Expert review of respiratory medicine最新文献

Introduction: Muscle weakness represents a significant clinical problem in chronic obstructive pulmonary disease (COPD). During exacerbations of COPD (ECOPD), inflammation, oxidative stress, malnutrition, disuse, hypoxia, and glucocorticoid (GC) levels increase and converge, further aggravating skeletal muscle impairment with GC signaling as a common denominator. No intervention currently exists that specifically prevents or counteracts GC-induced muscle weakness during ECOPD.

Areas covered: This review summarizes clinical and pre-clinical evidence on the role of GC signaling in muscle dysfunction during ECOPD. We discuss the underlying molecular mechanisms by which GCs drive muscle weakness, and critically evaluate emerging pharmacological strategies aimed at mitigating these effects. PubMed and Scopus were searched for peer-reviewed papers published before April 2025.

Expert opinion: GC-induced muscle weakness is an under-recognized but potentially modifiable contributor to muscle weakness in ECOPD. Particular promise lies in pharmacological interventions such as myostatin pathway inhibitors, selective androgen receptor modulators, and those inducing IGF-1-related protein synthesis. Dedicated translational and clinical research is urgently needed to evaluate these novel interventions in the setting of ECOPD. Effective countermeasures could preserve muscle mass and function, improve exercise capacity and recovery, shorten hospital stay, and lower the risk of recurrence, offering a new therapeutic opportunity in ECOPD management.

Introduction: Overgrowth and colonization by non-typeable Haemophilus influenzae (NTHi) is a common feature of increasing disease severity, treatment resistance and increased susceptibility to disease exacerbations across chronic airways diseases (CADs). Whether NTHi is a driver of respiratory disease or reflects that the damaged airway has become a permissive environment for growth remains to be proven.

Areas covered: In this review, we discuss the potential roles of hypermutation, biofilm formation and intracellular living in allowing NTHi to adapt to living in the lungs of individuals with CADs. Furthermore, we also highlight immunological, structural and mucosal changes in the lungs themselves that can create a permissive niche for NTHi colonization. Given the significance of the host-pathogen interaction in the pathophysiology of CADs, we also consider which host and bacterial mechanisms may serve as potential targets for novel therapeutics. To achieve this we performed a comprehensive literature search through PubMed to identify studies reporting on NTHi in chronic airways diseases published up to 1 December 2025.

Expert opinion: A deeper understanding of the dynamic interactions between NTHi and the diseased airway may help identify novel diagnostic and therapeutic interventions that can be effective across multiple CADs.

Background: Idiopathic pulmonary fibrosis (IPF) significantly increases lung cancer risk, with cumulative incidence exceeding 50% at 10 years. We evaluated whether antifibrotic therapies provide cancer-protective effects beyond their established antifibrotic actions.

Methods: We conducted a systematic review searching MEDLINE, EMBASE, and Cochrane databases through July 2025 per PRISMA guidelines. Observational studies comparing lung cancer incidence in IPF patients receiving antifibrotics (pirfenidone or nintedanib) versus untreated controls were included. Random-effects meta-analysis with sequential sensitivity analyses was performed.

Results: Four observational studies with 15,582 participants were included. Primary pooled risk ratio was 0.39 (95% CI: 0.13-1.14; I² = 98%). Sequential sensitivity analyses addressing confounding by indication and biological heterogeneity demonstrated statistically significant risk reductions: 73% (RR 0.27; 95% CI: 0.16-0.48; I² = 44%) and 76% (RR 0.24; 95% CI: 0.08-0.69; I² = 67%) in pirfenidone-specific analyses.

Conclusions: Pirfenidone specifically may reduce lung cancer risk in IPF patients by 73-76%, though evidence is limited by observational designs, geographic restriction to East Asian populations, and biological heterogeneity between mechanistically distinct antifibrotic agents. Insufficient data exist for nintedanib. Agent-specific prospective randomized controlled trials are warranted. Protocol registration: PROSPERO identifier CRD420251119104.

Introduction: Severe asthma (SA) is a heterogenous disease with multiple clinical phenotypes. 'Early atopic asthma' is the predominant phenotype in children with SA. This phenotype is also identified in adults with SA. However, the role of immunoglobulin E (IgE)-mediated allergy in SA is still under debate.

Areas covered: This review summarizes current evidence linking IgE-mediated sensitization to SA. Electronic search was realized in Medline and PubMed databases by using the following terms: 'severe asthma,' 'IgE-mediated' associated with 'environmental allergens,' 'aeroallergens,' 'house dust mites,' 'pollens,' 'pets,' 'moulds,' 'cockroach,' 'food allergy,' 'drug allergy,' 'venom allergy,' 'atopic dermatitis,' 'eczema,' 'anaphylaxis.' Exposure to most aeroallergens of SA patients with atopy is associated with an increased risk of severe exacerbations. Children with food allergy have more severe asthma, poor symptoms control, and a high hospitalization rate. More limited evidence exists for the other IgE-mediated conditions and SA.

Expert opinion: IgE-mediated pathways play central role in the pathogenesis of various allergic diseases, including asthma. However, the allergic burden seems to be more important in children with SA than in adults. Future research may provide a better understanding of the role of IgE-mediated allergy in SA and coexisting allergic diseases with improvement in their clinical outcomes.

