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Related Experiment Video

Updated: Oct 1, 2025

Primed Mycobacterial Uveitis PMU as a Model for Post-Infectious Uveitis

Primed Mycobacterial Uveitis PMU as a Model for Post-Infectious Uveitis

Published on: December 17, 2021

Brentuximab vedotin induced uveitis.

Stijn Therssen^1,2, Stef Meers³, Julie Jacob^1,4

¹University Hospitals Leuven, Herestraat 49, 3000, Leuven, Belgium.

American Journal of Ophthalmology Case Reports

|March 4, 2022

Summary

This summary is machine-generated.

Brentuximab vedotin (BV) can cause Vogt-Koyanagi-Harada (VKH)-like uveitis in classical Hodgkin lymphoma (CHL) patients. This adverse event may be linked to immune system changes induced by BV therapy.

Keywords:

Adcetris, CAS 914088-09-8 Drug-related side effects and adverse reactions Hodgkin disease Immunotoxins Vogt-koyanagi-harada disease/syndrome brentuximab vedotin

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Last Updated: Oct 1, 2025

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Area of Science:

Ophthalmology
Oncology
Immunology

Background:

Brentuximab vedotin (BV) is a CD30-targeted immunotherapy used for classical Hodgkin lymphoma (CHL).
Uveitis, particularly Vogt-Koyanagi-Harada (VKH) disease, involves inflammation of the uveal tract.
The role of CD30-expressing cells in ocular immunity is not fully understood.

Observation:

A patient with CHL developed bilateral panuveitis with VKH-like features after BV administration.
Ocular findings included anterior and posterior segment inflammation, serous optic disc detachments, RPE folds, and characteristic angiographic patterns.
No systemic features of VKH disease were present, and other causes were excluded.

Findings:

The uveitis responded to corticosteroid treatment and BV cessation.
Recurrence of uveitis upon BV reinitiation strongly suggested a drug-induced adverse event.
The Naranjo algorithm indicated a probable adverse drug reaction to brentuximab vedotin.

Implications:

Brentuximab vedotin may induce a VKH-like uveitis through disruption of CD30+ cells in the uveal tract.
Clinicians should be aware of this potential ocular side effect of BV therapy.
Further research into immunotherapy-induced immune mechanisms is crucial for understanding and managing such events.