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Allergic rhinitis (AR) is a prevalent IgE-mediated inflammatory disease characterized by nasal symptoms and elevated inflammatory biomarkers in nasal secretions. Eosinophil cationic protein (ECP), myeloperoxidase (MPO), and tryptase (TPS) are key mediators of AR pathogenesis, but their dynamic changes post-treatment remains underexplored. This study aimed to evaluate the effects of standard pharmacotherapy (fluticasone propionate nasal spray + fexofenadine hydrochloride) on nasal secretion levels of ECP, MPO, and TPS in AR patients and assess their diagnostic and prognostic utility. A total of 34 moderate to severe dust mite-sensitized AR patients and 20 healthy controls were enrolled. Nasal secretions were collected before and after 2 weeks of treatment. Biomarker concentrations (ECP, MPO, TPS) were measured using magnetic particle detection (MPD), and eosinophil percentages (EOS%) were analyzed via cytology smears. Statistical analyses included Mann-Whitney U tests and ROC curve evaluation. Post-treatment, AR patients showed significant reductions in ECP (5.95 ± 2.85 vs. 3.21 ± 1.82 ln (AU/μl), p < 0.001) and TPS (5.34±2.02 vs. 3.31±2.21 ln (AU/μl), p < 0.001), with ECP normalizing to HC levels (2.10 ± 0.84 ln (AU/μl)). TPS remained elevated compared to HC (-0.55 ± 0.99 ln (AU/μl), p < 0.05), while MPO levels were unchanged (143.2 ± 160.6 vs. 175.9 ± 174.8 AU/μl) but lower than HC (289.0±105.1 AU/μl, p < 0.01). ROC analysis revealed high diagnostic accuracy for TPS (AUC=0.959) and combined biomarkers (AUC=0.974) in distinguishing AR from HC, while ECP correlated best with symptom severity (AUC=0.819). Standard AR therapy effectively reduces ECP and TPS levels, with ECP serving as a sensitive marker for treatment response and TPS for early diagnosis. Persistent post-treatment TPS elevation suggests unresolved mast cell activation, highlighting the need for optimized therapies. Noninvasive nasal secretion analysis offers a reliable tool for monitoring AR inflammation.
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Long et al. (2026) studied this question.
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