# A case report of midodrine to treat protein-losing enteropathy for heart transplant candidacy

**Authors:** Sean M Conte, Daniel Tardo, Stephanie Wiltshire, Kavitha Muthiah

PMC · DOI: 10.1093/ehjcr/ytaf544 · European Heart Journal. Case Reports · 2025-10-23

## TL;DR

A young woman with heart failure and a rare condition called protein-losing enteropathy was successfully treated with midodrine, allowing her to become eligible for a heart transplant.

## Contribution

This is the first reported case of midodrine use bridging a patient with protein-losing enteropathy and Fontan heart failure to heart transplant candidacy.

## Key findings

- Midodrine therapy normalized serum albumin and improved edema, exercise tolerance, and frailty in a patient with Fontan circulation and protein-losing enteropathy.
- The treatment enabled the patient to become eligible for heart transplantation despite her advanced heart failure and complications.
- This case suggests midodrine could be a viable option for managing protein-losing enteropathy in Fontan patients to improve transplant eligibility.

## Abstract

Protein-losing enteropathy (PLE) is seen in up to 15% of patients with Fontan circulation and has important nutritional, immunologic, and haemodynamic consequences especially in the context of advanced heart failure. Midodrine, an alpha-1-receptor agonist, increases lymphatic tone, mitigating leak of lymph into the bowel, and has been shown to have clinical and biochemical benefit in patients with Fontan failure.

A young woman with Fontan circulation, end-stage heart failure, and PLE developed progressive hypoalbuminaemia, deconditioning, and frailty prohibitive to transplantation candidacy. Three months after commencing oral midodrine therapy, she experienced normalization of her serum albumin and improvements in her oedema, exercise tolerance, and frailty enabling candidacy and eventual successful heart transplantation.

The development of PLE in patients with Fontan circulations is an indication for cardiac transplantation, but there are often significant barriers due to the many complications. We performed a comprehensive Medline search, and this is the first case demonstrating the use of midodrine to bridge a frail patient with PLE and advanced Fontan heart failure to heart transplantation candidacy and eventual transplant.

## Linked entities

- **Chemicals:** midodrine (PubChem CID 4195)
- **Diseases:** protein-losing enteropathy (MONDO:0009174), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** frailty (MESH:D000073496), heart failure (MESH:D006333), end-stage heart failure (MESH:D007676), oedema (MESH:C536897), Fontan failure (MESH:D051437), PLE (MESH:D011504)
- **Chemicals:** Midodrine (MESH:D008879)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12644453/full.md

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Source: https://tomesphere.com/paper/PMC12644453