ORIGINAL RESEARCH article
Front. Immunol.
Sec. Molecular Innate Immunity
This article is part of the Research TopicHereditary angioedema - C1INH deficiency and beyondView all 5 articles
Eosinophilic inflammation in hereditary angioedema: a single-center real-world retrospective chart review study
Provisionally accepted
- 1Ludwig-Maximilians-Universitat Munchen, Munich, Germany
- 2University of Lübeck, Lübeck, Germany
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Background: Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurrent, unpredictable swelling attacks primarily driven by bradykinin-mediated vascular permeability. However, additional inflammatory mechanisms may contribute to disease heterogeneity. During routine diagnostics, we observed elevated serum eosinophil cationic protein (ECP) levels in HAE patients, suggesting increased eosinophil activation. To date, eosinophil involvement in HAE has not been systematically investigated, this study aimed to validate clinical observations and explore a potential link between bradykinin signaling and eosinophilic inflammation. Methods: We retrospectively analyzed data from 48 patients with confirmed HAE (32 HAE type I/II, 16 HAE with normal C1-INH) and 1,880 control patients treated at a tertiary university allergy and angioedema referral center. Using causal-inference Bayesian multilevel regression with bias-breaking post-stratification and propensity-score inverse probability weighting, we estimated the effect of HAE on serum ECP levels and absolute eosinophil counts while adjusting for age, sex, season, and allergic comorbidities. Results: HAE was associated with a 1.52-fold average increase in serum ECP levels (most conservative 95% credibility interval: 1.24–1.90; Bayesian p = 0.00088), consistent across all modeling specifications. Absolute eosinophil counts were not elevated, indicating enhanced eosinophil activation independent of cell number. Conclusions: Patients with HAE show biochemical evidence of increased eosinophil activation, suggesting a previously unrecognized inflammatory component beyond bradykinin-driven edema formation. Further studies should clarify clinical implications and the potential contribution to comorbidities and phenotypic variability.
Keywords: biomarker, Eosinophilic cationic protein, Eosinophilic inflammation, hereditary angioedema, Subclinical inflammation
Received: 25 Nov 2025; Accepted: 28 Jan 2026.
Copyright: © 2026 Boch, Ludwig, von Bubnoff and Recke. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Andreas Recke
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