[Pathogenesis of macular edema associated with branch retinal vein occlusion and strategy for treatment]

Hidetaka Noma1, Hideharu Funatsu, Seiyo Harino

  • 1Department of Ophthalmology, Yachiyo Medical Center, Tokyo Women's Medical University, 477-96 Owada-shinden, Yachiyo-shi, Chiba-ken 276-8524, Japan. nomahide@tymc.twmu.ac.jp

We summarize the pathogenesis and the treatment strategy for macular edema in patients with branch retinal vein occlusion (BRVO), focusing on the role of the cytokines. Various cytokines are involved in the pathogenesis of macular edema associated with BRVO. When BRVO occurs, it leads to retinal ischemia that induces the production of cytokines such as vascular endothelial growth factor (VEGF) by retinal cells such as glial cells and vascular endothelial cells in the occluded region affected by anoxia. These cytokines interact with each other (cytokine network) and this results in impairment of the blood-retinal barrier and an increase of vascular permeability, considered important in the development of macular edema associated with BRVO. Treatment for this condition includes triamcinolone acetonide, anti-VEGF antibody, laser therapy and vitrectomy, all of which lead to the suppression of cytokine production. To manage macular edema associated with BRVO, it is important to control cytokine production with a combination of treatments.

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