Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Clin Cases. May 26, 2026; 14(15): 120825
Published online May 26, 2026. doi: 10.12998/wjcc.v14.i15.120825
Published online May 26, 2026. doi: 10.12998/wjcc.v14.i15.120825
Kaposi sarcoma following dupilumab treatment for bullous pemphigoid: A case report and review of literature
Sheng-Nan Wang, Jin-Meng Wang, Mian Xu, Jing-Jing Wu, Department of Dermatology, Wenzhou Central Hospital, Wenzhou 325000, Zhejiang Province, China
Author contributions: Wang SN, Wang JM, Xu M, and Wu JJ designed the study and performed the data acquisition, analysis, and interpretation, performed critical revision of the manuscript for important intellectual content; Wang SN and Wu JJ wrote the manuscript; all authors have read and approved the submitted version.
Informed consent statement: Informed written consent was obtained from the patient for publication of this report and any accompanying images.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Corresponding author: Jing-Jing Wu, MD, Department of Dermatology, Wenzhou Central Hospital, No. 252 Baili East Road, Lucheng District, Wenzhou 325000, Zhejiang Province, China. 359680756@qq.com
Received: March 12, 2026
Revised: April 1, 2026
Accepted: April 22, 2026
Published online: May 26, 2026
Processing time: 61 Days and 19.6 Hours
Revised: April 1, 2026
Accepted: April 22, 2026
Published online: May 26, 2026
Processing time: 61 Days and 19.6 Hours
Core Tip
Core Tip: Dupilumab was used to treat bullous pemphigoid (BP) complicated with Kaposi sarcoma (KS). The causes were analyzed, and the immune drift induction hypothesis was proposed. STAT3 plays a key role in KS pathogenesis, as it supports human herpesvirus-8 latency and viral replication. It can be activated by virally encoded interleukin-6 via gp130 receptor signaling to promote the survival and proliferation of infected cells. Dupilumab-induced immune deviation (toward Th1/Th17/Th22 pathways) and STAT3 signaling activation may contribute to KS occurrence in susceptible BP patients. Further investigation is needed.