Ataxia-telangiectasia is a rare, autosomal recessive primary immunodeficiency caused by mutations in the ATM gene on chromosome 11, which encodes a serine-threonine kinase essential for the recognition and repair of DNA double-strand breaks. The disease is characterized by progressive neurological impairment, immunological dysfunction, and an increased susceptibility to recurrent infections and malignancies. Pulmonary involvement represents a major source of morbidity and frequently arises from chronic infections, aspiration, and impaired airway clearance, ultimately leading to the development of bronchiectasis. The case of a 15-year-old adolescent with a history of recurrent aspiration pneumonias, neuropsychomotor developmental delay, and severe malnutrition is reported, who was admitted for evaluation of chronic productive cough, fever, and dysphagia. Comprehensive clinical assessment and ancillary investigations revealed recurrent respiratory infections, gastroesophageal reflux, and typical features of ataxia-telangiectasia, including cerebellar ataxia, oculomotor apraxia, and conjunctival telangiectasias. Additionally, bronchiectasis was identified as a secondary consequence of the underlying neurological and immunological impairment. This case highlights the diagnostic challenges posed by ataxia-telangiectasia in pediatric patients presenting with chronic respiratory symptoms and emphasizes the importance of early recognition of the underlying systemic disorder. A multidisciplinary approach is essential for accurate diagnosis and optimized management, aiming to address both the primary disease and its pulmonary complications.

Non-cystic fibrosis bronchiectasis (NCFB) is a heterogeneous chronic airway disease characterized by irreversible bronchial dilatation, impaired mucociliary clearance, and recurrent infection. Historically, research and clinical practice have focused mainly on bacteria, particularly Pseudomonas aeruginosa, as major drivers of exacerbations and disease progression, whereas the contribution of fungi has received far less attention. Over the last decade, evidence from mycobiome studies, large registries, and prospective cohorts has increasingly identified Aspergillus spp. as clinically relevant contributors in a substantial subset of patients with bronchiectasis. Data from the European Bronchiectasis Registry (EMBARC) indicate that approximately one quarter of patients exhibit Aspergillus-related immunological signals, including allergic bronchopulmonary aspergillosis (ABPA), Aspergillus sensitization, and elevated Aspergillus-specific IgG, and that these phenotypes are associated with more severe disease and worse clinical outcomes. Mechanistic studies further suggest that Aspergillus-related disease in bronchiectasis is underpinned by distinct molecular and immunological programs involving epithelial dysfunction, impaired mucociliary clearance, innate fungal sensing, inflammasome-related signaling, and divergent type-2 versus non-type-2 inflammatory responses. In parallel, mycobiome and multi-biome studies indicate that Aspergillus should be interpreted within a broader airway interactome shaped by cross-kingdom relationships with bacterial pathogens and by host immune tone. In this review, we synthesize current evidence on the epidemiology, molecular pathobiology, inflammatory endotypes, biomarker profiles, clinical-radiologic spectrum, and therapeutic implications of Aspergillus in bronchiectasis. Current evidence suggests that Aspergillus-related findings in bronchiectasis should be interpreted within a structured clinical, radiological, microbiological, and immunological framework rather than considered solely as isolated culture results. However, most data remain observational or extrapolated from related airway diseases, and bronchiectasis-specific interventional evidence is limited. A cautious biomarker-informed approach may help standardize phenotyping, identify patients requiring closer follow-up, and define priorities for future prospective trials.

Background: Overuse of short-acting reliever inhalers, particularly short-acting β2-agonists (SABAs), is linked to poor asthma control, higher exacerbation risk, and increased mortality. Data on reliever overuse in severe asthma and the role of short-acting muscarinic antagonists (SAMAs) remain limited. Objective: This study aims to assess the prevalence of rescue inhaler overuse in adults with severe asthma and examine its associations with maintenance therapy adherence, biologic treatment, oral corticosteroid use, asthma control, lung function, allergic sensitization, and comorbidities. Methods: We conducted a retrospective observational study of 223 adults with severe asthma followed at a tertiary multidisciplinary clinic in 2024. Clinical, functional, pharmacological, and pharmacy-dispensing records were reviewed. Rescue inhaler overuse was defined as dispensing ≥ 3 SABA and/or SAMA canisters per 12 months. Associations with clinical and treatment variables were analyzed. Results: Among 223 patients, 144 (64.6%) had a prescribed rescue inhaler; 85 (38.1%) met the criteria for overuse. Of those prescribed rescue therapy, 59.0% overused, with 47.2% classified as low overuse and 11.1% as high overuse. Overuse was more frequent in patients with maintenance adherence > 50%. Biologic therapy was associated with reduced odds of overuse, while oral corticosteroid use showed no significant effect. Poor asthma control (ACT < 20) was strongly associated with overuse. Lung function did not differ significantly, though overusers tended to have lower FEV1. Allergic sensitization was not associated with overuse; bronchiectasis was the comorbidity most frequently linked. Conclusions: Rescue inhaler overuse is common in severe asthma and closely linked to inadequate disease control. Lower overuse rates among biologic-treated patients suggest improved control reduces reliance on short-acting relievers. Systematic monitoring of reliever use may help identify high-risk patients and guide individualized management strategies.

