Michele Mondoni

Severe asthma represents a major clinical challenge, accounting for disproportionate healthcare costs and morbidity despite affecting only 3–5% of patients with asthma. Traditional computed tomography (CT) can quantify bronchial wall thickening and mucus plugging, but concerns about cumulative radiation exposure limit its use for longitudinal monitoring, particularly in patients requiring frequent assessment. Recent advances in magnetic resonance imaging (MRI), specifically T2-weighted sequences combined with ultrashort echo time (UTE) imaging, have enabled quantitative assessment of bronchial wall signal intensity without ionizing radiation. Pilot studies demonstrate that bronchial wall T2-weighted MRI signal intensity (BrWall_T2-MIS) is significantly elevated in severe versus non-severe asthma, correlates with airflow obstruction and type-2 inflammatory markers, and has shown preliminary ability to predict exacerbation risk. Importantly, this biomarker may capture different pathophysiological information than CT-derived wall thickness measurements, potentially reflecting active inflammation rather than fixed remodelling. Although evidence remains preliminary and limited to single-centre studies with small sample sizes, BrWall_T2-MIS represents a promising investigational tool that could enhance phenotyping and therapeutic monitoring in the era of targeted biological therapies for severe asthma.

Pulmonary fibrosis (PF), particularly idiopathic pulmonary fibrosis (IPF), is a progressive and often fatal interstitial lung disease characterised by complex genetic and molecular heterogeneity. Traditional diagnostic approaches, which rely on clinical, radiological and histopathological assessment, are frequently insufficient to capture the underlying biological diversity of the disease. The advent of next-generation sequencing (NGS) has substantially advanced the understanding of PF by enabling comprehensive genomic and transcriptomic profiling. NGS technologies, including whole-exome sequencing (WES), whole-genome sequencing (WGS), RNA sequencing (RNA-seq), and targeted gene panels, have uncovered key genetic determinants. These include mutations in telomere-related genes (TERT, TERC, RTEL1) and surfactant-related genes (SFTPC, SFTPA2), as well as common variants like the MUC5B promoter polymorphism. These discoveries have clarified disease pathogenesis, revealed polygenic risk models, and may improve diagnostic accuracy, particularly in distinguishing overlapping interstitial lung disease (ILD) phenotypes. Beyond genetics, transcriptomic analyses have identified dysregulated pathways, including TGF-β, Wnt/β-catenin, and PI3K/Akt signalling, and have enabled the discovery of novel biomarkers for prognosis and therapeutic response. In selected clinical settings, NGS is beginning to support patient stratification and inform management decisions. Emerging applications, including liquid biopsy and integration with artificial intelligence, further expand the potential clinical utility of NGS. Despite challenges related to cost, data interpretation and standardisation, NGS represents a powerful research tool in PF.

The pathogenesis of interstitial lung diseases (ILDs) is significantly influenced by genetic factors, yet lack of consensus on the optimal timing for genetic testing and precise patient selection could hinder clinical practice. Position papers currently suggest testing patients presenting with a suspect of Familial Pulmonary Fibrosis (FPF) and with extra-pulmonary syndromic features (i.e., premature graying, cytopenias, liver cirrhosis) for genetic screening. Diagnostics rely on next-generation sequencing (NGS) to identify pathogenic/likely pathogenic variants in telomere-related and surfactant-related genes. A specialized genetic consultation is essential in the correct interpretation of test results, especially when variants of uncertain significance (VUS) are detected. Adoption of other tests, such as polygenic risk scores, could further support precision medicine in ILD care. Future research might address the knowledge gap regarding early test prescription and the role of therapy, including lung transplant stratification and antifibrotic therapy, in FPF.

Background and objective: Hypoxemia and respiratory failure (RF) in chronic obstructive pulmonary disease (COPD) are associated with exacerbations, comorbidities and increased mortality. However, the prevalence of hypoxemia and RF in stable COPD is unknown. We aimed at investigating the prevalence and determining predictive factors for chronic gas exchange abnormalities in COPD patients. Methods: A retrospective cohort study that enrolled clinically stable COPD patients referring to a pulmonary outpatient clinic. Anthropometrics, clinical characteristics, blood gas analysis and lung function were analyzed. Patients were grouped according to hypoxemia (PaO₂ 2 < 60 mmHg) or type II (PaO₂ < 60 and PaCO₂ > 45 mmHg) RF. A sensitivity analysis adopting an age-adjusted definition of hypoxemia was performed. Predictive factors for hypoxemia or RF were assessed with multifactorial analysis. Results: We analyzed data from 515 patients. Fixed-ratio hypoxemia, RF type 1 and type 2 were observed in 352 (68.3%), 27 (5.2%) and 43 (8.3%) patients, respectively. Risk of hypoxemia was associated with preserved alveolar volume, residual volume/total lung capacity, and lung diffusion capacity. Heart failure, ischemic heart disease, atrial fibrillation, and metabolic syndrome were predictive factors for RF. Patients with age-adjusted hypoxemia (n = 321 patients, 62.3%) showed no difference in terms of anthropometrics, lung function, and clinical characteristics as compared with fixed-threshold hypoxemia. Conclusions: Hypoxemia is frequent in stable COPD. Lung function parameters and comorbidities can support the identification of patients at risk of RF. Blood gas analysis should be always performed in patients with COPD to allow for personalized therapy and management.

