Transcriptome Profiling of Embryonic Retinal Pigment Epithelium Reprogramming.

The plasticity of human retinal pigment epithelium (RPE) has been observed during proliferative vitreoretinopathy, a defective repair process during which injured RPE gives rise to fibrosis. In contrast, following injury, the RPE of the embryonic chicken can be reprogrammed to regenerate neural retina in a fibroblast growth factor 2 (FGF2)-dependent manner. To better explore the mechanisms underlying embryonic RPE reprogramming, we used laser capture microdissection to isolate RNA from (1) intact RPE, (2) transiently reprogrammed RPE (t-rRPE) 6 h post-retinectomy, and (3) reprogrammed RPE (rRPE) 6 h post-retinectomy with FGF2 treatment. Using RNA-seq, we observed the acute repression of genes related to cell cycle progression in the injured t-rRPE, as well as up-regulation of genes associated with injury. In contrast, the rRPE was strongly enriched for mitogen-activated protein kinase (MAPK)-responsive genes and retina development factors, confirming that FGF2 and the downstream MAPK cascade are the main drivers of embryonic RPE reprogramming. Clustering and pathway enrichment analysis was used to create an integrated network of the core processes associated with RPE reprogramming, including key terms pertaining to injury response, migration, actin dynamics, and cell cycle progression. Finally, we employed gene set enrichment analysis to suggest a previously uncovered role for epithelial-mesenchymal transition (EMT) machinery in the initiation of embryonic chick RPE reprogramming. The EMT program is accompanied by extensive, coordinated regulation of extracellular matrix (ECM) associated factors, and these observations together suggest an early role for ECM and EMT-like dynamics during reprogramming. Our study provides for the first time an in-depth transcriptomic analysis of embryonic RPE reprogramming and will prove useful in guiding future efforts to understand proliferative disorders of the RPE and to promote retinal regeneration.

Effects of trans-resveratrol on type 1 diabetes-induced up-regulation of apoptosis and mitogen-activated protein kinase signaling in retinal pigment epithelium of Dark Agouti rats.

Microvascular changes and retinal degeneration precede diabetic retinopathy. Oxidative stress alters several intracellular signaling pathways, which form the basis of diabetic retinopathy. Many antioxidants have been investigated as possible preventive and therapeutic remedies for diabetic retinopathy. The current study investigated the modulatory effects of trans-resveratrol on streptozotocin-induced type 1 diabetes mediated changes in the transcription and levels of apoptosis-related proteins and mitogen-activated protein kinases (MAPKs) in the retinal pigment epithelium (RPE) of adult male dark Agouti rats. In control rats, 5 mg/kg/d trans-resveratrol administration for 30 days increased gene expressions of tumor suppressor protein 53, Bcl2-associated X protein, B-cell lymphoma-2 (Bcl2), Caspase-3 (CASP3), CASP8 and CASP9, p38αMAPK, c-Jun N-terminal kinase-1 (JNK1), and extracellular signal-regulated kinase-1 (ERK1). On the other hand, diabetes decreased gene expressions of CASP3, CASP8, p38αMAPK, JNK, and ERK1. Trans-resveratrol reversed the inhibited gene expressions of CASP8, p38αMAPK, JNK, and ERK1 to normal control levels in diabetic rats. Trans-resveratrol normalized diabetes-induced upregulation of CASP3 and -9, cytochrome-c, Bcl-2, and ERK1 proteins. In conclusion, Trans-resveratrol-induced alterations in gene expressions do not seem to affect RPE functions as they do not reflect as altered protein functions. Trans-resveratrol imparts its protective effects by normalizing apoptosis-related proteins and ERK1 but does not affect JNK proteins. Trans-resveratrol causes cytostasis in RPE of normal rats by upregulating Bcl2 protein and apoptotic proteins.

Investigations on Retinal Pigment Epithelial Damage at Laser Irradiation in the Lower Microsecond Time Regime.

Purpose: New lasers with a continuous wave power exceeding 15 W are currently investigated for retinal therapies, promising highly localized effects at and close to the Retinal Pigment Epithelium (RPE). The goal of this work is to evaluate mechanisms and thresholds for RPE cell damage by means of pulse durations up to 50 µs. Methods: A diode laser with a wavelength of 514 nm, a power of 15 W, and adjustable pulse durations between 2 µs and 50 µs was used. Porcine RPE-choroidal explants (ex vivo) and chinchilla bastard rabbits (in vivo) were irradiated to determine threshold radiant exposures for RPE damage \({\bar H_{Cell}}\) by calcein vitality staining and fluorescence angiography, respectively. Thresholds for microbubble formation (MBF) \({\bar H_{MBF}}\) were evaluated by time-resolved optoacoustics. Exemplary histologies support the findings. Results: \({\bar H_{{{MBF}}}}\) is significantly higher than \({\bar H_{Cell}}\) at pulse durations ≥ 5 µs (P < 0.05) ex vivo, while at 2 µs, no statistically significant difference was found. The ratios between \({\bar H_{{{MBF}}}}\) and \({\bar H_{Cell}}\) increase with pulse duration from 1.07 to 1.48 ex vivo and 1.1 to 1.6 in vivo, for 5.2 and 50 µs. Conclusions: Cellular damage with and without MBF related disintegration are both present and very likely to play a role for pulse durations ≥ 5 µs. With the lower µs pulses, selective RPE disruption might be possible, while higher values allow achieving spatially limited thermal effects without MBF. However, both modi require a very accurate real-time dosing control in order to avoid extended retinal disintegration in this power range.

