# Use of an IL-1 Inhibitor for Refractory Steroid-Dependent Lupus Pericarditis With Constrictive Physiology

**Authors:** Patrick Creechan, Megan Lockwood, Brittany N. Weber, Allan Klein, Syed W. Haider

PMC · DOI: 10.1016/j.jaccas.2025.105348 · JACC Case Reports · 2025-09-09

## TL;DR

A patient with difficult-to-treat lupus pericarditis improved after switching to a new treatment targeting interleukin-1, reducing steroid use and reversing heart inflammation.

## Contribution

This case demonstrates that IL-1 inhibition with rilonacept can be effective for steroid-dependent lupus pericarditis refractory to B cell-targeted therapies.

## Key findings

- Rilonacept led to rapid symptom resolution and reversal of pericardial inflammation.
- Steroid use was successfully discontinued after treatment with rilonacept.
- Interleukin-1 inhibition may break the autoinflammatory cycle in refractory lupus pericarditis.

## Abstract

Pericardial involvement is common in systemic lupus erythematosus (SLE) and can lead to recurrent episodes. B cell–targeted therapies are commonly used in the treatment of SLE pericarditis. The management of recurrent lupus pericarditis refractory to B cell–targeted therapy remains challenging.

A 33-year-old woman with SLE developed steroid-dependent, recurrent pericarditis with large effusions requiring 2 pericardial windows. Despite corticosteroids, colchicine, hydroxychloroquine, and the B cell–targeted therapy belimumab, she had persistent symptomatic recurrences with features of evolving constrictive physiology on cardiac magnetic resonance. Transition to rilonacept led to rapid symptom resolution, steroid discontinuation, and cardiac magnetic resonance–documented reversal of pericardial inflammation and constrictive physiology.

This case illustrates that interleukin-1 inhibition with rilonacept can be an effective steroid-sparing strategy for refractory lupus pericarditis after failure of traditional B cell–targeted therapy.

Lupus pericarditis can be steroid dependent and refractory to standard SLE immunosuppression, including B cell–directed biologics. Interleukin-1 inhibition offers a potential therapeutic strategy for breaking the autoinflammatory cycle that can sustain recurrent pericarditis.

## Linked entities

- **Proteins:** IL1A (interleukin 1 alpha)
- **Chemicals:** colchicine (PubChem CID 2833), hydroxychloroquine (PubChem CID 3652)
- **Diseases:** systemic lupus erythematosus (MONDO:0007915)

## Full-text entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}
- **Diseases:** pericardial inflammation (MESH:D007249), autoinflammatory (MESH:D056660), effusions (MESH:D000080324), Pericardial involvement (MESH:D008476), Lupus Pericarditis (MESH:D010493), SLE (MESH:D008180)
- **Chemicals:** Steroid (MESH:D013256), colchicine (MESH:D003078), hydroxychloroquine (MESH:D006886), belimumab (MESH:C511911)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12793853/full.md

## References

10 references — full list in the complete paper: https://tomesphere.com/paper/PMC12793853/full.md

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Source: https://tomesphere.com/paper/PMC12793853