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March 21, 2026BMC Ophthalmology2 citationsOpen Access

Tislelizumab-induced Vogt-Koyanagi-Harada-like uveitis: a case report

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YZYunyun ZhouXLXiaoqin LeiWMWeimei Ma

Key Points

  • To report a case of uveitis resembling Vogt-Koyanagi-Harada syndrome following treatment with tislelizumab.
  • Descriptive case report detailing clinical observations and symptoms.
  • Assessment of clinical history in relation to tislelizumab administration.
  • Monitoring symptoms and responses to treatment.
  • Patient developed uveitis symptoms after initiation of tislelizumab treatment.
  • Symptoms aligned with Vogt-Koyanagi-Harada characteristics, including visual changes.
  • Treatment adjustments led to resolution of uveitis symptoms.

Abstract

Background While immune checkpoint inhibitors like the anti-PD-1 agent tislelizumab have revolutionized the treatment of cancer, they pose a risk of immune-related adverse events (irAEs). Vogt-Koyanagi-Harada (VKH)-like uveitis is a rare, vision-threatening ocular irAE that poses significant diagnostic and therapeutic challenges, often mimicking its idiopathic counterpart. Case presentation Following ten cycles of adjuvant tislelizumab treatment, a 52-year-old female with a past medical history of esophageal cancer presented with acute monocular vision loss. Comprehensive ophthalmic evaluation revealed left optic disc edema, exudative retinal detachment, and characteristic serous retinal detachments on optical coherence tomography (OCT). Extensive systemic workup excluded infectious, neoplastic, and primary autoimmune etiologies. Notably, cerebrospinal fluid (CSF) analysis revealed a lymphocyte-dominant profile but no pleocytosis, a finding atypical for classic VKH disease. The uveitis responded markedly to systemic corticosteroid pulse therapy but flared unequivocally upon two subsequent tislelizumab infusions, establishing a clear drug-effect temporal relationship. After completing the planned 12 cycles of tislelizumab alongside a prolonged, carefully tapered oral corticosteroid regimen, the patient’s ocular inflammation resolved completely. At one-year follow-up, visual acuity remained stable with no recurrence, demonstrating sustained remission after cessation of the inciting agent. Conclusion This case strongly implicates tislelizumab as a trigger for VKH-like uveitis and highlights two critical learning points: the potential lack of CSF pleocytosis as a differentiating feature from primary VKH, and the risk of recurrence upon drug rechallenge. It underscores the necessity for close collaboration between oncologists and ophthalmologists to navigate the dual imperatives of cancer control and vision preservation. Clinical trial number Not applicable.

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Cite This Study

Zhou et al. (2026) studied this question.

synapsesocial.com/papers/69be37726e48c4981c67725ahttps://doi.org/10.1186/s12886-026-04743-7
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Also Consider

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  3. 3PD0325901, a Mitogen-Activated Protein Kinase Kinase Inhibitor, Produces Ocular Toxicity in a Rabbit Animal Model of Retinal Vein Occlusion2009 · 93 citations
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