# Treatment of Kimura disease with dupilumab: a case report and literature review

**Authors:** Wei Yang, Ze Wu, Jun Niu

PMC · DOI: 10.3389/fimmu.2026.1670489 · Frontiers in Immunology · 2026-02-16

## TL;DR

A 19-year-old man with Kimura disease showed significant improvement after treatment with dupilumab, a drug targeting type 2 inflammation.

## Contribution

This case report demonstrates dupilumab's efficacy in treating Kimura disease when conventional therapies fail.

## Key findings

- The patient's subcutaneous masses decreased in size during dupilumab treatment.
- Eosinophil count and IgE levels progressively declined with dupilumab therapy.
- Symptoms worsened after discontinuation of previous treatments but improved with dupilumab.

## Abstract

Kimura disease is a benign chronic inflammatory condition characterized by painless subcutaneous masses, peripheral blood eosinophilia, and increased serum immunoglobulin E levels. The pathogenesis of KD remains unclear, however, more and more evidence suggests that type 2 inflammation may play an important role in KD. We present a case of a 19-year-old male who complained of masses behind both ears for two months, ultimately diagnosed as KD. He showed a partial response to the initial systemic corticosteroid therapy. However, after tapering the dosage of corticosteroids, the patient’s symptoms did not improve, even with combined mycophenolate mofetil therapy. His symptoms worsened significantly after he discontinued treatment. Therefore, treatment with dupilumab was initiated at 600 mg, followed by 300 mg every two weeks. At week 20, the treatment was adjusted to 300 mg every four weeks for a duration of 32 weeks. The mass gradually reduced in size, accompanied by a progressive decrease in both the eosinophil count and IgE levels. These results show the significant efficacy of dupilumab in the management of KD.

## Linked entities

- **Chemicals:** mycophenolate mofetil (PubChem CID 5281078)
- **Diseases:** Kimura disease (MONDO:0018830)

## Full-text entities

- **Genes:** FCER1A (Fc epsilon receptor Ia) [NCBI Gene 2205] {aka FCE1A, FCERIA, FcERI}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, IL5RA (interleukin 5 receptor subunit alpha) [NCBI Gene 3568] {aka CD125, CDw125, HSIL5R3, IL5R}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, KRT20 (keratin 20) [NCBI Gene 54474] {aka CD20, CK-20, CK20, K20, KRT21}
- **Diseases:** ALHE (MESH:D000796), toxicity (MESH:D064420), subcutaneous (MESH:D013352), renal involvement (MESH:C565423), osteoporosis (MESH:D010024), leukemia (MESH:D007938), parotid gland swelling (MESH:D010309), atopic dermatitis (MESH:D003876), lymphoma (MESH:D008223), benign lymphoproliferative disorder (MESH:D008232), peripheral lymphadenopathy (MESH:D010523), KD (MESH:D009080), lymphatic granuloma (MESH:D006099), tuberculosis (MESH:D014376), allergic reactions (MESH:D004342), blood eosinophilia (MESH:D004802), inflammation (MESH:D007249), fibrosis (MESH:D005355), lymphadenopathy (MESH:D008206), KD (MESH:D000082242)
- **Chemicals:** Rituximab (MESH:D000069283), cefuroxime (MESH:D002444), Dupilumab (MESH:C582203), Omalizumab (MESH:D000069444), mepolizumab (MESH:C434107), mycophenolate mofetil (MESH:D009173), benralizumab (MESH:C571386), methyl-prednisolone (MESH:D008775), ribavirin (MESH:D012254)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12950764/full.md

## References

31 references — full list in the complete paper: https://tomesphere.com/paper/PMC12950764/full.md

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Source: https://tomesphere.com/paper/PMC12950764