100393 - TSLP Blockade in Severe Refractory Chronic Rhinosinusitis with Nasal Polyps: A Case Report

We present a report of a patient with severe, recurrent chronic rhinosinusitis with nasal polyps (CRSwNP) treated with anti-TSLP therapy. This case highlights the potential of TSLP blockade as a “top-level” intervention in type 2 inflammation and its impact on both nasal polyps and comorbid asthma.

This work helps to understand the clinical effectiveness of TSLP blockade in a patient with severe CRSwNP refractory to conventional therapies, demonstrating improvement in polyp size, olfaction, and quality of life.

Chronic rhinosinusitis with nasal polyps is associated with type 2 inflammation in up to 80% of patients. Recurrent polyps represent one of the most challenging scenarios in otolaryngology and allergy practice. TSLP is an epithelial “alarmin” that activates ILC2 cells and the type 2 inflammatory cascade, promoting IL-4/13 and IL-5 production, eosinophilic inflammation, IgE synthesis, tissue remodeling, and polyp growth. Blockade of TSLP represents an upstream intervention in the inflammatory pathway, offering a unique opportunity to interrupt fundamental immune mechanisms.

To describe the clinical presentation, laboratory findings, and outcomes of anti-TSLP therapy in a patient with severe, recurrent CRSwNP and comorbid asthma.

A 49-year-old female with a 6-year history of recurrent nasal polyps underwent two prior endoscopic sinus surgeries. Disease severity was evaluated using Lund–Kennedy endoscopic scoring (24), SNOT-22 questionnaire (88 points), and Lund–Mackay CT score (24, bilateral). Comorbidities included partially controlled asthma and NSAID/aspirin sensitivity. Laboratory data showed eosinophilia (0.98 ×10^9/L, 12.8%) and elevated total IgE (146 IU/mL). Anti-TSLP therapy with tezepelumab 210 mg monthly subcutaneously was initiated after inadequate response to intranasal steroids and standard therapies. Follow-up assessments included endoscopic scoring, SNOT-22, olfaction, and asthma control and laboratory parameters.

By 12 weeks of therapy, polyp size decreased by 60% (Lund–Kennedy 6/24, Lund–Mackay 7/24), and the patient reported recovery of olfaction for the first time in 6 years. SNOT-22 score dropped from 88 to 18 points. Eosinophils decreased from 0.98 ×10⁹/L (12.8%) to 0.45 ×10⁹/L (6.5%), total IgE from 146 to 103 IU/mL, ECP from 56 to 28 ng/mL, and rhinocytogram eosinophils from 40–50 to 5–10 per field. Asthma exacerbations ceased, and overall quality of life significantly improved. The case demonstrates that TSLP blockade can modulate upstream type 2 inflammation, reduce polyp burden, restore olfaction, and control comorbid asthma simultaneously.

TSLP blockade represents a high-level intervention in severe, refractory CRSwNP. Early clinical experience suggests substantial improvement in nasal polyps, olfaction, asthma control, and patient quality of life. Anti-TSLP therapy may provide a novel approach for patients who fail conventional biologics targeting IL-4/13 or IL-5.

Written informed consent for publication of anonymized clinical data was obtained from the patient.