Purpose 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. Methods 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. Results 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. Conclusion 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.

Purpose To analyse structural (OCT), microvascular (OCTA), and functional changes (BCVA, mfERG) associated with fovea plana and to compare it to healthy controls. Methods A retrospective observational study was performed on 13 patients (26 eyes; aged 34.46 y ± 20.26) with a clinical picture of fovea plana and 15 controls (30 eyes; aged: 41.47 y ± 14.03). Results In fovea plana, BCVA ranged from 0.25 to 1.0, with a spherical error of − 5.5 to + 18.0 dpt. Posterior segment changes included elevated papillomacular retinal fold, uveal effusion syndrome, crowded optic discs, and hypopigmented fundus. OCTA imaging of the superficial (FAZ-S), intermediate (FAZ-I), and deep foveal avascular zone (FAZ-D) confirmed absence of foveal avascular zone (FAZ-S in 13 eyes, FAZ-I in 21 eyes, and FAZ-D in 10 eyes). Fovea plana patients had a significantly smaller FAZ-S, FAZ-I, and FAZ-D than controls (p < 0.001). Within the fovea plana group, a smaller FAZ-S correlated with reduced BCVA (p = 0.004) and with reduced mfERGs in zones 1 and 2 (p = 0.001 and p = 0.017). Also, a smaller FAZ-D showed positive correlations with the mfERG, with statistically significant values in zones 1 and 2 (p = 0.003 and p = 0.017). Conclusion In conclusion, our results confirm an altered structural, microvascular, and functional pattern in patients with a clinical picture of fovea plana. As documented by the functional microvascular interactions in our study, the developmental arrest in foveation reflects the functional maturation by means of visual acuity and central retinal function.

▶ Fig. 4 OCT segmentation of the macula and optic disc OS, showing reduced thickness of the ganglion cell layer in the superotemporal area around the fovea, a month after the acute event.