Dupilumab is an IL-4Rα antibody approved for treatment of severe asthma. Real-world data on the continuation and cessation patterns of dupilumab and long-term treatment efficacy are scarce. We sought to analyze real-world, long-term treatment outcomes and to evaluate trajectories of patients continuing or discontinuing dupilumab therapy over a 3-year period. This multicenter, retrospective, real-world cohort study included patients with severe asthma who started dupilumab before March 2021. Data on asthma control, medication, lung function, and annualized exacerbation rates were collected at baseline and 3, 12, and 36 months after initiation of dupilumab therapy. Asthma remission was assessed at 12 months and 36 months after dupilumab initiation. Of 160 included patients, 95 patients (59%) continued dupilumab therapy for 36 months; 65 patients (41%) discontinued therapy after a median time of therapy of 8 months. Patients who continued dupilumab for 36 months had significant reductions in annual exacerbations (-1; P < .0001) and oral corticosteroid dose (-5.5 mg/day; P < .001) as well as significant improvements in asthma control (asthma control test +5; P < .0001) and lung function (percent predicted of FEV₁ +7%; P < .001) compared with baseline. Of patients who continued dupilumab, 30% achieved remission at 12 months, and 26% achieved remission at 36 months. Of the 65 patients who discontinued therapy, 55 switched to another antibody, and 10 did not receive further antibody treatment. Dupilumab represents an effective long-term treatment option for patients with severe asthma, with sustained treatment effects up to 36 months. Importantly, a relevant proportion of patients achieved remission in this pretreated population.

Objectives: To investigate the role of blood eosinophils in predicting PH in end-stage lung disease. Methods: We conducted a retrospective study of adults with CF, COPD, and ILD who underwent RHC during lung transplant evaluations (2010–2022). Patients were classified by the 2022 ECS/ERS PH guidelines with pulmonary function and laboratory tests, including hemograms. The eosinophil threshold was set at 0.30 G/L. Results: We analyzed 663 patients (n = 89 CF, n = 294 COPD, and n = 280 ILD). Severe PH was more common in ILD (16%) than in CF (4%) and COPD (7%) (p = 0.0002), with higher eosinophil levels in ILD (p = 0.0002). No significant correlation was found between eosinophil levels and hemodynamic parameters (PAPm, PVR, and CI) across CF, COPD, and ILD (PAPm: p = 0.3974, p = 0.4400 and p = 0.2757, respectively; PVR: p = 0.6966, p = 0.1489 and p = 0.1630, respectively; CI: p = 0.9474, p = 0.5705 and p = 0.5945, respectively), nor was a correlation observed in patients not receiving OCS. Linear regression analysis confirmed the lack of association (PAPm: p = 0.3355, p = 0.8552 and p = 0.4146, respectively; PVR: p = 0.6924, p = 0.8935 and p = 0.5459, respectively; CI: p = 0.4260, p = 0.9289 and p = 0.5364, respectively), controlling for 6-MWD, Nt-proBNP, and ICS/OCS dosages. ROC analysis indicated eosinophils were ineffective in distinguishing PH severity levels across these diseases (AUC 0.54, 0.51, and 0.53, respectively). The analysis of eosinophil levels measured 18 ± 6 months prior to baseline found no predictive correlation with the presence of PH either. Eosinophil levels did not differ significantly among PH groups, but eosinophilic COPD was linked to more unclassified PH, higher CO, and greater lung volumes than non-eosinophilic COPD. Conclusions: In our cohort of end-stage CF, COPD, and ILD patients, blood eosinophilia did not predict the presence of PH but was associated with hemodynamic parameters and lung volumes in COPD.