scholarly journals Intravitreal Aflibercept Injection and Treatment Regimens in Macular Edema due to Branch Retinal Vein Occlusion

2019 ◽  
pp. 92-98
Keyword(s):  
Growth Factor ◽  
Macular Edema ◽  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Vascular Endothelial ◽  
Treatment Regimens ◽  
Vein Occlusion ◽  
Anti Vegf ◽  
Intravitreal Aflibercept ◽  
Endothelial Growth Factor

Branch retinal vein occlusion (BRVO) is the most common form of retinal vein occlusions (RVO), which is the second most common retinal vascular disease after diabetic retinopathy. The most common cause of visual loss in BRVO is macular edema. Since the vascular endothelial growth factor (VEGF) was detected in the pathogenesis of macular edema due to BRVO, studies have been made with available anti-VEGF agents and different treatment regimens. Those treatment regimens can be listed as; monthly / bi-monthly fixed interval, as needed (Pro Re Nata; PRN), treat and extend (T&E). Aflibercept acts as a decoy receptor that binds to VEGF-A, VEGF-B, and placental growth factor. There are publications indicating that this agent binds VEGF with a higher affinity than other anti-VEGF agents and thus provides a longer treatment efficacy. This review summarizes the studies about the use of aflibercept in different regimens for the treatment of macular edema due to BRVO.

Change of cytokines after intravitreal ranibizumab in patients with recurrent branch retinal vein occlusion and macular edema

2019 ◽  
pp. 112067211988505 ◽  
Author(s):  
Hidetaka Noma ◽  
Kanako Yasuda ◽  
Masahiko Shimura
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Macular Edema ◽  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Intravitreal Ranibizumab ◽  
Vein Occlusion ◽  
Endothelial Growth Factor

Purpose: To investigate the relations of vascular endothelial growth factor, growth factors, soluble vascular endothelial growth factor receptors, and inflammatory factors to recurrence of macular edema after anti-vascular endothelial growth factor therapy in patients with branch retinal vein occlusion. Methods: This study retrospectively investigated 17 patients with branch retinal vein occlusion who received intravitreal ranibizumab injection three times within 6 months for recurrent macular edema. Aqueous humor samples were obtained from these patients at every recurrence. Levels of soluble vascular endothelial growth factor receptor-1, soluble vascular endothelial growth factor receptor-2, vascular endothelial growth factor, placental growth factor, platelet-derived growth factor-AA, soluble intercellular adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-6, interleukin-8, interleukin-12(p70), and interleukin-13 were measured by the suspension array method. Aqueous flare values were measured with a laser flare meter and central macular thickness was determined by optical coherence tomography. Results: Mean best-corrected visual acuity and central macular thickness improved significantly over time after intravitreal ranibizumab injection, but the aqueous flare value at recurrence after intravitreal ranibizumab injection showed no significant change compared with baseline. Aqueous humor levels of soluble vascular endothelial growth factor receptor-1, soluble vascular endothelial growth factor receptor-2, vascular endothelial growth factor, platelet-derived growth factor-AA, monocyte chemoattractant protein-1, and interleukin-8 decreased significantly over time after intravitreal ranibizumab injection. However, there were no significant changes of the other five factors/cytokines (placental growth factor, soluble intercellular adhesion molecule-1, interleukin-6, interleukin-12, and interleukin-13) at recurrence after intravitreal ranibizumab injection compared with baseline. Conclusion: These findings suggest that persistent inflammation may influence the recurrence of macular edema in branch retinal vein occlusion patients, and that adding steroid therapy might be an effective strategy for preventing recurrence.

scholarly journals Cytokines and the Pathogenesis of Macular Edema in Branch Retinal Vein Occlusion

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Hidetaka Noma ◽  
Kanako Yasuda ◽  
Masahiko Shimura
Keyword(s):  
Macular Edema ◽  
Retinal Vein Occlusion ◽  
Branch Retinal Vein Occlusion ◽  
Vascular Endothelial ◽  
Intraocular Injection ◽  
Vein Occlusion ◽  
Anti Vegf ◽  
Lifestyle Related Diseases ◽  
Endothelial Growth Factor

Branch retinal vein occlusion (BRVO) is a very common retinal vascular problem in patients with lifestyle-related diseases, such as hypertension and arteriosclerosis. In patients with BRVO, development of macular edema is the main cause of visual impairment. BRVO is still a controversial condition in many respects. Over the years, various methods such as laser photocoagulation have been tried to treat macular edema associated with BRVO, but the results were not satisfactory. After vascular endothelial growth factor (VEGF) was found to have an important role in the pathogenesis of macular edema in BRVO patients, treatment of this condition was revolutionized by development of anti-VEGF therapy. Although macular edema improves dramatically following intraocular injection of anti-VEGF agents, repeated recurrence and resistance of edema is a major problem in some BRVO patients. This suggests that factors or cytokines other than VEGF may be associated with inflammation and retinal hypoxia in BRVO and that the pathogenesis of macular edema is complicated. The present review assesses the role of various factors and cytokines in the pathogenesis of macular edema associated with BRVO. We present a mechanism that is not only plausible but should also be useful for developing new therapeutic strategies.

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