# Unmasking EGPA with near fatal diffuse alveolar haemorrhage in severe eosinophilic asthma under treatment with benralizumab: a case report

**Authors:** Nora Drick, Till Frederik Kaireit, Jannik Ruwisch, Sven Schallhorn, Johann Bauersachs, Heiko Schenk, Marius M. Hoeper, Torsten Witte, Benjamin Seeliger

PMC · DOI: 10.1186/s12890-026-04106-4 · BMC Pulmonary Medicine · 2026-01-10

## TL;DR

A patient with severe eosinophilic asthma developed a life-threatening lung condition and heart issues while on benralizumab, highlighting complications in treating EGPA.

## Contribution

This case report highlights the emergence of vasculitis and myocardial injury in EGPA despite IL-5-targeted therapy.

## Key findings

- Diffuse alveolar haemorrhage occurred as a manifestation of overt vasculitis during corticosteroid tapering.
- Elevated troponin T levels indicated myocardial involvement consistent with EGPA and an acute myocardial infarction.

## Abstract

Eosinophils are key factors to the pathogenesis of severe eosinophilic asthma and eosinophilic granulomatosis with polyangiitis (EGPA). Monoclonal antibodies targeting the interleukin-5 (IL-5) pathway (mepolizumab and benralizumab) often lead to rapid symptom control and enable tapering of oral corticosteroids (OCS) in many patients.

We present the case of a 51-year-old male patient with severe eosinophilic asthma, peripheral blood eosinophilia, and ear, nose, and throat (ENT) involvement, treated with benralizumab (30 mg every 8 weeks) and oral corticosteroids. During tapering of corticosteroids, the patient developed diffuse alveolar haemorrhage as a manifestation of overt vasculitis. Subsequently, elevated troponin T levels were detected, and further diagnostic work-up revealed both myocardial involvement consistent with EGPA and an acute myocardial infarction due to occlusion of the left anterior descending (LAD) artery.

Central immunopathogenic pathways involved in vasculitis are not targeted by IL-5 antibodies and vasculitic manifestations may relapse or even newly emerge despite ongoing biological therapy. Elevated troponin levels in EGPA patients should only be attributed to EGPA once other potential causes of myocardial injury are ruled out.

## Linked entities

- **Proteins:** TNNT3 (troponin T3, fast skeletal type)
- **Diseases:** acute myocardial infarction (MONDO:0004781)

## Full-text entities

- **Genes:** IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}
- **Diseases:** throat ( (MESH:C538390), eosinophilia (MESH:D004802), myocardial involvement (MESH:C564676), haemorrhage (MESH:D006470), occlusion of the left anterior descending (LAD) artery (MESH:D001157), eosinophilic asthma (MESH:D001249), EGPA (MESH:D014890), vasculitis (MESH:D014657), acute myocardial infarction (MESH:D009203), myocardial injury (MESH:D009202)
- **Chemicals:** OCS (-), benralizumab (MESH:C571386), mepolizumab (MESH:C434107)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12849275/full.md

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Source: https://tomesphere.com/paper/PMC12849275