黄斑维塔病变（VLs）与多种黄斑疾病有关，但其共同的病理机制是视网膜色素上皮（RPE）受损和吞噬功能障碍。 VLs由黄色亚视网膜物质的堆积定义。在多模式先进的视网膜成像时代，VLs可以通过光学相干断层扫描下的亚视网膜超反射和通过荧光素自发荧光检查下的高自发荧光进一步表征。 VLs可能是遗传性或获得性视网膜疾病的结果。在年轻患者中，VLs通常发生在Best病的情况下。 VL的其他遗传原因包括形态畸形或成人发病的黄斑维塔状肌营养不良症。在老年患者中，获得性VLs可以与牵引性、旁肿瘤性、毒性和退行性疾病的广泛谱系有关。 VLs眼中的视觉不适主要是因为黄斑萎缩和黄斑新生血管的发生导致的。组织病理学研究提供了有关维塔样物质（由黑色素体，脂色素，黑色素脂色素和位于RPE和感光细胞层之间的外段残留物组成）的位置，性质和生命周期的新见解。视网膜上皮细胞的吞噬功能受损是导致VL发展的统一机制。我们讨论和总结了维塔样黄斑病变的性质，发病机制，多模式成像特征，病因和自然病程。由Elsevier Inc.发表

Vitelliform lesions (VLs) are associated with a wide array of macular disorders but are the result of one common pathway: retinal pigment epithelium (RPE) impairment and phagocytic dysfunction. VLs are defined by the accumulation of yellowish subretinal material. In the era of multimodal advanced retinal imaging, VLs can be further characterized by subretinal hyperreflectivity with optical coherence tomography and hyperautofluorescence with fundus autofluorescence. VLs can be the result of genetic or acquired retinal diseases. In younger patients, VLs usually occur in the setting of Best disease. Additional genetic causes of VL include pattern dystrophy or adult-onset vitelliform macular dystrophy. In older patients, acquired VLs can be associated with a broad spectrum of etiologies, including tractional, paraneoplastic, toxic, and degenerative disorders. The main cause of visual morbidity in eyes with VLs is the onset of macular atrophy and macular neovascularization. Histopathological studies have provided new insights into the location, nature, and lifecycle of the vitelliform material comprised of melanosomes, lipofuscin, melanolipofuscin, and outer segment debris located between the RPE and photoreceptor layer. Impaired phagocytosis by the RPE cells is the unifying pathway leading to VL development. We discuss and summarize the nature, pathogenesis, multimodal imaging characteristics, etiologies, and natural course of vitelliform maculopathies.Published by Elsevier Inc.