Risuteganib Protects against Hydroquinone-induced Injury in Human RPE Cells.

Purpose: Cigarette smoking has been implicated in the pathogenesis of AMD. Integrin dysfunctions have been associated with AMD. Herein, we investigate the effect of risuteganib (RSG), an integrin regulator, on RPE cell injury induced by hydroquinone (HQ), an important oxidant in cigarette smoke. Methods: Cultured human RPE cells were treated with HQ in the presence or absence of RSG. Cell death, mitochondrial respiration, reactive oxygen species production, and mitochondrial membrane potential were measured by flow cytometry, XFe24 analyzer, and fluorescence plate reader, respectively. Whole transcriptome analysis and gene expression were analyzed by Illumina RNA sequencing and quantitative PCR, respectively. F-actin aggregation was visualized with phalloidin. Levels of heme oxygenase-1, P38, and heat shock protein 27 proteins were measured by Western blot. Results: HQ induced necrosis and apoptosis, decreased mitochondrial bioenergetics, increased reactive oxygen species levels, decreased mitochondrial membrane potential, increased F-actin aggregates, and induced phosphorylation of P38 and heat shock protein 27. HQ, but not RSG alone, induced substantial transcriptome changes that were regulated by RSG cotreatment. RSG cotreatment significantly protected against HQ-induced necrosis and apoptosis, prevented HQ-reduced mitochondrial bioenergetics, decreased HQ-induced reactive oxygen species production, improved HQ-disrupted mitochondrial membrane potential, reduced F-actin aggregates, decreased phosphorylation of P38 and heat shock protein 27, and further upregulated HQ-induced heme oxygenase-1 protein levels. Conclusions: RSG has no detectable adverse effects on healthy RPE cells, whereas RSG cotreatment protects against HQ-induced injury, mitochondrial dysfunction, and actin reorganization, suggesting a potential role for RSG therapy to treat retinal diseases such as AMD.

Injury of photoreceptors and retinal pigment epithelium in macular area of a preterm infant: A case analysis.

RATIONAL: Injury of photoreceptors and retinal pigment epithelium (RPE) in macular area of premature infants is very rare. PATIENT CONCERNS: A preterm infant delivered under general anesthesia. The infant was born at 28 weeks' and 4 days' gestation, with a birth weight of 1.15 kg and a treatment of oxygen inhalation after birth. According to the related protocol formulated by the Ophthalmology Branch of the Chinese Medical Association in 2014, the infant was regularly checked in our hospital. DIAGNOSIS: Optical coherence tomography (OCT) examination showed injuries of the photoreceptors and RPE in macular area. INTERVENTIONS: The fundus screening at 40 weeks' and 4 days' gestation (corrected gestational age) showed retinopathy of prematurity in bilateral eyes, with round yellow-white lesions at the macular area of right eye and sub-temporal macular area. OCT examination showed interrupted signals in the external limiting membrane (ELM), inner segment of the photoreceptors (IS)/outer segment of the photoreceptors (OS) layer, interdigitation zone (IZ), and RPE of the central fovea of macula of the right eye, with the area of defect of approximately 184 µm. Enhanced signal reflection was found under the defect area. Interrupted signals were also found in the IS/OS layer of the central fovea of macula of the left eye, with the area of defect of approximately 222 µm. Fundus fluorescence angiography (FFA) examination showed transmitted fluorescence at the macular area of the right eye and sub-temporal macular area of the left eye, suggesting retinopathy of prematurity in bilateral eyes. OUTCOMES: Several factors, such as photic damage, eye injuries, hyperpyrexia, and underlying diseases, could cause macular retinal injuries. However, the baby had not received any radiation from high energy intense light sources, and had no history of hyperpyrexia or trauma. Fundamental screening was performed 1 year and 4 months of age and no obvious change was found in the round yellow-white lesions of the eyes compared with that in earlier stages. We have contacted with the patient for the follow-up OCT and FFA examinations a month later to check the possible structural changes of the macular area. LESSONS: The retina of a preterm infant is underdeveloped, we speculated that the bilateral retinal injuries in this baby could be caused by various factors.

hsa_circ_0041795 contributes to human retinal pigment epithelial cells (ARPE 19) injury induced by high glucose via sponging miR-646 and activating VEGFC.