Background: The clinical burden of pulmonary diseases associated with the genus Aspergillus is increasing, although diagnostic focus remains largely on A. fumigatus. This study evaluated the diagnostic value of testing for A. flavus and A. niger-specific IgG in patients with chronic respiratory conditions. Methods: A retrospective study was conducted on 274 subjects (156 with chronic respiratory diseases, Bronchiectasis, Hypersensitivity Pneumonitis [HP], and Interstitial Lung Disease [ILD] non-HP, and 67 healthy controls). Cut-off values were established at the 97.5th percentile of the control group: 30 mg/L for A. fumigatus, 13 mg/L for A. flavus, and 8 mg/L for A. niger. Results: Among 109 patients who tested negative for A. fumigatus, 49.5% showed positivity to at least one other species, preventing a significant diagnostic gap in exposure detection. Notably, 40.4% of these patients exhibited simultaneous positivity for both A. flavus and A. niger. In the HP subgroup, 100% of patients who were A. fumigatus-positive also showed concurrent positivity to the two other species. Furthermore, the Bronchiectasis group showed the highest rate of isolated A. flavus at 11.8%. Conclusions: Testing solely for A. fumigatus IgG leads to substantial underestimation of Aspergillus exposure. Integrating A. flavus and A. niger into diagnostic panels is essential for a comprehensive immunological assessment of fungal interaction, particularly in HP and ILD, where identifying specific antigenic exposure is crucial for managing chronic inflammation and preventing disease progression.

Bronchiectasis is a chronic respiratory disease characterised by irreversible bronchial dilatation, persistent airway inflammation and recurrent infections. Symptoms, particularly cough, sputum production and dyspnoea, are the most immediate and patient-relevant expression of the disease, linking clinical presentation, airway biology and outcomes. While asthma and COPD management algorithms already integrate symptom burden into therapeutic decision-making, bronchiectasis care has historically relied on exacerbation history to guide preventive interventions. Over the past decade, an expanding body of evidence has demonstrated that daily symptoms mirror current infection and inflammation, profoundly impact quality of life, and predict future exacerbations. Comparative analyses across chronic lung diseases further highlight the central role of symptom monitoring in defining disease activity and risk. The updated European Respiratory Society guidelines translate this evidence into clinical practice, marking a paradigm shift from an exacerbation-driven to a symptom-centred and treatable-traits model. This review synthesises clinical, biological and therapeutic insights linking symptoms to bronchiectasis pathophysiology, disease activity and treatment response. We discuss how airway clearance, mucoactive therapy, antibiotics, pulmonary rehabilitation and targeted anti-inflammatory strategies, including dipeptidyl peptidase-1 inhibition, can address specific symptom profiles. We also mention the role of comorbidities and psychosocial management, establishing symptoms as the cornerstone of a holistic, multidimensional care approach. Recognising symptoms as both biomarkers of activity and therapeutic targets represents a major step toward precision medicine in bronchiectasis, aligning clinical management with patient experience and the biological drivers of disease.

