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Asthma is a chronic inflammatory disease characterized by airflow limitation and variable respiratory symptoms. It is characterized by variable symptoms such as cough, wheeze, chest tightness, and shortness of breath which vary in intensity and time. In order to reach a comprehensive approach of disease management, the importance of non-pharmacological treatment in addition to pharmacological therapy has been recently highlighted. Studies have documented that pulmonary rehabilitation has beneficial effects in patients with asthma, at any stage of the disease, improving exercise capacity, asthma control, and quality of life and reducing wheezing, anxiety, depression, and bronchial inflammation. Although several evidences suggest a role of pulmonary rehabilitation in patients with asthma, additional information is required to identify a specific program in order to improve clinical care based on specific patient's needs.

Background: Mepolizumab improves asthma control in severe eosinophilic asthma (SEA). However, its multidimensional effects on airway and systemic biomarkers are still incompletely understood. Methods: In this prospective study, 15 SEA patients were evaluated at baseline (T0), 6 (T6), and 12 months (T12) after starting mepolizumab. Lung function, FeNO values, asthma control, blood eosinophil count (BEC), cytokines, and metabolomic profiles (1H-NMR) were evaluated in serum, nasal secretions, and exhaled breath condensate (EBC). Univariate and multivariate (PCA, OPLS-DA) analyses were performed. Results: Mepolizumab reduced exacerbations, from a median of 2 at T0 to 0 at both T6 (p = 0.001) and T12 (p = 0.003). ACT improved from 18.7 ± 4.7 at baseline to 23.0 ± 2.8 at T6 (p = 0.026) and 23.4 ± 3.3 at T12 (p = 0.032), while FEV1 increased by 270 mL at T6 (p = 0.032) and remained stable at T12. Median BEC decreased from 450.0 (350.0–560.0) to 65.0 (50.0–87.5) cells/μL at T6 and to 50.0 (35.0–160.0) at T12 (p < 0.001), while FeNO showed a non-significant downward trend. IL-13 significantly decreased in serum and nasal secretions at T6 and T12, while IL-5 increased in nasal secretions at both timepoints and remained unchanged in serum. IL-2 showed opposite trends in serum and nasal samples, whereas GM-CSF and IFN-γ increased in nasal secretions at T12. Metabolomic profiling suggested compartment-specific changes, with decreased short-chain alcohols in EBC, increased amino acids in nasal secretions and serum at T6, and elevated pyruvate in serum at T12, although none reached statistical significance in univariate analysis. Conclusions: Mepolizumab induced consistent clinical, immunologic, and metabolic changes across compartments, supporting the use of integrated cytokine and 1H-NMR metabolomic profiling as a complementary approach for response assessment in SEA.

Chronic Obstructive Pulmonary Disease (COPD) is a heterogeneous lung condition characterised by chronic respiratory symptoms, fixed airway obstruction and persistent inflammation that leads to a progressive airflow limitation. Although COPD has traditionally been linked to neutrophilic inflammation, recent studies have identified a subset of patients – approximately 20%–40% – with elevated eosinophil levels in blood and sputum. Emerging evidence suggests that eosinophilic inflammation has a pivotal role in a subset of COPD patients and may influence disease progression, exacerbation frequency and therapeutic responses. This narrative review provides a comprehensive analysis of the role of eosinophils in COPD with particular attention to their role as biomarkers in blood and sputum. We evaluate the prevalence of eosinophilic inflammation in COPD exanimating different thresholds used in blood and in sputum to define it. In addition, we focus on eosinophilic COPD phenotype as a treatable trait, emphasising recent evidence that supports the effectiveness of biological target therapy.

Arterial hypertension is the most frequent cardiovascular risk factor all over the world, and it is one of the leading drivers of the risk of cardiovascular events and death. It is a complex trait influenced by heritable and environmental factors. To date, the World Health Organization estimates that 1.28 billion adults aged 30–79 years worldwide have arterial hypertension (defined by European guidelines as office systolic blood pressure ≥ 140 mmHg or office diastolic blood pressure ≥ 90 mmHg), and 7.1 million die from this disease. The molecular genetic basis of primary arterial hypertension is the subject of intense research and has recently yielded remarkable progress. In this review, we will discuss the genetics of arterial hypertension. Recent studies have identified over 900 independent loci associated with blood pressure regulation across the genome. Comprehending these mechanisms not only could shed light on the pathogenesis of the disease but also hold the potential for assessing the risk of developing arterial hypertension in the future. In addition, these findings may pave the way for novel drug development and personalized therapeutic strategies.

