Generalised granuloma annulare following ustekinumab therapy for palmoplantar psoriasis

We report the case of a woman in her 70s who developed generalised granuloma annulare (GA) after 3 years of successful ustekinumab therapy for severe palmoplantar psoriasis. Ustekinumab, an interleukin (IL)-12/23 inhibitor, was ceased as the most likely trigger. GA remained persistent despite multiple treatments but resolved gradually over 5 years. This resolution was followed by a severe flare of her psoriasis, requiring initiation of guselkumab, an IL-23 inhibitor. This case illustrates a probable paradoxical T-helper (Th)1-mediated granulomatous reaction to ustekinumab, likely due to immune dysregulation between Th1 and Th17 pathways. It adds to the limited but growing body of evidence suggesting ustekinumab may trigger delayed granulomatous inflammation via phenotypic switching, including GA. Clinicians should be aware of this potential complication, even after long-term stable use of ustekinumab. Managing biologically induced paradoxical inflammation is complex and may require switching to an alternative biological agent, particularly when cessation leads to rebound flare of the underlying condition.

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Publication Details

Journal
BMJ Case Reports
Published
2025-12-01
DOI
https://doi.org/10.1136/bcr-2025-268668
Citations
1
Primary Topic
Skin Diseases and Diabetes
Type
article
Field-Weighted Citation Impact
2.00
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article

Generalised granuloma annulare following ustekinumab therapy for palmoplantar psoriasis

Jenny Nicolopoulos, Con Dolianitis, Samuel Morriss
1 citations
BMJ Case Reports
Skin Diseases and Diabetes
2.00
article

Generalised granuloma annulare following ustekinumab therapy for palmoplantar psoriasis

Jenny Nicolopoulos, Con Dolianitis, Samuel Morriss
article en
1 citations

Abstract

We report the case of a woman in her 70s who developed generalised granuloma annulare (GA) after 3 years of successful ustekinumab therapy for severe palmoplantar psoriasis. Ustekinumab, an interleukin (IL)-12/23 inhibitor, was ceased as the most likely trigger. GA remained persistent despite multiple treatments but resolved gradually over 5 years. This resolution was followed by a severe flare of her psoriasis, requiring initiation of guselkumab, an IL-23 inhibitor. This case illustrates a probable paradoxical T-helper (Th)1-mediated granulomatous reaction to ustekinumab, likely due to immune dysregulation between Th1 and Th17 pathways. It adds to the limited but growing body of evidence suggesting ustekinumab may trigger delayed granulomatous inflammation via phenotypic switching, including GA. Clinicians should be aware of this potential complication, even after long-term stable use of ustekinumab. Managing biologically induced paradoxical inflammation is complex and may require switching to an alternative biological agent, particularly when cessation leads to rebound flare of the underlying condition.

BMJ Case ReportsVol. 18(12)
The Royal Melbourne Hospital (AU)
Good health and well-being
Openalex Percentile: Top 9%
Skin Diseases and Diabetes
2.00
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