Macular Edema of Choroidal Origin

Soubrane, G.

doi:10.1159/000455282

Cited by 6 publications

(2 citation statements)

References 66 publications

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“…ME is clinically defined as an accumulation of serous fluid within the neurosensory retina, with increased thickness of the central retina. Some researches have shown that the leakage from the choroidal new vessels, predominantly VEGF-induced, may produce a large accumulation of fluid under the neurosensory retina [ 15 ]. Anti-VEGF has now become the cutting-edge treatment choice for ME, due to its excellent visual and anatomic improvement [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Association between Inflammatory Factors in the Aqueous Humor and Hyperreflective Foci in Patients with Intractable Macular Edema Treated with Antivascular Endothelial Growth Factor

Chen

et al. 2021

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Background. To evaluate the correlations between the inflammatory factors in the aqueous humor and hyperreflective foci (HRF) in patients with intractable macular edema treated with antivascular endothelial growth factor (anti-VEGF). Methods. This study included 17 patients with intractable macular edema (ME) treated with anti-VEGF agents. Inflammatory factors in the aqueous humor were measured by the Cytometric Beads Array before injection, and the numbers of HRF pre- and post-anti-VEGF treatment were counted from four different directions (90 degrees, 45 degrees, 180 degrees, and 135 degrees) in the SD-OCT images, respectively, before treatment and one month after treatment. The correlations between inflammatory factors and the numbers of HRF were assessed. Results. The numbers of HRF were reduced significantly after anti-VEGF treatment. The change in the HRFs at the 90-degree location was significantly positively correlated with IL-8 and VCAM-1. The change of all HRFs was significantly positively correlated with IL-8. The HRFs before the treatment also had a positive correlation with IL-8 and VCAM-1. Conclusion. After anti-VEGF treatment, the numbers of HRF in intractable ME declined greatly. The higher the levels of IL-8 and VCAM-1 before treatment, the more significant the reduction of HRF after anti-VEGF treatment, which indicated that HRF could be an effective noninvasive imaging indicator for evaluating the effect of anti-VEGF on intractable macular edema. The OCT images at the 90-degree location could better show the inflammatory reaction of patients and also had better clinical significance for the prognosis evaluation of ME associated with inflammation.

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Section: Discussionmentioning

confidence: 99%

Association between Inflammatory Factors in the Aqueous Humor and Hyperreflective Foci in Patients with Intractable Macular Edema Treated with Antivascular Endothelial Growth Factor

Chen

et al. 2021

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“…Although the choroid sits outside the site of the outer BRB, together with Bruch’s membrane, it may still influence fluid homeostasis across the barrier. For instance, the hydraulic conductivity of Bruch’s membrane decreases with age ( 80 ), which is a possible factor in the accumulation of subretinal fluid in exudative age-related macular degeneration ( 81 ). Changes to the choroid are also likely to affect processes of retinal fluid absorption across the RPE cells.…”

Section: Mechanisms Of Macular Edemamentioning

confidence: 99%

Mechanisms of macular edema

et al. 2023

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Macular edema is the pathological accumulation of fluid in the central retina. It is a complication of many retinal diseases, including diabetic retinopathy, retinal vascular occlusions and uveitis, among others. Macular edema causes decreased visual acuity and, when chronic or refractory, can cause severe and permanent visual impairment and blindness. In most instances, it develops due to dysregulation of the blood-retinal barrier which permits infiltration of the retinal tissue by proteins and other solutes that are normally retained in the blood. The increase in osmotic pressure in the tissue drives fluid accumulation. Current treatments include vascular endothelial growth factor blockers, corticosteroids, and non-steroidal anti-inflammatory drugs. These treatments target vasoactive and inflammatory mediators that cause disruption to the blood-retinal barrier. In this review, a clinical overview of macular edema is provided, mechanisms of disease are discussed, highlighting processes targeted by current treatments, and areas of opportunity for future research are identified.

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