Patients with carcinomas often share symptoms of vision
deterioration as part of paraneoplastic retinopathy (PNR), based on
a cross-reaction between antigens expressed by the underlying tumor
and retinal proteins. However, some of the underlying symptoms may
be explained by a drug-induced toxicity. The application of new
therapeutic strategies with mitogen-activated protein kinase (MEK)
and fibroblast growth factor receptor (FGFR) inhibitors in advanced
cancers are still under evaluation for safety and tolerability, but
also for dose-limiting toxicities. In the presented data, we
identified a drug-induced pseudo-central serous chorioretinopathy
(pCSC) to be the reason for central vision deterioration.
A retrospective, observational, case-controlled study included seven
patients receiving MEK and six patients receiving FGFR inhibitor
treatment for bronchopulmonal cancer. We compared the clinical and
diagnostic pictures of pCSC patients with that of 50 CSC patients
(100 eyes) and 7 patients (14 eyes) with PNR. The activity of pCSC
was assessed by clinical examination, supported by multimodal
imaging. The relationships between clinical symptomatology and
systemic disease activity were evaluated.
Three out of thirteen patients (23.1%) showed signs of pCSC (one
FGFR and two MEK inhibitor patients). All three pCSC patients showed
central bilateral detachment of the neurosensory retina on OCT
imaging, but also paracentral multifocal lesions in the second
subject. Compared to our CSC and PNR patients, the lesions in pCSC
patients showed no lipofuscin irregularities on FAF. With reduction
of the MEK treatment, the lesions on one MEK subject disappeared and
BCVA restored to 0.8. In one MEK- and the FGFR subject, the lesions
reduced in size without therapy discontinuation.
Based on our data, MEK and FGFR inhibitor-associated pCSC is a mild,
self-limited retinopathy that seems to disappear simultaneously or
shortly after discontinuation of medication, with subsequent
restoration of the central visual function.