Background: Monoclonal antibody therapy is currently an additional treatment option to reduce exacerbations and improve symptom control in patients with severe eosinophilic asthma (SEA) that is uncontrolled despite treatment with high-dose inhaled corticosteroids and long-acting beta-2 agonists. Benralizumab, a monoclonal antibody that binds to the interleukin-5 receptor (IL-5), significantly reduces symptoms and annual exacerbations, as well as the use of systemic corticosteroids in patients with SEA. However, few studies are available on the effectiveness of this biological treatment in real life. The aim of this case series was to evaluate the efficacy of benralizumab by analyzing changes in clinical parameters and blood eosinophils in patients with SEA. Methods: We analyzed four patients with SEA who started treatment with benralizumab. The history of symptoms and exacerbations, eosinophil counts, data regarding the oral corticosteroid dose, need for rescue treatment, spirometry measurements and asthma control questionnaires (ACT) regarding the level of asthma control were recorded. A positive response to treatment was defined by a significant reduction in eosinophil counts, increased ACT scores, and lower rates of exacerbations. Results and conclusions: Benralizumab monoclonal antibody was effective in all four patients. This was shown by a reduction in exacerbation rates, symptom severity, and lower dose of oral corticosteroids and rescue medication. This novel treatment was well tolerated by the analyzed patients, thus indicating that benralizumab is an attractive choice for patients due to eosinophilic count reduction as well as the less frequent dosing schedule. However, further studies are required, on larger populations.

Dysregulated cytokine responses are a hallmark of severe COVID-19; however, the persistence of these responses following hospital discharge remains inadequately understood. This study aimed to characterize the inflammatory profile of hospitalized COVID-19 patients in Mureș County, Romania, at the point of admission and one month post-discharge. We conducted a prospective observational study involving 68 patients with RT-PCR-confirmed SARS-CoV-2 infection, classified according to disease severity. Blood samples were collected at baseline and after one month. Macrophage migration inhibitory factor (MIF) levels were quantified using ELISA, while other cytokines, including MCP-1, IP-10, IFN-γ, IL-4, IL-10, IL-13, IL-17, and TNF-α, were measured via Luminex multiplex assays. Patients with severe disease exhibited significantly elevated levels of MIF, IFN-γ, IL-17, and TNF-α at admission (p < 0.0001). Although cytokine concentrations generally declined over time, patients with severe disease continued to display persistently elevated MIF (mean 31,035 pg/mL), IFN-γ, and TNF-α, indicative of ongoing inflammatory processes. Clinical parameters such as respiratory rate and oxygen saturation correlated with disease severity. These findings suggest that severe COVID-19 induces a prolonged inflammatory response, with MIF and IFN-γ remaining elevated beyond the acute phase. Cytokine profiling holds potential for improving prognostic assessments and identifying patients at risk of long-term immune dysregulation, with MIF emerging as a potential candidate marker for immune recovery and a possible target for therapy.

Introduction: Severe eosinophilic asthma (SEA) is marked by persistent airway inflammation and recurrent exacerbations, unmitigated by standard high-dose inhaled therapies. Benralizumab, a humanized monoclonal antibody, targets the interleukin 5 receptor alpha chain on eosinophils, providing a unique treatment option. Materials and Methods: In this study, 24 SEA patients (11 women and 13 men, average age 60) received benralizumab 30 mg. The regimen consisted of 30 mg injections every 4 weeks for the initial three doses, then every 8 weeks thereafter, aiming to assess the therapy's long-term impact on eosinophil counts, lung function, and quality of life over three years. Results: Treatment significantly reduced blood eosinophil levels (p=0.001) and improved lung function, as shown by increases in the Tiffeneau-Pinelli index (p=0.002) and forced vital capacity (p < 0.001). Quality of life significantly improved from the first dose (p < 0.001). However, after over three years, 5 patients developed side effects, notably chronic sinusitis, leading to discontinuation in 2 cases due to non-response to sinusitis treatment. Conclusion: Benralizumab effectively reduces eosinophil counts, enhances lung function, and improves quality of life in SEA patients over the long term. Yet, a small fraction experienced adverse effects such as chronic sinusitis, highlighting the need for vigilant monitoring and management in prolonged treatments. This study confirms benralizumab's sustained efficacy and underscores the importance of tailored patient care strategies.

