scholarly journals Сlinical analysis of the series of A-VEGF therapy in patients with retinal pigment epithelium tear complicating of wet form age-related macular degeneration

Author(s):  
E.V. Kozina ◽  
◽  
S.N. Sakhnov ◽  
V.V. Myasnikova ◽  
E.V. Bykova ◽  
...  

Purpose. Analysis A-VEGF therapy for wet form age-related macular degeneration (AMD) complicated by retinal pigment epithelium tear (RPET), different in involvement of macular zone (MZ), with different time of RPET regarding A-VEGF therapy. Material and methods. The results of treatment 18 patients with wet AMD complicated by RPET during monthly A-VEGF injection were analyzed. In first group (10 eyes) – RPET occurred before treatment, the second (8 eyes) – RPET arisen during A-VEGF. Visometry, ophthalmoscopy, fundus photoregistration, MZ OCT before and in month after each injection. Age – 65–83 years. Results. RPET (1,5 DD) captured fovea in 7 first group patients, in 3 patients RPET (0,5 DD) didn't affect fovea, In macula registered subretinal fluid (SRF) and hemorrhage (SRH). After 2 A-VEGF injections, resorption of SRF and SRH was observed. VA increased from 0,2 to 0,7 in cases RPET without capture of the fovea. RPET involving fovea occurred in 8 patients of the second group after the first A-VEGF injection. SRH and SRF resorbed. VA of patients decreased from 0,7 to 0,15. In both groups relapses of the SRF in macula after the development of RPET were not observed. Conclusion. Wet AMD complicated by RPET as a result of the pathological process and on the background of A-VEGF therapy. When RPET is involved fovea, VA decreases to 0.15. In case of preservation RPE in fovea – VA is high. A-VEGF therapy for wet AMD with RPET leads to resorption of SRH and SRF, to stop SRF for a long time. Key words: wet form macular degeneration, Anti-VEGF therapy, retinal pigment epithelium tear, macular zone

2016 ◽  
Vol 8 ◽  
pp. OED.S38863 ◽  
Author(s):  
Ryan Enslow ◽  
Sai Bhuvanagiri ◽  
Sravanthi Vegunta ◽  
Benjamin Cutler ◽  
Michael Neff ◽  
...  

Age-related macular degeneration (AMD) is one of the leading causes of blindness in developed countries in people over the age of 60 years. One of the forms of advanced AMD is wet AMD. Wet AMD is a result of leakage and bleeding from abnormal neovascularization. The principal treatment for wet AMD is intravitreal anti-VEGF injections. A second form of advanced AMD is geographic atrophy (GA). GA refers to large areas of retinal pigment epithelium loss. In the literature, there is some concern that anti-VEGF injections administered to treat wet AMD may be associated with progression of GA. This review discusses evidence suggesting the association of anti-VEGF injections with progression of GA.


2021 ◽  
Vol 22 (16) ◽  
pp. 8387
Author(s):  
Alexa Klettner ◽  
Johann Roider

(1) Background: Inflammation is a major pathomechanism in the development and progression of age-related macular degeneration (AMD). The retinal pigment epithelium (RPE) may contribute to retinal inflammation via activation of its Toll-like receptors (TLR). TLR are pattern recognition receptors that detect the pathogen- or danger-associated molecular pattern. The involvement of TLR activation in AMD is so far not understood. (2) Methods: We performed a systematic literature research, consulting the National Library of Medicine (PubMed). (3) Results: We identified 106 studies, of which 54 were included in this review. Based on these studies, the current status of TLR in AMD, the effects of TLR in RPE activation and of the interaction of TLR activated RPE with monocytic cells are given, and the potential of TLR activation in RPE as part of the AMD development is discussed. (4) Conclusion: The activation of TLR2, -3, and -4 induces a profound pro-inflammatory response in the RPE that may contribute to (long-term) inflammation by induction of pro-inflammatory cytokines, reducing RPE function and causing RPE cell degeneration, thereby potentially constantly providing new TLR ligands, which could perpetuate and, in the long run, exacerbate the inflammatory response, which may contribute to AMD development. Furthermore, the combined activation of RPE and microglia may exacerbate neurotoxic effects.


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