Exacerbations of chronic obstructive pulmonary disease (COPD) carry significant consequences for patients and are responsible for considerable health-care costs—particularly if hospitalization is required. Despite the importance of hospitalized exacerbations, relatively little is known about their determinants. This study aimed to analyze predictors of hospitalized exacerbations and mortality in COPD patients. This was a retrospective population-based cohort study. We selected 900 patients with confirmed COPD aged ≥35 years by simple random sampling among all COPD patients in Cantabria (northern Spain) on December 31, 2011. We defined moderate exacerbations as events that led a care provider to prescribe antibiotics or corticosteroids and severe exacerbations as exacerbations requiring hospital admission. We observed exacerbation frequency over the previous year (2011) and following year (2012). We categorized patients according to COPD severity based on forced expiratory volume in 1 second (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 1–4). We estimated the odds ratios (ORs) by logistic regression, adjusting for age, sex, smoking status, COPD severity, and frequent exacerbator phenotype the previous year. Of the patients, 16.4% had ≥1 severe exacerbations, varying from 9.3% in mild GOLD grade 1 to 44% in very severe COPD patients. A history of at least two prior severe exacerbations was positively associated with new severe exacerbations (adjusted OR, 6.73; 95% confidence interval [CI], 3.53–12.83) and mortality (adjusted OR, 7.63; 95%CI, 3.41–17.05). Older age and several comorbidities, such as heart failure and diabetes, were similarly associated. Hospitalized exacerbations occurred with all grades of airflow limitation. A history of severe exacerbations was associated with new hospitalized exacerbations and mortality.

Tezepelumab, an anti–TSLP monoclonal antibody, has shown broad efficacy across severe asthma phenotypes. However, real-world evidence evaluating multidomain remission—integrating clinical, functional, and inflammatory domains—remains limited. The primary objective was to assess 12-month effectiveness and multidomain remission (clinical, biological, and complete remission) stratified by inflammatory phenotype, in a prospective multicentre real-world cohort of patients with severe asthma treated with tezepelumab. This prospective observational study included adults with severe asthma initiating tezepelumab across 14 specialised severe asthma units in Spain. Clinical outcomes (exacerbations, ACT, OCS use), lung function, and type 2 (T2) biomarkers (blood eosinophils, FeNO) were evaluated at baseline and 12 months. Clinical remission was defined using strict (no exacerbations, no maintenance OCS, ACT ≥ 20, FEV₁ ≥80%) and pragmatic criteria (no exacerbations, no OCS, ACT ≥ 20, and no FEV₁ decline > 5%). Biological remission required FeNO < 25 ppb and eosinophils < 300/µL. Ninety-three patients were included. The annualised exacerbation rate decreased by 68% (3.59 to 1.14; p < 0.001). ACT improved from 13.7 to 19.9 (p < 0.001) and 77.8% of patients achieved an ACT increase ≥ 3 points. Maintenance OCS use fell from 40% to 21% (p < 0.01). FEV₁ (% predicted) increased from 70.7% to 75.6% (p < 0.001). T2 biomarkers significantly decreased (eosinophils p = 0.004; FeNO p = 0.034). Of the 93 patients included, 86 had complete data for strict clinical remission analysis. Among evaluable patients, 22.1% (19/86) achieved strict clinical remission and 38.4% (33/86) pragmatic remission. Biological remission occurred in 73.1% (38/52), and complete remission in 22.0% (11/50). In this multicentre real-world cohort, tezepelumab produced sustained multidomain improvements with consistent benefit across phenotypes, including marked exacerbation reductions in allergic biologic-naïve patients. Incorporating biological remission into a multidomain framework provides new insight into the depth and heterogeneity of response achievable with upstream TSLP blockade. The online version contains supplementary material available at 10.1186/s12931-026-03597-3.

We aimed to determine whether exposure to particulate matter PM, measured as the oxidative potential (OP) of filters collected from 24 h personal samplers, is associated with increased airway inflammation in asthmatic and non-asthmatic volunteers. Forty-two adult asthmatic patients (25 women and 17 men) and 37 matched controls wore a personal sampler for a day collecting fine (PM2.5) and coarse (PM10-2.5) particles, and determining 24 h afterwards their fractional exhaled nitric oxide (FeNO). The PM-OP was determined by two methods: dithiothreitol (DTT) and ascorbic acid (AA) being OP levels dichotomized based on the median, to calculate adjusted mean differences (aMDs) and odds ratios (aORs) with sex, age, study level, body mass index and interleukin-6 (IL-6) levels as confounders. Statistically significant associations between PM-OP and FeNO levels in non-asthmatic volunteers were observed: aMD for OP-DTT PM2.5 = 11.64 ppbs; 95 %CI (0.13-22.79); aMD for OP-AA PM10-2.5 = 15.67; 95 %CI (2.91-28.43) with aORs = 4.87 and 18.18 respectively. In asthmatic patients an association was also observed in the form of aORs, but of lower magnitude (1.91 and 1.94 respectively). Non-significant higher FeNO levels (aMD = 5.22) and an aOR = 3.92 were also observed in non-asthmatic volunteers for OP-AA in the fine fraction. As a conclusion, the effect of personal PM-OP on airway inflammation appears to be differential between asthmatic and non-asthmatic volunteers suggesting a potential implication of inhaled corticosteroids diminishing the reactivity of airway epithelium since adjusted associations were higher in volunteers without asthma.