Background: Chronic Obstructive Pulmonary Disease (COPD) is a major global health challenge, primarily driven by exposures to tobacco smoke and biomass smoke. While Tobacco-Smoke-Induced COPD (TSCOPD) has been extensively studied, the diagnostic challenges and distinct pathogenesis of Biomass-Smoke-Induced COPD (BSCOPD), particularly in low- and middle-income countries, remain underexplored. Objective: To explore the differences in clinical manifestations, pulmonary function, and inflammatory profiles between BSCOPD and TSCOPD and highlight the diagnostic complexities of BSCOPD. Methods: This review analyzes the current literature comparing BSCOPD with TSCOPD, focusing on distinctive pathophysiological mechanisms, inflammatory markers, and oxidative stress processes. Results: BSCOPD presents differences in clinical presentation, with less emphysema, smaller airway damage, and higher rates of pulmonary hypertension compared to TSCOPD. BSCOPD is also characterized by bronchial hyperresponsiveness and significant hypoxemia, unlike TSCOPD, which exhibits severe airflow obstruction and emphysema. Additionally, the inflammatory profile of BSCOPD includes distinct mucous hypersecretion and airway remodeling. Conclusions: The unique genetic, epigenetic, and oxidative stress mechanisms involved in BSCOPD complicate its diagnosis and management. Biomass smoke’s underrecognized impact on accelerated lung aging and exacerbation mechanisms emphasizes the need for targeted research to refine diagnostic criteria and management strategies for BSCOPD. Future directions: Further research should focus on identifying specific biomarkers and molecular pathways to enhance early diagnosis and improve clinical outcomes in populations exposed to biomass smoke.

Background/Objectives: Asthma is a heterogeneous inflammatory airway disease. Periostin, a matricellular protein induced by interleukin-13, contributes to airway inflammation and remodeling. This study evaluated serum periostin as a diagnostic biomarker and explored multidimensional phenotypes in adult asthma. Methods: A cross-sectional study included 76 adults, with 25 healthy controls, 25 moderate, and 26 severe asthma patients, classified per Global Initiative for Asthma (GINA)-2020 guidelines. Serum periostin was measured using an enzyme-linked immunosorbent assay (ELISA). Diagnostic accuracy was assessed using receiver operating characteristic (ROC) analysis, Firth-penalized logistic regression, bootstrap calibration (1000 resamples), decision curve analysis (DCA), and gradient boosting machine (GBM) validation. Principal component analysis (PCA) followed by k-means clustering identified distinct phenotypes based on clinical, functional, and inflammatory variables. Results: Asthma patients had higher serum periostin than controls (median 52.9 vs. 32.5 pg/mL; p < 0.01), with excellent diagnostic accuracy (AUC = 0.987; sensitivity = 94.1%, specificity = 100%). Firth regression identified periostin as the only independent predictor of asthma diagnosis (β = 0.387; OR = 1.47; 95% CI 1.23–2.08; p < 0.001). Calibration showed minimal error (MAE = 0.042) and DCA demonstrated clear net benefit. GBM confirmed periostin as the dominant diagnostic predictor. PCA revealed three clusters: Cluster 1: younger, lower periostin, preserved lung function, good symptom control; Cluster 2: intermediate periostin, greater airflow limitation, poorer control; and Cluster 3: highest periostin, elevated systemic inflammation (NLR, PLR, SII), with moderate functional impairment. Conclusions: Serum periostin is a reliable diagnostic biomarker for asthma. Multidimensional clustering highlights clinically relevant phenotypes linked to periostin, inflammatory burden, and lung function, supporting its role in personalized asthma management.

Steroid-resistant asthma (SRA) is clinically significant, approximately 10–15% of individuals with asthma do not exhibit a positive response to standard treatments. While this subset represents a relatively small proportion of asthma patients, severe refractory asthma places a substantial burden on healthcare resources and contributes significantly to illness and death. Additionally, the quality of life of patients is greatly affected by the adverse effects of excessive steroid consumption, there is a need to identify individuals who do not react well to steroid medication and the ongoing difficulties of these asthma patients in controlling their diseases, which have a large socio-economic impact. The current short article reviews the common molecular mechanisms responsible for steroid resistance in asthma patients.

This review delves into the complex role of 12/15-lipoxygenase (12/15-LOX) in asthma pathogenesis, focusing on its contributions to mitochondrial dysfunction, oxidative stress, epithelial injury, and airway remodeling. We provide new insights into potential therapeutic strategies aimed at improving asthma management. Additionally, we examine the pro-inflammatory functions of interleukin-4 (IL-4) and its regulatory mechanisms that upregulate 12/15-LOX, leading to increased oxidative stress and airway remodeling. Key interventions such as vitamin E, esculetin, and baicalein are highlighted for their potential to inhibit 12/15-LOX activity, reduce oxidative stress, and restore mitochondrial function. Vitamin E suppresses IL-4 transcription, reducing 12/15-LOX expression and its inflammatory metabolites, while esculetin and baicalein directly inhibit 12/15-LOX, mitigating inflammation and oxidative damage. These antioxidants also promote mitochondrial biogenesis, protect mitochondrial DNA, and enhance respiratory efficiency, contributing to improved cellular metabolism and reduced apoptosis. This comprehensive approach emphasizes the therapeutic potential of targeting 12/15-LOX pathways to alleviate asthma symptoms and improve patient outcomes, paving the way for novel treatment strategies that significantly enhance asthma therapy.