Explore the vast range of titles available.

BackgroundChronic obstructive pulmonary disease (COPD) is a prevalent, debilitating condition linked to significant morbidity and mortality. While glucagon-like peptide-1 receptor agonists (GLP-1RAs) have demonstrated clinical benefits for COPD, the effect of tirzepatide on COPD outcomes remains to be fully elucidated.MethodsThis study utilized the TriNetX Global Collaborative Network to analyze data from adults with COPD who were prescribed tirzepatide between 1 January 2022, and 28 February 2025. Patients were divided into two groups: those prescribed tirzepatide and those receiving standard care (control group). Propensity score matching (PSM) was applied to balance covariates. The primary outcome was the risk of COPD exacerbations.ResultsAfter PSM, the study included 12,110 patients (6,055 in each group). The tirzepatide group was associated with a lower risk of COPD exacerbations (HR, 0.77; 95% CI, 0.63–0.93) compared to the control group. Additionally, tirzepatide use was associated with a lower risk of mortality (HR, 0.52; 95% CI, 0.37–0.73), pneumonia (HR, 0.71; 95% CI, 0.59–0.86), and acute respiratory failure (HR, 0.59; 95% CI, 0.48–0.73).ConclusionTirzepatide use was associated with a potentially reduced risk of COPD exacerbations, lower mortality, and a decreased incidence of pneumonia and acute respiratory failure. These findings should be interpreted with caution, given the inherent limitations of observational study designs, including the possibility of residual confounding and selection bias. The observed associations do not establish causality, and the clinical generalizability of these results remains uncertain. Prospective randomized controlled trials are warranted to confirm these preliminary findings.

Asthma exacerbations are associated with significant childhood morbidity and mortality. Recurrent asthma attacks contribute to progressive loss of lung function and can sometimes be fatal or near-fatal, even in mild asthma. Exacerbation prevention becomes a primary target in the management of all asthmatic patients. Our work reviews current advances on exacerbation predictive factors, focusing on the role of non-invasive biomarkers and genetics in order to identify subjects at higher risk of asthma attacks. Easy-to-perform tests are necessary in children; therefore, interest has increased on samples like exhaled breath condensate, urine and saliva. The variability of biomarker levels suggests the use of seriate measurements and composite markers. Genetic predisposition to childhood asthma onset has been largely investigated. Recent studies highlighted the influence of single nucleotide polymorphisms even on exacerbation susceptibility, through involvement of both intrinsic mechanisms and gene-environment interaction. The role of molecular and genetic aspects in exacerbation prediction supports an individual-shaped approach, in which follow-up planning and therapy optimization take into account not only the severity degree, but also the risk of recurrent exacerbations. Further efforts should be made to improve and validate the application of biomarkers and genomics in clinical settings.

Alterations of the airway microbiome are often associated with pulmonary diseases. For example, detection of the bacterial pathogen in the upper airways is linked with an increased risk to develop or exacerbate asthma. However, the mechanisms by which augments allergic airway inflammation (AAI) remain unclear. We here characterized the cellular and soluble mediators of triggered excacerbation of AAI in wt and IL-17 deficient as well as in animals treated with TNF-α and IL-6 neutralizing antibodies. We compared the type of inflammatory response in infected, house dust mite (HDM)-allergic and animals infected with at different time points of HDM sensitization. We found that airway infection of mice with triggers a strong inflammatory response with massive neutrophilic infiltrates, high amounts of IL-6 and TNF-α and moderate levels of CD4 T-cell-derived IFN-γ and IL-17. If bacterial infection occurred during HDM allergen sensitization, the allergic airway response was exacerbated, particularly by the expansion of Th17 cells and increased TNF-α levels. Neutralization of IL-17 or TNF-α but not IL-6 resulted in accelerated clearance of and effectively prevented infection-induced exacerbation of AAI. Taken together, our data demonstrate an essential role for TNF-α and IL-17 in infection-triggered exacerbation of AAI.

Chronic obstructive pulmonary disease (COPD) comprises a significant number of emergency department (ED) presentations, and hematological phenotypes may have prognostic significance. The aim of this study was to investigate the effect of hematological phenotypes on serious outcomes in COPD exacerbations. A prospective cohort study was carried out in patients with COPD exacerbation presenting to the ED. The patients were classified into three groups, including neutrophilic, eosinophilic, and mixed-type (including neutrophilic and eosinophilic features) COPD exacerbation. Outcome measures were defined as mortality, hospitalization, and need for intensive care unit (ICU) care within three months, and these outcomes were compared among groups. A total of 173 COPD patients were assessed for eligibility, and 147 of them were included in the final analysis. The study population consisted of 90 patients with neutrophilic exacerbation (61.2%), 26 patients with eosinophilic exacerbation (17.7%), and 31 patients with mixed-type exacerbation (21.1%). The neutrophilic exacerbation group was older, was more often tachycardic and desaturated, and had more sputum production compared with the eosinophilic exacerbation group. Mortality was seen in 35 patients in the neutrophilic exacerbation group (38.9%), whereas 5 patients in the eosinophilic group (19.2%) and 6 patients in the mixed-type group (19.4%) died (p = .044). No difference was observed among groups in terms of hospital and ICU admission. COPD exacerbations with neutrophilic phenotypes presented to the ED with more serious clinical findings compared with eosinophilic exacerbations. This may also have a possible effect on mortality.

