VOGT-KOYANAGI-HARADA DISEASE-LIKE UVEITIS IN A PATIENT WITH ADVANCED MELANOMA TREATED BY SEQUENTIAL ADMINISTRATION OF NIVOLUMAB AND DABRAFENIB/TRAMETINIB THERAPY.

Autor:	Madoe A; Department of Ophthalmology, University Hospital of Leuven, Leuven, Belgium., Schauwvlieghe PP; Department of Ophthalmology, University Hospital of Leuven/Middelheim Hospital in Antwerp, Leuven, Belgium; and., Jacob J; Department of Ophthalmology, University Hospital of Leuven, Leuven, Belgium.
Jazyk:	angličtina
Zdroj:	Retinal cases & brief reports [Retin Cases Brief Rep] 2023 Sep 01; Vol. 17 (5), pp. 611-615.
DOI:	10.1097/ICB.0000000000001251
Abstrakt:	Purpose: To describe a case of bilateral Vogt-Koyanagi-Harada (VKH)-like uveitis during treatment with dabrafenib and trametinib and three months after discontinuation of nivolumab for malignant melanoma, and discuss the possible (synergistic) role(s) of mitogen-activated protein kinase (MAPK) inhibitors and immune checkpoint inhibitors in its pathophysiology. Methods: Retrospective case report with fluorescein angiography and optical coherence tomography. Results: A 55-year old patient with metastatic melanoma presented with a complaint of gradually worsening blurry vision in the right eye during treatment with dabrafenib and trametinib, three months after discontinuation of nivolumab. Based on the clinical examination, optical coherence tomography and fluorescein angiography findings, and a thorough laboratory work-up, he was diagnosed with a bilateral VKH-like uveitis without extraocular manifestations. The uveitis responded well to oral corticosteroids. Conclusion: Vogt-Koyanagi-Harada-like uveitis is a rare adverse effect of MAPK inhibitors and immune checkpoint inhibitors. Similar pathogenetic mechanisms including a drug-induced autoimmunity targeted against benign and malignant melanocytes may underlie MAPK inhibitor-induced and immune checkpoint inhibitors-induced VKH-like uveitis. In our report, the patient developed a VKH-like uveitis during MAPK inhibition therapy, four months after discontinuation of nivolumab. It is difficult to delineate whether MAPK inhibition alone was responsible for this adverse effect, or whether, on the contrary, potentiation occurred as a result of immune modulation by previous treatment with an immune checkpoint inhibitor. Further cases are needed to further clarify this latter hypothesis.
Databáze:	MEDLINE
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