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Introduction: Severe eosinophilic asthma (SEA) is an asthma subtype defined by chronic airway inflammation with episodes of acute exacerbations despite high doses of inhaled beta-agonists and glucocorticoids (ICS). Benralizumab is a humanized recombinant monoclonal antibody that specifically binds to the alpha chain of the interleukin 5 receptor (IL-5R) expressed on eosinophils and basophils. Material and Methods: We followed 21 patients with SEA and monoclonal antibody therapy during the pandemic, 10 women and 11 men, with a mean age of 62 years. All patients started therapy with benralizumab 30 mg (30 mg injection every 4 weeks for the first 3 doses, then every 8 weeks) before the covid pandemic. We aimed to monitor the patients9 blood eosinophil count, changes in their lung capacity, and quality of life during the pandemic. Results: All patients experienced a significant decrease in blood eosinophils after the first treatment with benralizumab 30 mg (p=0.001), which persisted during the pandemic. We observed a significant increase in the Tiffeneau-Pinelli index (TI) (p=0.002) and forced vital capacity (FVC) (p < 0.001) from the start of therapy. Quality of life, as measured by the asthma control score ACT, had significantly increased since the first dose of benralizumab (p < 0.001), with no changes during the pandemic. None of the patients discontinued their therapy during the pandemic. Conclusion: The pandemic had no impact on the benefit of monoclonal antibody therapy in patients with SEA. We were unable to diagnose new SEA patients during the pandemic, and we were not able to enroll new patients in our study due to the pandemic.

Background and Objectives: Persistent cough, dyspnea, chest tightness, and exercise limitation after SARS-CoV-2 infection are common in people with asthma but are not specific to uncontrolled asthma. This critical narrative review evaluates inhaled corticosteroid (ICS) delivery optimization after COVID-19 while distinguishing direct post-COVID evidence from established asthma evidence. Materials and Methods: PubMed/MEDLINE was searched from January 2020 through 6 July 2026 for literature on asthma after COVID-19, ICS, inhaler technique, adherence, device selection, small-airway disease, chronic cough, rehabilitation, and severe-asthma care; relevant GINA (Global Initiative for Asthma), WHO (World Health Organization), NICE (National Institute for Health and Care Excellence), ERS (European Respiratory Society), and ATS (American Thoracic Society) guidance was also reviewed. The narrative synthesis drew on 89 cited sources, grouped by relevance, study design, and evidentiary directness. Results: Direct post-acute evidence is limited and predominantly observational. Post-acute asthma-control outcomes vary across cohorts; observational evidence suggests increased exacerbation risk, particularly after severe or hospitalized COVID-19. In the most directly relevant observational study, Tichopad et al. evaluated 654 patients with asthma and COVID-19 and found that a higher combined adherence/inhaler-technique score was associated with better recovery of lung-function measures and quality of life, without establishing causality. Evidence for adherence assessment, inhaler-technique correction, device-patient matching, and appropriate ICS-containing therapy is stronger in established asthma care. Extra-fine formulations may improve peripheral deposition in selected asthma phenotypes, whereas post-COVID air trapping alone does not establish corticosteroid responsiveness. Conclusions: COVID-19 history should trigger better asthma assessment, not automatic treatment intensification. Persistent symptoms should prompt confirmation of asthma relevance, assessment of objective and inflammatory features when appropriate, verification of adherence, inhaler technique, and device suitability, and consideration of non-asthma mechanisms before pharmacological escalation.