nbsp;=&nbsp;82) resulted in significantly higher reduction of blood eosinophil and basophil levels in patients treated with benralizumab compared to mepolizumab. Mepolizumab did not significantly modified the levels of blood total IgE during the study period, whereas benralizumab significantly reduced (−35%, p&nbsp;&lt;&nbsp;0.001) total blood IgE levels. In patients treated with benralizumab the reduction of blood total Ig-E levels correlated with the reduction of blood basophils (but not eosinophils) and weakly with the improvement of asthma control. Conclusion: Benralizumab but not mepolizumab, treatment led to a significant reduction of circulating IgE level. The study provides different and specific mechanisms of action for anti-IL5-pathway treatments

    Nasal pressure swings as the measure of inspiratory effort in spontaneously breathing patients with de novo acute respiratory failure.

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    Background- Excessive inspiratory effort could translate into self-inflicted lung injury, thus worsening clinical outcomes of spontaneously breathing patients with acute respiratory failure (ARF). Although esophageal manometry is a reliable method to estimate the magnitude of inspiratory effort, procedural issues significantly limit its use in daily clinical practice. The aim of this study is to describe the correlation between esophageal pressure swings (\u394P es ) and nasal (\u394P nos ) as a potential measure of inspiratory effort in spontaneously breathing patients with de novo ARF. Methods- From January 1 st , 2021 to September 1 st , 2021, 61 consecutive patients with ARF (83.6% related to COVID-19) admitted to the Respiratory Intensive Care Unit (RICU) of the University Hospital of Modena (Italy) and candidate to escalation of noninvasive respiratory support (NRS) were enrolled. Clinical features and tidal changes in esophageal and nasal pressure were recorded on admission and 24 hours after starting NRS. Correlation between \u394P es and \u394P nos served as primary outcome. The effect of \u394P nos measurements on respiratory rate and \u394P es was also assessed. Results- \u394P es and \u394P nos were strongly correlated at admission (R 2 =0.88, p&lt;0.001) and 24 hours apart (R 2 =0.94, p&lt;0.001). The nasal plug insertion and the mouth closure required for \u394P nos measurement did not result in significant change of respiratory rate and \u394P es . The correlation between measures at 24 hours remained significant even after splitting the study population according to the type of NRS (high-flow nasal cannulas [R 2 =0.79, p&lt;0.001] or non-invasive ventilation [R 2 =0.95, p&lt;0.001]). Conclusions- In a cohort of patients with ARF, nasal pressure swings did not alter respiratory mechanics in the short term and were highly correlated with esophageal pressure swings during spontaneous tidal breathing. \u394P nos might warrant further investigation as a measure of inspiratory effort in patients with ARF
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