Introduction: T2-comorbidities are the most common in severe asthma (SA) patients and have a negative impact on disease outcomes but also an important socio-economic burden. Treating SA and its comorbidities by one medication is a very exciting possibility for the clinicians. Several biologics used for SA showed benefits on T2-comorbidities, but currently more limited data exists for tezepelumab, most recently developed in this domain.

Areas covered: This paper summarizes the available evidence regarding the efficacy of tezepelumab on T2-comorbidities of SA. Electronic search queries were applied to PubMed and Medline databases by using the following terms: 'tezepelumab,' 'severe asthma,' 'allergic rhinitis' (AR), 'chronic rhinosinusitis,' 'nasal polyps' (CRSwNP), 'aspirin exacerbated disease (AERD),' 'atopic dermatitis' (AD), 'eczema,' 'chronique spontaneous urticaria' (CSU),'food allergy' (FA), 'eosinophilic esophagitis' (EE).

Expert opinion: Tezepelumab treatment showed undeniable benefits on CRSwNP and AERD by improving sino-nasal and asthma outcomes. If the efficacy of tezepelumab on severe allergic asthma is well documented, current data are insufficient to conclude on its impact on AR. The effects of tezepelumab on AD and CSU were disappointing. No consistent data exists regarding FA and EE. Future studies are needed to confirm the efficacy of tezepelumab on AR, FA, and EE.

Objective: The aim of this study is to assess the effectiveness of an Internet-based comprehensive nursing intervention in improving lung function, treatment adherence, and quality of life in COPD patients.

Methods: A total of 104 COPD patients admitted to our hospital between October 2023 and January 2024 were randomly assigned to either a control group (n = 52) or an experimental group (n = 52). The control group received routine nursing interventions, including general education and routine care. The experimental group received Internet-based comprehensive nursing, which included personalized action plans, telehealth consultations, health education, dietary guidance, and psychological support delivered via the WeChat platform.

Results: The experimental group demonstrated significantly higher compliance (92.3%) compared to the control group (76.9%, p = 0.034). The improvement in PaO₂ and PaCO₂ levels, as well as lung function indicators (FEV₁, FVC, and FEV₁/FVC ratio), was significantly greater in the experimental group (p < 0.001). Moreover, the experimental group experienced a more substantial reduction in SGRQ scores (p < 0.001), indicating improved quality of life. Notably, a strong correlation between increased compliance and better clinical outcomes was observed (p < 0.001).

Conclusions: The application of Internet-based comprehensive nursing interventions significantly enhances treatment adherence, lung function, and quality of life in COPD patients.

Introduction: Severe therapy-resistant pediatric asthma (STRA) is an uncommon but high-impact form of childhood asthma, affecting 2-5% of patients yet causing disproportionate morbidity, healthcare use, and corticosteroid exposure. It is defined by uncontrolled disease despite optimized high-dose inhaled corticosteroids plus additional controllers, after exclusion and correction of modifiable factors. Accurate distinction from difficult-to-treat asthma is essential to avoid unnecessary treatment escalation and enable timely advanced interventions.

Areas covered: This narrative review summarizes current knowledge on STRA pathophysiology, diagnosis, and management in children, with a focus on precision medicine. Mechanistic insights include epithelial barrier dysfunction, distinct inflammatory endotypes, early airway remodeling, and microbial - immune interactions. Biomarker-guided endotyping supports individualized care. The article evaluates the efficacy, safety, and positioning of approved biologics, while noting gaps in treating non-T2 phenotypes and in predicting biologic response.

Expert opinion: STRA management is shifting from empirical escalation to endotype-driven strategies. Biologics benefit biomarker-selected patients by reducing exacerbations, improving lung function, and lowering steroid dependence, sometimes addressing comorbid allergies. Future priorities include expanding options for non-T2 and mixed phenotypes, validating predictive biomarkers, integrating digital monitoring, and reducing global inequities in access to advanced therapy.

Introduction: Dupilumab is a monoclonal antibody which selectively targets T2 inflammation by binding the IL-4 and 13 receptor and blocking its contribution to the immune activation. Clinical trials and real-life studies on severe asthma and nasal polyps patients have reported blood eosinophils fluctuation over the treatment course.

Areas covered: In the present narrative review the authors aim to provide a practical perspective on the recent evidence related to hypereosinophilia occurring during dupilumab therapy in respiratory indications, its underlying mechanisms, frequency, and clinical relevance, and to critically revise the currently proposed approaches to its management. Eosinophils increase is in most cases transient, spontaneously resolving, without any clinical relevance and no impact on efficacy. In fact, dupilumab safety profile is overall comparable with the other monoclonal antibody of the same drug class.

Expert opinion: Blood eosinophil count itself should not preclude dupilumab prescription, neither lead to dupilumab discontinuation, especially in the presence of ascertained drug efficacy and in the absence of signs suggesting a eosinophils-related complication. However, an extensive diagnostic work-up and regular follow-up monitoring is indicated, especially in patients with increased baseline eosinophils and coexisting nasal polyps and asthma.