D3.364 - Effect of Omalizumab on Inflammatory and Immune Biomarkers in Mast Cell-Mediated Angioedema

Poster abstract

Background

Mast cell-mediated angioedema (AE-MC) is a rare condition characterized by episodic localized swelling due to mast cell activation and inflammatory mediator release. Identifying reliable biomarkers is crucial for accurate diagnosis, monitoring disease activity and guiding therapeutic strategies. This study aims to evaluate the changes in inflammatory and immune biomarkers in patients with AE-MC before and after Omalizumab treatment.

Method

This retrospective descriptive study analyzed laboratory data from AE-MC patients managed at our Angioedema Unit between 2018 and 2024. Eligible patients were refractory to antihistamines up to four times the standard dose and required treatment with Omalizumab. Biomarkers assessed pre- and post-treatment included eosinophils, basophils, fibrinogen, D-dimer, erythrocyte sedimentation rate (ESR), lactate dehydrogenase (LDH), C-reactive protein (CRP), amyloid A, and tryptase. Statistical analyses were performed using the Shapiro-Wilk test for normality, Student’s t-test for normally distributed variables and the Wilcoxon test for non-normal variables.

Results

A total of 40 patients (21 women) with a mean age of 54.2 ± 16.3 years were included. Statistically significant differences were found between the two measurements of the following biomarkers: ESR (p = .019), LDH (p < .001), amyloid A (p = .045) and tryptase (p = .026), indicating potential improvements in inflammatory and immune responses. In contrast, no statistically significant differences were observed in eosinophils (p = .723), basophils (p = 1.000), fibrinogen (p = .102), D-dimer (p = .126) or CRP (p = 0.918).

Conclusion

Omalizumab demonstrates a statistically significant effect on reducing inflammatory biomarkers such as ESR, LDH, amyloid A and tryptase, highlighting its potential role as an effective therapeutic option for optimizing AE-MC management. Further large-scale studies are needed to confirm these findings and clarify the mechanisms underlying the differential biomarker responses.