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

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.

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.

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.

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