# Successful Treatment of Adalimumab-Induced Pustular Psoriasis With Guselkumab in a Patient With Hidradenitis Suppurativa

**Authors:** Kostandin Valle, Divya Pothuri, Travis Jackson, Ashley M Jenkins

PMC · DOI: 10.7759/cureus.84626 · 2025-05-22

## TL;DR

A patient with hidradenitis suppurativa developed pustular psoriasis after adalimumab treatment but improved significantly with guselkumab.

## Contribution

Demonstrates successful treatment of adalimumab-induced pustular psoriasis using guselkumab, an IL-23 inhibitor.

## Key findings

- Adalimumab therapy led to a diffuse pustular rash in a patient with hidradenitis suppurativa.
- Switching to guselkumab resulted in significant improvement within a week and continued resolution at follow-up.
- TNF-alpha inhibitors may cause pustular psoriasis, and IL-23 inhibitors like guselkumab may be a better alternative.

## Abstract

Pustular psoriasis is a rare and severe form of psoriasis, characterized by the presence of desquamative plaques with pustules on an erythematous base. Psoriasis is thought to result from plasmacytoid dendritic cell (PDC)-mediated T-cell activation, which stimulates keratinocyte proliferation via type 1 interferon signaling. Studies suggest that TNF-alpha inhibition can paradoxically enhance interferon-alpha activity, leading to the development of pustular psoriasis in some cases. A 58-year-old patient with hidradenitis suppurativa began adalimumab therapy. One month later, she presented with a diffuse pustular rash. A punch biopsy revealed pustular psoriasis with negative direct immunofluorescence (DIF) and periodic acid-Schiff (PAS) stain. Despite treatment with topical steroids, the rash worsened. Her therapy was switched to guselkumab, alongside continued topical steroids. This resulted in significant improvement within a week, with continued resolution at the one-month follow-up. Psoriasis and hidradenitis suppurativa are driven by chronic inflammation involving TNF-alpha and the IL-23/IL-17 axis. While TNF-alpha inhibitors like adalimumab reduce inflammation, paradoxical reactions like pustular psoriasis can occur due to enhanced interferon-alpha activity. In patients on this therapy who develop a new-onset diffuse pustular rash, an index of suspicion for this condition should be maintained. TNF-alpha inhibitors should be discontinued if pustular psoriasis develops, with IL-23 inhibitors providing a viable alternative.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IL37 (interleukin 37), IL17A (interleukin 17A)
- **Diseases:** pustular psoriasis (MONDO:0022205), hidradenitis suppurativa (MONDO:0006559)

## Full-text entities

- **Genes:** IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** Psoriasis (MESH:D011565), pustular rash (MESH:D005076), Hidradenitis Suppurativa (MESH:D017497), inflammation (MESH:D007249)
- **Chemicals:** Guselkumab (MESH:C000588857), steroids (MESH:D013256), Adalimumab (MESH:D000068879)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12182880/full.md

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Source: https://tomesphere.com/paper/PMC12182880