Abstract Acute asthma remains an important medical emergency, the most frequent cause of acute admissions in children and a major source of morbidity for adults with asthma. In all ages with asthma, the presence of exacerbations is an important defining characteristic of asthma severity. In this review, we assess the epidemiology of acute asthma, the triggers of acute exacerbations, and the mechanisms that underlie these exacerbations. We also assess current treatments that prevent exacerbations, with an emphasis on the role of type 2 airway inflammation in the context of acute exacerbations and the novel treatments that effectively target this. Finally we review current management strategies of the exacerbations themselves.

Abstract Acute exacerbation of idiopathic pulmonary fibrosis has been defined as an acute, clinically significant, respiratory deterioration of unidentifiable cause. The objective of this international working group report on acute exacerbation of idiopathic pulmonary fibrosis was to provide a comprehensive update on the topic. A literature review was conducted to identify all relevant English text publications and abstracts. Evidence-based updates on the epidemiology, etiology, risk factors, prognosis, and management of acute exacerbations of idiopathic pulmonary fibrosis are provided. Finally, to better reflect the current state of knowledge and improve the feasibility of future research into its etiology and treatment, the working group proposes a new conceptual framework for acute respiratory deterioration in idiopathic pulmonary fibrosis and a revised definition and diagnostic criteria for acute exacerbation of idiopathic pulmonary fibrosis.

BackgroundThere is emerging evidence suggesting a link between ambient heat exposure and chronic obstructive pulmonary disease (COPD) hospitalisations. Individual and contextual characteristics can affect population vulnerabilities to COPD hospitalisation due to heat exposure. This study quantifies the effect of ambient heat on COPD hospitalisations and examines population vulnerabilities by age, sex and contextual characteristics.MethodsIndividual data on COPD hospitalisation at high geographical resolution (postcodes) during 2007–2018 in England was retrieved from the small area health statistics unit. Maximum temperature at 1 km ×1 km resolution was available from the UK Met Office. We employed a case-crossover study design and fitted Bayesian conditional Poisson regression models. We adjusted for relative humidity and national holidays, and examined effect modification by age, sex, green space, average temperature, deprivation and urbanicity.ResultsAfter accounting for confounding, we found 1.47% (95% Credible Interval (CrI) 1.19% to 1.73%) increase in the hospitalisation risk for every 1°C increase in temperatures above 23.2°C (lags 0–2 days). We reported weak evidence of an effect modification by sex and age. We found a strong spatial determinant of the COPD hospitalisation risk due to heat exposure, which was alleviated when we accounted for contextual characteristics. 1851 (95% CrI 1 576 to 2 079) COPD hospitalisations were associated with temperatures above 23.2°C annually.ConclusionOur study suggests that resources should be allocated to support the public health systems, for instance, through developing or expanding heat-health alerts, to challenge the increasing future heat-related COPD hospitalisation burden.

This paper aims to systematically review the literature to identify clinically important factors that predict mortality after hospitalization for acute exacerbation of chronic obstructive pulmonary disease (COPD). Eligible studies considered adults admitted to hospital with COPD exacerbation. Two authors independently abstracted data. Odds ratios were then calculated by comparing the prevalence of each predictor in survivors versus nonsurvivors. There were 37 studies included with risk of death ranging from 3.6% for studies considering short-term mortality, 31% for long-term mortality, and 29% for studies that considered solely intensive care unit (ICU)-admitted study subjects. Twelve prognostic factors (age, male sex, low bodymass index, cardiac failure, chronic renal failure, confusion, long-term oxygen therapy, lower limb edema, Global Initiative for Chronic Lung Disease criteria stage 4, cor pulmonale, acidemia, and elevated plasma troponin level) were significantly associated with increased short-term mortality. Different factors correlate with mortality from COPD exacerbation in the short term, long term, and after ICU admission.

There is continuing debate about whether to define airflow obstruction by a post-bronchodilator ratio of forced expiratory volume in 1 second (FEV ) and forced vital capacity (FVC) below 0.70, or by ratio values falling below the age-dependent lower limit of normal (LLN) derived from general population data. To determine whether using the LLN criterion affects the classification and outcomes of patients previously defined as having chronic obstructive pulmonary disease by the fixed FEV /FVC ratio. We applied the LLN definition to pooled data from the Tiotropium Safety and Performance in Respimat study that used the fixed FEV /FVC ratio for the clinical diagnosis of chronic obstructive pulmonary disease. A total of 17,072 patients were analyzed; of these, 1,807 (10.6%) patients had a ratio greater than or equal to LLN. Patients with a ratio greater than or equal to LLN had similar risks of death from any cause and fatal major adverse cardiovascular (CV) event as those below LLN. Patients with a ratio below LLN had a significantly lower risk of major adverse CV events (hazard ratio = 0.69; 95% confidence interval [CI] = 0.55-0.86; P = 0.001), and had significantly greater risks of moderate to severe exacerbation (rate ratio = 1.48; 95% CI = 1.36-1.61; P < 0.0001) and severe exacerbation (rate ratio = 2.01; 95% CI = 1.68-2.40; P < 0.0001) when compared with patients greater than or equal to LLN. Study outcomes by treatment arm (5 μg tiotropium Respimat vs. 18 μg HandiHaler) were comparable. Using the LLN to define airflow obstruction would have excluded patients in the Tiotropium Safety and Performance in Respimat study with a higher risk of nonfatal major adverse CV events and a lower risk of exacerbation; study outcomes by treatment arm (2.5 μg/5 μg tiotropium Respimat vs. 18 μg HandiHaler) remained similar. Clinical trial registered with www.clinicaltrials.gov (NCT01126437).