# Crisaborole as a Potential Treatment for Pediatric Alopecia Areata: A Case Report and Literature Review

**Authors:** Qiannan Xu

PMC · DOI: 10.7759/cureus.102854 · Cureus · 2026-02-02

## TL;DR

A 10-year-old girl with hair loss showed significant regrowth after using crisaborole, a non-corticosteroid treatment, suggesting it could be a safer option for children.

## Contribution

This case report explores crisaborole as a novel, non-corticosteroid treatment for pediatric alopecia areata.

## Key findings

- A 10-year-old patient showed significant hair regrowth after two weeks of crisaborole treatment.
- Follow-up at three months confirmed full hair regrowth with no corticosteroid-related side effects.
- Crisaborole may work by reducing inflammation and improving hair follicle blood flow and stem cell activity.

## Abstract

Alopecia areata (AA) is an autoimmune disorder that causes non-scarring hair loss, often affecting pediatric patients, where it can significantly impact both psychological well-being and quality of life. While corticosteroids and other systemic therapies are commonly used to treat AA, their side effects, especially in children, highlight the need for safer alternatives. This case report evaluates the use of crisaborole, a topical phosphodiesterase 4 (PDE4) inhibitor, as a potential treatment for pediatric AA. A 10-year-old female patient, who initially presented with a small patch of hair loss and failed to respond to topical corticosteroid therapy, was switched to crisaborole after concerns about corticosteroid-related side effects. After two weeks of treatment, significant hair regrowth was observed, and a follow-up at three months confirmed full regrowth. The mechanisms through which crisaborole may benefit AA include modulation of inflammation, improvement in blood flow to hair follicles, and promotion of follicular stem cell activity. Crisaborole's safety profile, with minimal systemic absorption, makes it a promising non-corticosteroidal alternative for pediatric patients. This case suggests that crisaborole may be an effective treatment for pediatric AA, but further studies with larger sample sizes and longer follow-up periods are needed to validate these findings.

## Linked entities

- **Chemicals:** crisaborole (PubChem CID 44591583)
- **Diseases:** alopecia areata (MONDO:0004907)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CCL20 (C-C motif chemokine ligand 20) [NCBI Gene 6364] {aka CKb4, Exodus, LARC, MIP-3-alpha, MIP-3a, MIP3A}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, PDE4A (phosphodiesterase 4A) [NCBI Gene 5141] {aka DPDE2, PDE4, PDE46}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}
- **Diseases:** vitiligo (MESH:D014820), anxiety (MESH:D001007), skin atrophy (MESH:D001284), adrenal suppression (MESH:D000310), scalp pain (MESH:D010146), growth retardation (MESH:D006130), Inflammation (MESH:D007249), telangiectasia (MESH:D013684), pruritus (MESH:D011537), ischemia (MESH:D007511), psoriasis (MESH:D011565), alopecia (MESH:D000505), autoimmune (MESH:D001327), infection (MESH:D007239), autoimmune or endocrine disorders (MESH:D004700), rheumatoid arthritis (MESH:D001172), AA (MESH:D000506), immune dysregulation (OMIM:614878), atopic dermatitis (MESH:D003876), erythema (MESH:D004890), thyroid disease (MESH:D013959), skin thinning (MESH:D013851)
- **Chemicals:** cAMP (MESH:D000242), mometasone (MESH:D000068656), corticosteroidal (-), Crisaborole (MESH:C543085), steroid (MESH:D013256)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

21 references — full list in the complete paper: https://tomesphere.com/paper/PMC12960067/full.md

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Source: https://tomesphere.com/paper/PMC12960067