# An Uncommon Case of Bowel Angioedema Due to Lisinopril

**Authors:** Cristina Vidal Carrion, Hannah Warshaw, Sree Uppalapati, Zubia Ahmed, Margi Desai

PMC · DOI: 10.7759/cureus.100319 · Cureus · 2025-12-29

## TL;DR

A 54-year-old man developed bowel angioedema after starting lisinopril, highlighting a rare side effect of ACE inhibitors that can mimic acute abdominal conditions.

## Contribution

This case report presents a rare instance of bowel angioedema caused by lisinopril, expanding the known complications of ACE inhibitors.

## Key findings

- Bowel angioedema can occur as a complication of ACE inhibitor use and may present with acute abdominal symptoms.
- Discontinuation of lisinopril and treatment with steroids, antihistamines, and acid suppression resolved the patient's symptoms.
- Bowel angioedema due to ACE inhibitors should be considered in the differential diagnosis of acute abdomen.

## Abstract

In general, angioedema can be caused by a hereditary C1 esterase deficiency or by an allergy-related cascade involving either a histamine or a bradykinin-induced cascade. Angioedema secondary to angiotensin-converting enzyme inhibitors (ACEi) typically induces an allergy-related angioedema and typically presents complications associated with the upper airway, and rarely presents intra-abdominally. This case discussed how a 54-year-old male with a recent diagnosis of hypertension presented with acute abdominal pain. He was started on a lisinopril-hydrochlorothiazide combination two days before the presentation. Differentials were considered for an acute abdomen, and a CT abdomen was obtained, which was significant for the thickening of the jejunum and sigmoid colon with surrounding mucosal edema and inflammatory changes. The patient was ultimately treated for bowel angioedema successfully with dexamethasone, diphenhydramine, and famotidine, and his lisinopril was discontinued. This case report aims to discuss and evaluate bowel angioedema in the setting of ACEi use and how it should be considered as a differential for an acute abdomen and its relevant empirical management with steroids due to the indistinguishable etiology of histamine or bradykinin mediated.

## Linked entities

- **Chemicals:** lisinopril (PubChem CID 5362119), hydrochlorothiazide (PubChem CID 3639), dexamethasone (PubChem CID 5743), diphenhydramine (PubChem CID 3100), famotidine (PubChem CID 5702160)
- **Diseases:** angioedema (MONDO:0010481)

## Full-text entities

- **Genes:** KNG1 (kininogen 1) [NCBI Gene 3827] {aka BDK, BK, HAE6, HK, HMWK, KNG}
- **Diseases:** abdominal pain (MESH:D015746), mucosal edema (MESH:D004487), Angioedema (MESH:D000799), acute abdomen (MESH:D000006), allergy (MESH:D004342), inflammatory (MESH:D007249), hypertension (MESH:D006973), C1 esterase deficiency (MESH:D054179)
- **Chemicals:** Lisinopril (MESH:D017706), famotidine (MESH:D015738), steroids (MESH:D013256), diphenhydramine (MESH:D004155), hydrochlorothiazide (MESH:D006852), histamine (MESH:D006632), dexamethasone (MESH:D003907)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12848952/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12848952/full.md

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Source: https://tomesphere.com/paper/PMC12848952