Coronavirus disease 2019 (COVID-19) vaccines proved a strong clinical efficacy against symptomatic or moderate/severe COVID-19 and are considered the most promising approach for curbing the pandemic. However, some questions regarding the safety of COVID-19 vaccines have been recently raised. Among adverse events to vaccines and despite a lack of signal during phase III clinical trials, an increase in blood pressure (BP) after COVID-19 vaccination has been reported as a potential adverse reaction. We systematically analyze this topic and undertook a meta-analysis of available data to estimate the proportion of patients with abnormal BP or raise in BP after vaccination. Six studies entered the final analysis. Overall, studies accrued 357,387 subjects with 13,444 events of abnormal or increased BP. After exclusion of outlier studies, the pooled estimated proportion of abnormal/increased BP after vaccination was 3.20% (95% CI: 1.62–6.21). Proportions of cases of stage III hypertension or hypertensive urgencies and emergencies was 0.6% (95% CI: 0.1% to 5.1%). In conclusion, abnormal BP is not rare after COVID-19 vaccination, but the basic mechanisms of this phenomenon are still unclear and require further research.

Background High blood eosinophils seem to predict exacerbations and response to inhaled corticosteroids (ICS) treatment in patients with chronic obstructive pulmonary disease (COPD). The aim of our study was to prospectively evaluate for 2 years, blood and sputum eosinophils in COPD patients treated with bronchodilators only at recruitment. Methods COPD patients in stable condition treated with bronchodilators only underwent monitoring of lung function, blood and sputum eosinophils, exacerbations and comorbidities every 6 months for 2 years. ICS was added during follow-up when symptoms worsened. Results 63 COPD patients were enrolled: 53 were followed for 1 year, 41 for 2 years, 10 dropped-out. After 2 years, ICS was added in 12/41 patients (29%) without any statistically significant difference at time points considered. Blood and sputum eosinophils did not change during follow-up. Only FEV 1 /FVC at T0 was predictive of ICS addition during the 2 year-follow-up (OR:0.91; 95% CI: 0.83–0.99, p  = 0.03). ICS addition did not impact on delta (T24-T0) FEV 1 , blood and sputum eosinophils and exacerbations. After 2 years, patients who received ICS had higher blood eosinophils than those in bronchodilator therapy ( p  = 0.042). Patients with history of ischemic heart disease increased blood eosinophils after 2 years [ p  = 0.03 for both percentage and counts]. Conclusions Blood and sputum eosinophils remained stable during the 2 year follow-up and were not associated with worsened symptoms or exacerbations. Almost 30% of mild/moderate COPD patients in bronchodilator therapy at enrollment, received ICS for worsened symptoms in a 2 year-follow-up and only FEV 1 /FVC at T0 seems to predict this addition. History of ischemic heart disease seems to be associated with a progressive increase of blood eosinophils.

After assessing the levels of spread and severity of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, academic literature focused on the pathophysiology of coronavirus disease 2019 (COVID-19) [...]