Diabetic retinopathy (DR)is a common diabetes complication, resulting in the loss of vision. circRNAshave been reported to serve as ceRNA via targeting corresponding miRNAs and modulating mRNA expression in various diseases. Recently, increasing reports has indicated circRNAs can exert a significant role inDR progression. However, the expression and mechanism of hsa_circ_0041795 in human retinal pigment epithelial cells ARPE-19 treated by high glucose remains poorly known. Hence, we aimed to work figure out the effect of hsa_circ_0041795 in high glucose (HG)-induced ARPE-19 cell damage and study its molecular mechanisms. In our current research, we found that hsa_circ_0041795 was obviously up-regulated in HG-treated ARPE-19 cells. High dose of glucose greatly depressed ARPE-19 cell survival and contributed to cell apoptosis. In addition, we observed that loss of hsa_circ_0041795 enhanced cell proliferation and inhibit ARPE-19 cell apoptosis, after HG incubation. Furthermore, data of ELISA indicated that hsa_circ_0041795 siRNA significantly restrained inflammatory factors expression, such as TNF-α, IL-1ß and IL-6 in ARPE-19 cells treated with HG. miR-646 has been recognized in multiple diseases and currently, we predicted that miR-646 acted as a target of hsa_circ_0041795. Moreover, we found that miR-646 inhibitors dramatically reversed the effect of hsa_circ_0041795 siRNA on ARPE-19 cells. Additionally, a dual-luciferase reporter assay proved that VEGFC was a direct target of miR-646. Our results demonstrated that hsa_circ_0041795 might exhibit a novel therapeutic potential in the treatment of DR.

CHOROIDAL NEOVASCULARIZATION ASSOCIATED WITH RETINAL PIGMENT EPITHELIAL TEAR IMAGED BY OPTICAL COHERENCE TOMOGRAPHY ANGIOGRAPHY.

PURPOSE: To report a patient presenting a retinal pigment epithelial tear in which optical coherence tomography angiography enabled the visualization of subfoveal choroidal neovascularization (CNV) not evidenced by the fluorescein angiography. She was treated with 3 monthly intravitreous anti-VEGF injections and intraretinal fluid resolution occurred. METHODS: Observational case report. RESULTS: A 62-year-old Caucasian woman presented with decreased visual acuity in the right eye for 3 months. Fundus biomicroscopy revealed a yellowish macular lesion associated with intraretinal hemorrhage. Fluorescein angiography showed a large hyperfluorescent area consistent with window defect. Optical coherence tomography showed a retinal pigment epithelial tear with subretinal fluid. However, there was no clear evidence of CNV on fluorescein angiography or OCT. Optical coherence tomography angiography confirmed the presence of an active CNV by the visualization of the neovascular network in the region corresponding to the scrolled up retinal pigment epithelium. CONCLUSION: This case report demonstrates that optical coherence tomography angiography can be useful to confirm the presence of CNV in cases where fluorescein angiography and OCT cannot establish the diagnosis. The reported case suggests the applicability of optical coherence tomography angiography in patients in whom retinal pigment epithelial tear is detected and associated CNV is suspected.

Protective effects of delphinidin against H2O2-induced oxidative injuries in human retinal pigment epithelial cells.

Age-related macular degeneration (AMD) is now one of the leading causes of blindness in the elderly population and oxidative stress-induced damage to retinal pigment epithelial (RPE) cells occurs as part of the pathogenesis of AMD. In the present study, we evaluated the protective effect of delphinidin (2-(3,4,5-trihydroxyphenyl) chromenylium-3,5,7-triol) against hydrogen peroxide (H2O2)-induced toxicity in human ARPE-19 cells and its molecular mechanism. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and flow cytometry demonstrated that pretreatment of ARPE-19 cells with delphinidin (25, 50, and 100 µg/ml) significantly increased cell viability and reduced the apoptosis from H2O2 (0.5 mM)-induced oxidative stress in a concentration-dependent manner, which was achieved by the inhibition of Bax, cytochrome c, and caspase-3 protein expression and enhancement of Bcl-2 protein. The same tendency was observed in ARPE-19 cells pre-treated with 15 mM of N-acetylcysteine (NAC) before the addition of H2O2 Furthermore, pre-incubation of ARPE-19 cells with delphinidin markedly inhibited the intracellular reactive oxygen species (ROS) generation and Nox1 protein expression induced by H2O2 Moreover, the decreased antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GSH-PX) and elevated (MDA) level in H2O2-treated cells were reversed to the normal standard by the addition of delphinidin, which was regulated by increasing nuclear Nrf2 protein expression in ARPE-19 cells. Our results suggest that delphinidin effectively protects human ARPE-19 cells from H2O2-induced oxidative damage via anti-apoptotic and antioxidant effects.

