FGFR Inhibitors in Metastatic Urothelial Cancer and the Management of Ocular Toxicity

Arlene O. Siefker-Radtke, MD: Central serous retinopathy is 1 of those novel eye toxicities that we see with FGF-targeted therapy. And it’s estimated to occur in 25% of patients receiving that FGF-targeted agent. It’s thought to be because of inhibition through the MAP and MEK kinase pathways. It’s been seen with other MEK inhibitors, and some have decided or thought maybe we should call it MEK-associated retinopathy because it’s a little different compared with the typical serous retinopathy associated with diabetes. When it happens, it usually it’s early within the first 4 to 6 months of treatment. It rarely occurs after that period.

Ophthalmologic testing at baseline and then monthly intervals for the first 4 months has been suggested, including vision testing and optical coherence tomography, which helps look at the retinal layer for any thickening along the retina. If a patient does experience an adverse effect, they usually report blurry vision. It’s important to distinguish that blurred vision from the intermittent blurred vision from dry eyes and mucous that may go across the cornea. I usually tell patients to blink, and if it goes away, it’s probably not retinopathy. But if they have blurred vision—persistent wavy lines on the Amsler grid testing—then they should hold treatment and see the ophthalmologist every 2 weeks.

Once their symptoms have resolved back to their normal vision, they can resume erdafitinib or theirFGF-targeted agent at a dose-level reduction. Managing these toxicities becomes very important and very helpful in keeping patients on therapy longer. I’ll be honest: I think ofFGF inhibition as an induction/maintenance strategy. Using the higher dose up front to induce a better and perhaps deeper response, but then we can control the response, even if we need to dose reduce it down to 8 or 6 mg daily. The ability to manage toxicity can be very helpful.

Transcript edited for clarity.