Interstitial lung diseases (ILDs) encompass a heterogeneous group of disorders characterized by varying degrees of inflammation and fibrosis. Despite advances in understanding the pathogenesis, therapeutic options remain limited, particularly for patients with progressive phenotypes. Current international guidelines for idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF) emphasize the need for antifibrotic strategies and call for novel pharmacological interventions targeting key molecular pathways involved in fibrogenesis. This review provides a comprehensive overview of the most promising emerging pharmacological agents for ILDs, with particular attention to their mechanisms of action, efficacy, and safety profiles as reported in recent preclinical and clinical studies. The recent approval of Nerandomilast and the ongoing phase III trials of other agents mark a pivotal transition toward a new generation of antifibrotic therapies, aiming to achieve more effective disease control and improved patient outcomes. In view of an enlargement of active drugs aiming at controlling the disease with different mechanisms, the Authors underline the need for a “precision medicine” model to be applied to each ILD phenotyped patient, mirroring what already happens for other respiratory diseases.

Purpose of Review: To review current evidence on biologic therapies targeting type 2 inflammation in patients with eosinophilic COPD and respiratory comorbidities who remain uncontrolled despite optimized triple inhaled therapy. Recent Findings: Recent phase 3 trials have shown that dupilumab provides the most consistent benefit in eosinophilic COPD, reducing exacerbations and improving lung function and quality of life. Mepolizumab has shown a more limited effect, mainly on exacerbation reduction, whereas benralizumab has not demonstrated clear clinical benefit. Blood eosinophil count remains the main biomarker for treatment selection. Summary: Biologic therapies are advancing precision medicine in COPD, with dupilumab currently showing the strongest overall evidence. Careful patient selection is essential. Broader phenotyping may further improve management, as comorbidities such as chronic rhinosinusitis may contribute to symptom burden and support a multidisciplinary approach. Future studies should clarify long-term outcomes and optimal biologic selection.

Tuberculous pleural effusion (TPE) is currently the most common form of extrapulmonary tuberculosis and remains a significant cause of pleural disease worldwide, particularly in endemic regions. It often presents with non-specific clinical symptoms, such as fever, chest pain, cough and weight loss, thereby complicating the diagnostic process. This narrative review provides an expert comprehensive clinical practice overview covering the following issues correlated with diagnosis and management of TPE: 1- epidemiology, clinical presentation and underlying pathophysiology; 2- limitations of conventional diagnostic procedures on pleural fluid; 3- usefulness of thoracic ultrasound (TUS) in the stepwise pathway 4- role of thoracoscopy as a golden diagnostic tool, with the proposal of a step by step algorithm. A large iconography enriches the review from the educational point of view by presenting a pictorial series of characteristic sonographic and thoracoscopic findings.

Small-airway disease (SAD) is a key feature of severe asthma and is associated with poor symptom control and frequent exacerbations. Dupilumab has demonstrated efficacy in improving lung function and reducing exacerbations, but real-world evidence on its effects in SAD remains limited. The aim of this study is to evaluate the impact of 12 months of dupilumab treatment on SAD, clinical outcomes, and type 2 inflammation. We included 21 patients. Small-airway function was assessed by impulse oscillometry (R5–R20) and spirometry FEF25–75% predicted at baseline (T0) and after 3 (T3), 6 (T6), and 12 (T12) months of treatment. Additional assessments included FEV₁, the Asthma Control Test (ACT), exacerbation frequency, oral corticosteroid (OCS) use, the blood eosinophil count (BEC), and fractional exhaled nitric oxide (FeNO). At baseline, 62% of patients exhibited SAD (R5–R20 > 0.07 kPa/L/s). Dupilumab treatment led to a significant and sustained improvement in small-airway function: mean R5–R20 decreased from 0.18 ± 0.17 kPa/L/s to 0.09 ± 0.07 at T12 (p = 0.04), while predicted FEF25–75% increased from 29.5 ± 20.8% to 47.0 ± 21.1% (p < 0.001). ACT scores improved from 13.1 ± 4.9 to 19.6 ± 3.8 (p < 0.001). FeNO levels declined from 64.1 ± 50.7 ppb to 24.8 ± 20.9 ppb (p = 0.01). Improvements in R5–R20 correlated with better ACT and FeNO reductions. In this real-world cohort, dupilumab significantly improved SAD, lung function, and asthma control, while reducing exacerbations, OCS dependence, and type 2 inflammation over 12 months.

The therapeutic goals related to chronic airway diseases are evolving from short-term symptom control toward sustained suppression of disease activity and prevention of future risk. In severe asthma, this shift has been captured by the concept of clinical remission, generally defined by absence of exacerbations, no need for oral corticosteroids, symptom control, and stable or improved lung function. In chronic obstructive pulmonary disease (COPD), the analogous concept has more often been described as disease stability. Although remission in asthma and stability in COPD have developed within different biological and clinical frameworks, they may reflect disease-specific expressions of the same therapeutic ambition. Recent studies support COPD stability as a measurable and clinically meaningful state, associated with reduced exacerbation risk and mortality. Evidence from optimized inhaled triple therapy, particularly with fluticasone furoate/umeclidinium/vilanterol, indicates that multidimensional stability can be achieved and maintained in a proportion of patients, while real-world studies reinforce its applicability beyond randomized trials. The emergence of biologic therapies for selected patients with eosinophilic or type 2 COPD further strengthens the rationale for considering stability as an ambitious treatment target. In this narrative review, informed by a structured literature search, we discuss the conceptual relationship between asthma remission and COPD stability, and summarize the evidence supporting disease stability as an attainable and prognostically relevant outcome. In addition, we propose a pragmatic multidimensional definition based on symptom stability, absence of moderate or severe exacerbations, no systemic corticosteroid use, and maintained lung function over 12 months. COPD stability should not be viewed as a weaker goal than asthma remission, but rather as the most appropriate COPD-specific expression of sustained low disease activity.