Background/Objectives: Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and sleep fragmentation, assessed using the Apnea–Hypopnea Index (AHI). Systemic inflammation is central to OSA progression, and the systemic inflammatory response index (SIRI) has emerged as a potential biomarker for inflammatory diseases. This study investigates the relationship between SIRI and OSA severity while comparing other inflammatory markers. Methods: A retrospective study was conducted among 150 OSA patients at a tertiary care hospital. Based on AHI, patients were categorized into mild, moderate, and severe OSA groups. Blood parameters, including neutrophil, monocyte, and lymphocyte counts, were analyzed, and inflammatory indices (SIRI, NLR, PLR) were calculated. Correlation, ROCs, and regression analyses assessed associations between inflammatory markers and OSA severity. Results: SIRI demonstrated an excellent predictive ability for severe OSA with an AUC of 0.960 (cut-off: 1.105; sensitivity: 92.2%; specificity: 91.4%). The STOP-BANG score alone had lower discriminatory power (AUC: 0.737), but combining it with SIRI improved accuracy (AUC: 0.983). The best performance was observed when SIRI, STOP-BANG, PLR, and CRP were combined, yielding an AUC of 1.00, indicating perfect discrimination. Conclusions: SIRI shows strong predictive value for identifying severe OSA, underscoring its utility as a simple, cost-effective biomarker to aid early recognition and referral, particularly in primary care and resource-limited settings.

Background: Chronic Obstructive Pulmonary Disease (COPD) remains a leading cause of morbidity and mortality worldwide, particularly in low- and middle-income countries (LMICs), where both tobacco and biomass smoke exposure are major risk factors. While spirometry is the diagnostic gold standard, reliable non-invasive biomarkers are needed for early detection and disease monitoring. The soluble receptor for advanced glycation end-products (sRAGE), a circulating decoy receptor with anti-inflammatory activity, has shown potential in this context. Methods: In this prospective, exposure-stratified, cross-sectional study, 150 adults were enrolled into four groups of 25 each—tobacco-smoke COPD, male tobacco-exposed controls, biomass-smoke COPD, and female biomass-exposed controls—along with 50 healthy controls (25 males, 25 females). Participants underwent clinical evaluation, spirometry, and serum sRAGE quantification (ELISA). Systemic inflammation was assessed using neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR). Correlation and receiver operating characteristic (ROC) analyses determined diagnostic performance. Results: Serum sRAGE levels were significantly lower in tobacco-induced (545 ng/mL) and biomass-induced COPD (540 ng/mL) versus controls (1207–1462 ng/mL; p < 0.001). sRAGE correlated positively with FEV₁, FVC, and FEV₁/FVC (r = 0.54–0.75, p < 0.001), and negatively with CAT, mMRC, and SGRQ-C. ROC analysis showed excellent discrimination (AUC = 0.990; 94% sensitivity; 96% specificity at 946 ng/mL cutoff). Conclusions: Serum sRAGE is a robust, non-invasive biomarker for COPD diagnosis and severity assessment across exposure phenotypes. Its integration into clinical practice may enhance early detection and risk stratification, particularly in LMICs.

Introduction: Asthma is a heterogeneous chronic airway disease marked by variable airflow limitation and bronchial hyperresponsiveness. While eosinophilic inflammation is well studied, neutrophil-driven and mixed eosinophilic–neutrophilic patterns are increasingly recognized in severe or poorly controlled asthma. Olfactomedin-4 (OLFM4), a neutrophil-expressed glycoprotein involved in immune regulation, has emerged as a potential biomarker of neutrophilic inflammation, though its role in asthma is underexplored. This study aimed to evaluate serum OLFM4 levels in asthma patients and examine their association with disease severity and control. Methods: A pilot cross-sectional, hospital-based comparative study was conducted at JSS Medical College, Mysore, between June 2023 and December 2024. Eighty participants were recruited: 60 asthmatics (20 each with mild, moderate, and severe asthma) and 20 healthy controls. Serum OLFM4 was measured using ELISA. Asthma severity was assessed by spirometry, and asthma control by the Asthma Control Test (ACT). Associations with hematological and pulmonary function parameters were analyzed. Results: Serum OLFM4 levels were significantly higher in asthmatics compared to controls (4,309.23 ± 1,533.97 vs. 1,344.41 ± 256.38 pg/mL; p < 0.001), with progressive elevation across severity (mild: 2,947.49; moderate: 4,371.45; severe: 5,608.75 pg/mL). OLFM4 correlated negatively with ACT scores (r = −0.820, p < 0.001) and lung function indices, and positively with leukocyte, neutrophil, and eosinophil counts. Multivariate Firth’s penalized logistic regression identified serum OLFM4 as an independent predictor of asthma severity (p < 0.001). ROC analysis showed excellent discrimination between asthmatics and controls (AUC = 0.997) and between non-severe and severe asthma (AUC = 0.89). Conclusion: Elevated serum OLFM4 levels correlate with asthma severity, poor control, and lower lung functions, highlighting its potential as a biomarker for disease stratification. These findings suggest that OLFM4 may be a useful biomarker reflecting overall disease burden and control status in asthma. Although the biological role of OLFM4 in asthma pathophysiology requires further investigation, its consistent association with clinical severity and control supports its potential utility in asthma stratification and monitoring.