1. Severe asthma (SA) is a heterogeneous and debilitating condition, often associated with a high burden of exacerbations, dependence on oral corticosteroids (OCS), and poor quality of life [1–3]. ...

Interstitial lung diseases (ILDs) are frequently characterized by the presence of pulmonary fibrosis (PF), which may lead to respiratory failure secondary to irreversible parenchymal distortion. Although idiopathic pulmonary fibrosis (IPF) is the clinical prototype, the emergence of the progressive pulmonary fibrosis (PPF) phenotype has shifted the therapeutic paradigm toward shared pathogenic pathways while preserving the need to recognize the biological and clinical heterogeneity of the underlying ILDs. This state-of-the-art review integrates recent experimental and clinical data to provide a comprehensive overview of the transition from inflammatory models to the current epithelial-centric framework of fibrogenesis. In particular, the shift from ineffective anti-inflammatory strategies to the success of nintedanib and pirfenidone in both IPF and non-IPF progressive diseases is discussed. Furthermore, recent advances from phase II and III clinical trials targeting specific molecular drivers of fibrosis and vascular remodeling are analyzed, with a focus on pathway-oriented therapies, including nerandomilast, admilparant, and inhaled treprostinil. Understanding this molecular crosstalk is essential for the development of new therapeutic strategy based on precision medicine and it may support a new era of combination approaches aimed at stabilizing disease and improving patient outcomes in both idiopathic and progressive pulmonary fibrosis.

Background: Endosonography (i.e., endoscopic ultrasound with bronchoscope fine-needle aspiration, EUS-B-FNA and endobronchial ultrasound-guided transbronchial needle aspiration, EBUS-TBNA) is a widely used technique in the diagnosis and staging of non-small cell lung cancer. Limited data are available in diagnosing small cell lung cancer (SCLC), and no studies have specifically investigated the diagnostic accuracy of EUS-B-FNA in these patients. The study aims at evaluating the sensitivity and safety of endosonography in the diagnosis of SCLC. Methods: A prospective, single-center, observational study was conducted in Italy. All patients diagnosed with SCLC who underwent EUS-B-FNA and/or EBUS-TBNA were enrolled. The sensitivity of EUS-B-FNA and EBUS-TBNA were assessed using pathological confirmation as the gold standard. Results: A total of 72 patients (38 (53%) males) with confirmed SCLC were included in the study. EUS-B-FNA was performed in 31 (43%) patients and EBUS-TBNA in 44 (61.1%) patients; both procedures were performed in three (4.2%). The overall sensitivity of endosonography was 97.2%. The sensitivity of EUS-B-FNA and EBUS-TBNA was 96.8% and 90.9%, respectively. No differences were observed in the sensitivity of both techniques when sampling lymph nodes vs. pulmonary parenchymal lesions (p = 0.99). The overall complication rate was 5.6%. No major complications were reported. Conclusions: Endosonography is a highly accurate and safe technique in diagnosing SCLC. EUS-B-FNA alone demonstrates excellent sensitivity, supporting its extensive role as a valuable diagnostic tool. The combined use of both techniques may further optimize diagnostic yield in the diagnosis of SCLC.

Acute exacerbation of idiopathic pulmonary fibrosis (IPF) is the most severe complication and one of the main causes of death in these patients. No proven

The Italian National Congress of Imaging in Pulmonology, held in Milan on November 21st, provided a unique educational platform exploring the evolving role of thoracic imaging in respiratory medicine. Organized by the Italian Respiratory Society (SIP-IRS) Imaging Study Group, the congress brought together over 160 participants, including pulmonologists, radiologists, interventional specialists, and early-career professionals, reflecting the essential role of multidisciplinary collaboration in modern respiratory care. Topics included functional imaging approaches to small airway disease in COPD and asthma, multimodal imaging in lung transplantation, the role of CT angiography for haemoptysis management, and radiomics applications for quantifying emphysema patterns and fibrotic changes. The role of imaging in guiding inhaled and biological therapies was explored, alongside a lively debate on thoracic ultrasound for interstitial lung disease screening. Advanced sessions covered medical thoracoscopy techniques, quantitative ultrasound and artificial intelligence in pleural diseases, shape-sensing robotic-assisted bronchoscopy for peripheral nodules, expanding cryobiopsy applications, and imaging’s role in monitoring progressive pulmonary fibrosis therapeutics. A distinctive feature was the first “Images in Pulmonology” contest, won by a remarkable case simultaneously depicting lung cancer and new life. This meeting report summarizes key congress highlights and underscores the importance of fostering multidisciplinary collaboration and structured imaging education to bridge the gap between technological capabilities and clinical expertise in respiratory medicine.

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) may affect multiple organs and interstitial lung disease (ILD) might be the first ma