Chronic obstructive pulmonary disease (COPD) represents a significant global health challenge, affecting millions worldwide, with an estimated prevalence of 5.9% specifically for Singapore, and a projected increase driven by population aging. Despite comprehensive healthcare infrastructure, COPD remains underdiagnosed and undertreated in Singapore. Real-world evidence indicates that most patients present with moderate-to-severe disease and exhibit high rates of comorbidities, including cardiovascular disorders, diabetes, and bronchiectasis, which complicate COPD management and increase healthcare utilization. Smoking remains the predominant risk factor, although non-smoking phenotypes linked to prior tuberculosis, biomass exposure, and environmental allergens are increasingly recognized. COPD imposes a significant economic burden, primarily driven by hospitalizations, and disproportionately affects certain ethnic groups, underscoring the need for culturally tailored interventions. Current treatment strategies for moderate-to-severe COPD emphasize smoking cessation, pulmonary rehabilitation, and inhaled bronchodilator therapy; however, substantial gaps persist, with frequent exacerbations despite triple therapy (long-acting β2-agonists and long-acting muscarinic antagonists along with inhaled corticosteroids) and inappropriate oral corticosteroid use contributing to adverse outcomes. Recent advances in biologic therapies targeting type 2 inflammation, notably dupilumab, approved in Singapore in 2025 offer promising options for patients with uncontrolled COPD characterized by elevated blood eosinophils. Emerging biomarkers, such as fractional exhaled nitric oxide, may further refine patient selection for precision therapy. This review focuses on the current evidence on COPD epidemiology, clinical characteristics, risk factors, treatment patterns, and evolving therapeutic approaches in Singapore, highlighting opportunities to optimize patient care through early diagnosis and adoption of novel biologics to improve outcomes in this heterogeneous population.

Non-cystic fibrosis and non-tuberculous bronchiectasis are being increasingly recognized as a result of improved imaging techniques, particularly high-resolution computed tomography, which remains the diagnostic gold standard, and greater clinical awareness. The disease encompasses a broad spectrum of etiologies, leading to marked heterogeneity in clinical presentation, severity, and progression. Understanding the underlying cause is essential, as it directly influences prognosis and therapeutic decision-making. Medical management represents the cornerstone of treatment and should be individualized according to disease etiology and severity. Core strategies include airway clearance techniques, long-term antibiotic therapy, and optimized management of associated comorbidities.

Adjuvant surgical resection in the setting of pulmonary nontuberculous mycobacterial infection removes focal parenchymal disease thought to serve as a poorly perfused reservoir for organisms, thus relatively resistant to standard antimicrobial therapy. Removal of these areas of damaged lung is felt to enhance the effectiveness of the medical treatment. In general, these operations are associated with low morbidity and mortality, although resections that are more extensive carry higher risk. Many of the planned operations may be performed with minimally invasive techniques. More data are needed regarding long-term outcomes in these patients.

Post-tuberculosis lung disease (PTLD) is a frequent and underrecognized cause of chronic respiratory morbidity, characterized by heterogeneous structural and functional sequelae following microbiological cure of tuberculosis. Although most patients are managed with medical therapy, rehabilitation, and bronchoscopic interventions, a selected subset develops irreversible disease requiring surgical treatment. This article focuses on PTLD, emphasizing the role of surgical management within multidisciplinary care, and discusses the underlying pathophysiology, clinical phenotypes, diagnostic approach, and surgical indications, including bronchiectasis, hemoptysis, destroyed lung, aspergillosis, and airway stenosis.

This study aims to examine the differences in microbial community abundance and species distribution in the bronchoalveolar lavage fluid (BALF) obtained from non-cystic fibrosis bronchiectasis (NCFB) patients between those with and without Pseudomonas aeruginosa (P. aeruginosa) colonization, and to assess the impact of P. aeruginosa colonization on airway microecological imbalance in NCFB. Sixty-four patients were enrolled, grouped into P. aeruginosa-colonized (PA, 29) and non-colonized (NPA, 35) groups. Among patients with NCFB, those with P. aeruginosa colonization had greater disease severity than those without colonization, with significantly higher bronchiectasis severity index (BSI) scores (P < 0.05). The proportions of patients with higher Bhalla and E-FACED scores were also greater in the PA group than in the NPA group (62.1% vs 42.8% and 34.1% vs 20%, respectively). Annual hospitalization frequency was numerically higher in PA (2.14 ± 2.43 vs 1.47 ± 0.86; P = 0.543). The PA group exhibited poorer pulmonary function, with significantly lower FEV1 and FEV1% predicted (both P < 0.01). In addition, NCFB patients in the PA group showed higher proportions of elevated white blood cell counts (31% vs 17.1%) and neutrophil percentages (41.4% vs 31.4%). Microbiota analysis of BALF demonstrated reduced alpha diversity in NCFB patients with P. aeruginosa colonization, with a predominance of Pseudomonas, whereas non-colonized NCFB patients had relatively higher abundances of Streptococcus, Acinetobacter, Rothia, Veillonella, and Prevotella. Overall, P. aeruginosa colonization in NCFB is associated with increased disease severity, heightened inflammation, and impaired lung function, accompanied by decreased microbial diversity, Pseudomonas dominance, and suppression of commensal taxa.