Choroidal vasculature analysis in MEK inhibitor-associated retinopathy

Abstract

Purpose: To evaluate choroidal vascularity index (CVI) in patients developing mitogen-activated protein kinase kinase (MEK) inhibitor-associated retinopathy (MEKAR).

Methods: In this prospective observational study, extensive ophthalmic examination was performed, including enhanced-depth-imaging-optical coherence tomography (EDI-OCT). EDI-OCT scans of patients receiving Cobimetinib, taken at baseline and at MEKAR manifestation, were considered for choroid analysis. Choroidal thickness (CT) was measured on high-resolution b-scans passing through the fovea at three different locations. Same scans were therefore imported for binarization into a previously reported software and CVI was calculated as the ratio of luminal area (LA) to total choroid area (TCA).

Results: When compared to baseline, eyes with MEKAR (14 eyes) did not show significative CT variation in subfoveal region (p = 0,57), 750-µm-nasal to the fovea (p = 0,08) and 750-µm-temporal to the fovea (p = 0,07). Similarly, there were no statistically significant differences for TCA (p = 0.54), LA (p = 0.85), stromal area (SA) (p = 0.13), LA/SA (p = 0.34) and CVI (p = 0.47). Best-corrected visual acuity was significantly reduced at fluid accumulation when compared to baseline values (p = 0.03), with complete recovery after fluid resolution (p = 0.73).

Conclusion: Multiple parameters reflecting the status of the choroid seemed not influenced by Cobimetinib administration. Retinal pigment epithelium toxic disfunction likely represents the crucial step in MEKAR pathogenesis.

Keywords: MEK inhibitor-associated retinopathy; choroid; choroidal vascularity index; retinal toxicity; serous retinopathy.