Vitelliform maculopathy: Diverse etiologies originating from one common pathway.

Area of Science:

• Ophthalmology
• Retinal Diseases
• Cell Biology

Background:

• Vitelliform lesions (VLs) are hallmarks of various macular disorders.
• They stem from a common pathway: impaired retinal pigment epithelium (RPE) function and phagocytosis.
• VLs manifest as yellowish subretinal material accumulation.

Purpose of the Study:

• To summarize the nature, pathogenesis, imaging, etiologies, and natural course of vitelliform maculopathies.
• To highlight the unifying role of RPE phagocytic dysfunction in VL development.
• To discuss the clinical implications of VLs in both younger and older patients.

Main Methods:

• Review of histopathological studies.
• Analysis of multimodal advanced retinal imaging (OCT, fundus autofluorescence).
• Synthesis of clinical data on genetic and acquired causes of VLs.

Main Results:

• VLs are characterized by subretinal hyperreflectivity (OCT) and hyperautofluorescence (FAF).
• Causes include genetic (Best disease, pattern dystrophy) and acquired (tractional, toxic) disorders.
• Visual morbidity is primarily due to macular atrophy and neovascularization.

Conclusions:

• Impaired RPE phagocytosis is the central mechanism in vitelliform maculopathy.
• Understanding VL pathogenesis aids in diagnosing and managing these conditions.
• Multimodal imaging is crucial for characterizing VLs and their underlying causes.