100692 - Effect of Mepolizumab on Tissue and Blood Eosinophils in Patients with Chronic Rhinosinusitis With Nasal Polyps
Background
Chronic rhinosinusitis with nasal polyposis (CRSwNP) is a chronic inflammatory disease of the sinonasal mucosa characterized by type-2 inflammation, primarily driven by proinflammatory cytokines such as IL-5, IL-4, and IL-13 along with elevated levels of eosinophils in the surrounding tissue. Mepolizumab, a humanized monoclonal antibody targeting IL-5, is an approved and effective treatment for CRSwNP.
The aim of this study was to evaluate changes in eosinophil counts in nasal polyp (NP) tissue and peripheral blood (PB) in patients with CRSwNP before and after 6 months of treatment with mepolizumab.
Method
We performed a retrospective descriptive study including adult patients with CRSwNP treated with mepolizumab according to current guideline recommendations. All patients had undergone at least one endoscopic sinus surgery (EES) prior to initiation of mepolizumab. Eosinophil counts in NP tissue were obtained from pathology reports of prior surgeries and after six months of mepolizumab treatment. Peripheral blood (PB) eosinophils counts were measured at baseline and six months of mepolizumab treatment
Results
Five patients (2 men and 3 women) with CRSwNP were included, with a median (IQR) age 58 (51-67) years. All patients had comorbid asthma, and one patient had aspirin-exacerbated respiratory disease. The median (IQR) number EES per patient was 2 (1-4). Median eosinophils count in NP tissue from previous EES were 180 per high power field (HPF) (100-500), which decreased to 4.5/HPF (3-36) after six months of mepolizumab treatment.
PB eosinophils counts decreased from a median of 480/μL (80-770) to 60/μL (40-80) after six months of treatment with mepolizumab.
Conclusion
Mepolizumab treatment was associated with reduction in eosinophil counts in both NP tissue and PB in patients with CRSwNP. These findings support the role of IL-5 blockade in reducing local and systemic eosinophilic inflammation in type 2 driven airway disease.