Background: Benralizumab is a monoclonal antibody treatment for severe eosinophilic asthma (SEA). Few studies investigated its role in airway inflammation and its correlation with lung function. Objectives: The aim of the present study is to assess its effect after 1 year of treatment, focusing on airway inflammation. Design: This is a retrospective observational study, in an Italian tertiary reference centre specialised in diagnosis and management of severe asthma patients. Methods: We conducted a monocentric retrospective study including SEA patients treated with benralizumab for 1 year. Clinical, functional and inflammatory data were collected at baseline, 6 (T6) and 12 (T12) months. Results: Twenty-two SEA patients on benralizumab were included. We observed a reduction in exacerbations rate and systemic steroid treatment (p < 0.0001) as well as an improvement in asthma control (p < 0.0001), health-related quality of life (p = 0.017) and lung function pre-BD FEV1 (L) (p = 0.02) and percentage (p = 0.004) and post-BD FEV1 (L) (p = 0.01) and percentage (p = 0.003) from baseline to T6 and T12. A reduction in sputum eosinophil percentage was observed at T6 and T12 (p < 0.005). We found a positive correlation between the variation of sputum eosinophils percentage and FEV1 (L) at T12 (rho = −0.79, p = 0.04). Moreover, the improvement of FEF25%–75% from baseline to 6 (rho = −0.53, p = 0.03) and 12 (rho = −0.62, p = 0.01) months negatively correlated with the duration of asthma disease. In our cohort 12/22 patients were super-responders at T6 and 15/22 at T12. Furthermore, clinical remission was reached by 12/22, and all of them obtained blood and sputum eosinophils counts normalisation. Conclusion: Our data confirm that it is a rapid and effective treatment for SEA acting on clinical, functional, systemic and airway inflammatory outcomes. Our results highlight the role of induced sputum as a promising non-invasive technique to investigate pathophysiologic mechanisms in severe asthma treated with biologics. Finally, a negative correlation between small airway improvement and the duration of asthma may suggest that a prompt referral to asthma centres may delay lung function worsening. Additional studies are needed to investigate more in-depth the role of induced sputum in the management of asthma, response to treatment and remission. Plain language summary Analysis of the effect of a biological therapy on severe asthma Background: Asthma is estimated to affect almost 5%-8% of the European adult population, and 5%–10% of these patients suffer from a severe asthma form. Severe asthma is characterised by chronic airway inflammation despite traditional inhaled treatment and patients may experience acute flare ups requiring courses of steroids and eventually hospitalization leading to a poor quality of life. New biological drugs have been introduced to treat severe asthma characterized by inflammation in the blood and in the lungs. Benralizumab is a well known biological option for severe asthmatic patients. Methods: We provide data on 22 patients followed up in our tertiary severe asthma centre in Tradate, Italy, affected by severe eosinophilic asthma treated with benralizumab for at least one year. Results: Our data confirmed a rapid effect of benralizumab on respiratory symptoms, exacerbations and quality of life. In addition, we documented a significant improvement in lung function along with a normalization of inflammation in the blood and in the lungs, assessed with a non-invasive tool: the induced sputum. Conclusions: Interestingly, our data highlight the importance of induced sputum as a promising non-invasive technique to investigate pathophysiologic mechanisms in severe asthma treated with biologics. Additional studies are needed to implement its role in the management of asthma also in terms of response to treatment towards a personalized approach.

Background: Benralizumab has been shown to restore good control of severe eosinophilic asthma (SEA). Robust data on benralizumab effectiveness over periods longer than 2 years are scarce. Methods: This retrospective multicentric study was conducted on 108 Italian SEA patients treated with benralizumab for up to 36 months. Partial and complete clinical remission (CR) were assessed. Data were analyzed with descriptive statistics or using linear, logistic, and negative binomial mixed-effect regression models. Results: At 36 months, benralizumab reduced the exacerbation rate by 89% and increased the forced expiratory volume in 1 second (FEV1) (+440 mL at 36 months, p < 0.0001). Benralizumab improved asthma control as well as sinonasal symptoms in patients with chronic rhinosinusitis with nasal polyposis (CRSwNP). Up to 93.33% of patients either reduced or discontinued OCS; benralizumab also decreased ICS use and other asthma medications. Overall, 84.31% of patients achieved partial or complete CR. Conclusions: Benralizumab improved asthma and sinonasal outcomes up to 36 months. These findings support the potential of benralizumab to induce CR, emphasizing its role as a disease-modifying anti-asthmatic drug for the management of SEA. Further research is warranted to expand these findings by minimizing data loss and assessing benralizumab’s long-term safety.

Hypertension is the most frequent cardiovascular risk factor all over the world. It remains a leading contributor to the risk of cardiovascular events and death. In the year 2015, about 1.5 billion of adult people worldwide had hypertension (as defined by office systolic blood pressure ≥ 140 mmHg or office diastolic blood pressure ≥ 90 mmHg). Moreover, the number of hypertensive patients with age ranging from 30 to 79 years doubled in the last 30 years (from 317 million men and 331 million women in the year 1990 to 652 million men and 626 million women in 2019) despite stable age-standardized prevalence worldwide. Despite such impressive growth, the proportion of controlled hypertension is very low. A better understanding of the pathogenesis of hypertension may contribute to the development of innovative therapeutic strategies. In this context, alterations of the messenger RNA metabolism have been recently evaluated as contributors to the pathogenesis of hypertension, and pharmacological modulation of RNA metabolism is under investigation as potential and novel therapeutic armamentarium in hypertension.