Uncontrolled, severe asthma remains a significant clinical challenge, affecting a small proportion of asthma patients worldwide. Despite advancements in treatment options, a subset of patients continues to experience frequent exacerbations, uncontrolled symptoms, and impaired quality of life. The advent of biological therapies has revolutionized the management of severe asthma, offering targeted treatments that address specific inflammatory pathways. This review provides a comprehensive overview of the efficacy and response criteria of biological treatments in severe asthma, focusing on clinical, functional, and inflammatory markers used to help in the evaluation of the biologic treatment. Key response criteria include symptom control, reduction in exacerbations, improvement in lung function, and a reduction in or the discontinuation of oral corticosteroids. Biomarkers such as blood eosinophils and exhaled nitric oxide (FeNO) are essential tools in guiding treatment adjustments. Real-world studies underscore the importance of personalized treatment strategies, as variability in response to biological therapies can be significant. The emergence of tools such as the FEOS score and EXACTO questionnaire offer quantitative measures for assessing biological response and guiding clinical decisions. Additionally, predictive factors for better or poorer responses, such as pre-treatment lung function and comorbidities, like obesity and rhinosinusitis, are critical in patient selection. This review highlights the need for ongoing reassessments and potential modifications of therapy in cases of suboptimal response. Practical considerations for switching biological therapies are discussed, emphasizing the importance of tailoring treatments to individual patient profiles and disease phenotypes. With the continued development of personalized medicine, the outlook for patients with severe asthma is improving, selecting specific biomarkers to improve the selection of the biologic treatment.

Background/Objectives: Patients with severe asthma (SA) commonly present with coexisting nasal polyposis (NP), often requiring treatment with intranasal corticosteroids (INC). However, adherence to INC in this population remains inadequately characterized despite its clinical significance. This study aimed to evaluate adherence to INC in patients with SA and NP and to identify clinical and pharmacological factors associated with adherence levels. Methods: We conducted a retrospective observational study including adult patients with SA and NP treated with INC and followed at a tertiary asthma unit in Madrid during 2024. Adherence was assessed via medication possession ratio (MPR) over six months, with poor adherence defined as MPR < 50%. Pharmacological, clinical and demographic variables were analyzed for associations with adherence. Results: Of the 188 patients evaluated, 86 (45.7%) were prescribed INC. Poor adherence was observed in 53.5% of these patients. Women exhibited significantly lower adherence compared to men (p < 0.05). Fluticasone was the most commonly prescribed INC (54.6%), with no significant adherence differences across corticosteroid types. Patients on maintenance systemic corticosteroids had higher adherence (85.7%, p < 0.05), whereas those receiving biologic therapies tended toward lower adherence (51% poor adherence), though this was not statistically significant. Higher adherence was associated with increased disease severity, as indicated by multiple endoscopic sinus surgeries (p < 0.05). No significant differences were observed in spirometry or Asthma Control Test scores. Conclusions: Adherence to INC in patients with SA and NP is suboptimal, particularly among women and patients on biologics. Greater disease severity correlates with improved adherence. Targeted interventions are necessary to enhance adherence and optimize disease management in this population.

Background: The prevalence of cardiovascular events (CVEs) in patients with asthma varies amongst studies, with little evidence as to their prevalence in patients treated with monoclonal antibodies (mAbs). In this retrospective, observational study, we aimed to evaluate the prevalence of CVEs in patients with T2 and non-T2 asthma and to identify risk factors associated with CVEs. Methods: A total of 206 patients with severe asthma were included. Demographic variables, respiratory comorbidities and cardiovascular risk factors were collected, along with respiratory function, laboratory parameters and respiratory pharmacotherapy, including treatment with mAbs. Results: A total of 10.7% of the patients had any CVE from the date of asthma diagnosis, with a higher risk in those patients with chronic obstructive pulmonary disease (odds ratio [OR] = 5.36, 95% CI 1.76–16.31; p = 0.003), arterial hypertension (OR = 2.71, 95% CI 1.13–6.55; p = 0.026) and dyslipidaemia (OR = 9.34, 95% CI 3.57–24.44; p < 0.001). No association between mAb treatment and a CVE or between time of mAb treatment and the event was found. No significant differences were observed between the T2 and non-T2 cohort. After a multivariate analysis, dyslipidaemia was identified as an independent risk factor (OR = 13.33, 95% CI 4.49–39.58; p < 0.001), whereas regular use of inhaled corticosteroids was associated with a reduced risk of a CVE (OR = 0.103, 95% CI 0.021–0.499; p = 0.005). Further research is needed to fully understand the relationship between severe asthma and CVEs. Conclusions: This study suggests that patients with severe asthma experience a higher percentage of CVEs compared with the general population.