Predicting the effectiveness of omalizumab in patients with refractory chronic rhinosinusitis with nasal polyps comorbid with asthma based on inflammatory biomarkers.

BACKGROUND

The treatment of refractory chronic rhinosinusitis with nasal polyps (CRSwNP) with omalizumab has been well studied based on clinical evaluation. Nevertheless, ideal quantitative or qualitative biomarkers for predicting a different response to biologics urgently need to be explored. We aim to identify potential biomarkers for predicting a good or poor response in patients with refractory CRSwNP.

METHODOLOGY

Patients received an endoscopic and radiological evaluation, a visual analogue scale (VAS) assessment, and a 22-item sinonasal outcome test (SNOT-22). Forty-eight biomarkers involving type 1 (T1), type 2 (T2), and type 3 (T3) inflammatory factors, chemokines, and remodeling factors were detected in nasal secretion and serum samples at baseline and after 24 weeks of omalizumab treatment.

RESULTS

Eighteen patients with CRSwNP and 16 patients as control were enrolled. Patients with CRSwNP who received oamlizumab treatment with the SNOT-22 and VAS scores improved by 8.9 and 2 points in 72.22% and 50%, respectively. The nasal polyp score (NPS) and Lund-Mackay score were significantly improved in 55.56% of patients. The concentrations of T2 inflammatory biomarker, granulocyte-macrophage colony-stimulating factor (GM-CSF), T3 inflammatory biomarkers, granulocyte colony-stimulating factor (G-CSF), chemokine (C-X-C motif) ligand (CXCL)-1, and chemokine (C-C motif) ligand-20 (CCL-20), T1 inflammatory biomarker, IP-10 (CXCL-10), and granzyme B in nasal secretion and serum periostin were significantly decreased. Serum CCL-3 (AUC = 0.836) and CCL-4 (AUC = 0.909) levels predicted the improvement of SNOT-22 score, respectively. Serum IL-8 (AUC = 0.883) predicted poor improvement in nasal congestion score. Nasal secretion CXCL-1 (AUC = 0.812), GM-CSF (AUC = 0.813), IgE (AUC = 0.900) and IP-10 (AUC = 0.800) effectively predicted none or less improvement in nasal polyp score.

CONCLUSIONS

Omalizumab remarkably affects inflammatory mediators in different pathways. CCL-3 and CCL-4 in serum and IgE, CXCL-1, GM-CSF, and IP-10 in nasal secretion may be considered as preferable biomarkers for predicting favorable or ineffective response to omalizumab therapy in patients with refractory CRSwNP comorbid with asthma, based on various clinical indicators.