INCIDENCE AND LONG-TERM VISUAL ACUITY OUTCOMES OF RETINAL PIGMENT EPITHELIUM TEARS AFTER INTRAVITREAL ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR TREATMENT OF NEOVASCULAR AGE-RELATED MACULAR DEGENERATION.

PURPOSE: To report the incidence of retinal pigment epithelium tears in eyes treated with aflibercept for neovascular age-related macular degeneration and compare it with ranibizumab, and to describe long-term visual outcomes of retinal pigment epithelium tears after intensive anti-vascular endothelial growth factor treatment. METHODS: Retrospective analysis of clinical charts, spectral domain optical coherence tomography and fundus fluorescein angiography imaging of consecutive naive patients treated with intravitreal aflibercept or ranibizumab for neovascular age-related macular degeneration. RESULTS: Eight hundred consecutive eyes were included in the study (300 treated with ranibizumab and 500 with aflibercept) with 34.0 ± 9.1 months of follow-up. The incidence of tears in the aflibercept group was 3.2% and 2.3% after ranibizumab (P = 0.52). Twenty-nine eyes with retinal pigment epithelium tears were followed for a mean of 30.76 months. Visual acuity at baseline was 20/100 (50.7 ± 19.3 Early Treatment Diabetic Retinopathy Study letters) and 20/200 (36.1 ± 26.1 Early Treatment Diabetic Retinopathy Study letters) at the end of follow-up. The mean number of injection was 7.3 at 12 months and 13.9 ± 8.1 at the end of the study. The number of injections positively correlated with the final visual outcome. CONCLUSION: There was a low rate of retinal pigment epithelium tears after aflibercept injections, similar to ranibizumab. The correlation between the number of anti-vascular endothelial growth factors received and visual outcomes supports the need for continuing anti-vascular endothelial growth factor therapy.

Retinal pigment epithelial tears.

A retinal pigment epithelial (RPE) tear is a well-known complication of retinal pigment epithelial detachments (PED) and may cause a significant visual impairment. The most common cause is a vascularized PED in patients with exudative age-related macular degeneration (AMD). The development of diagnostic imaging techniques brings us closer to the etiology and pathophysiological mechanisms of this entity, offering us new strategies for treatment and follow-up. The advent of intravitreal antiangiogenic treatment (anti-VEGF) has led to an increase in the number of reported cases of RPE tears, which are an important vision-limiting factor during treatment. However, RPE tears may occur spontaneously or as a consequence of thermal laser treatment, photodynamic therapy or anti-VEGF therapy. It is accepted that the mechanism of RPE tears is multifactorial. The optimization of the functional outcome of this complication has been described with continuous treatment with antiangiogenic drugs. The goal of the present review is to evaluate the incidence, risk factors and treatment of RPE tears.

Blueberry Polyphenols Ameliorate Visible Light and Lipid-Induced Injury of Retinal Pigment Epithelial Cells.

Although dietary polyphenols are known to be beneficial to vision, the protective distinctions among different types of polyphenols are unclear. In this work, the visual benefits of various blueberry polyphenols were evaluated using an in vitro model of visible light-lipid-induced injury of retinal pigment epithelial cells. Results showed that, at 10.0 µg/mL, the phenolic acid-rich fraction was superior in inhibiting cell death (93.6% ± 2.8% of cell viability). Anthocyanin- and flavonoid-rich fractions shared similar advantages in preventing the expression of senescence-associated ß-galactosidase (34.8% ± 11.1% and 32.2% ± 9.7% of aged cells, respectively) and overexpression of vascular endothelial growth factor (51.8 ± 3.5 and 54.1 ± 6.5 pg/mL, respectively). The flavonoid-rich fraction also showed high activity in ameliorating phagocytosis (70.3% ± 12.6%) and cellular oxidative stress. These results were further confirmed by using the corresponding polyphenol standards. Improved inhibitory effects of polyphenol mixture on cell death and senescence-associated ß-galactosidase expression were also observed. Therefore, various polyphenols play diverse roles and exert synergistic effects in nourishing the retina.

Bilateral maculopathy after exposure to a laser pointer: Optical coherence tomography angiography findings. / Maculopatía bilateral por exposición a puntero láser: hallazgos en la angiografía mediante tomografía de coherencia óptica.

CASE REPORT: A 36-year-old man went to the emergency department the day after exposure to a laser pointer. Funduscopy revealed dispersed macular pigment alterations, and optical coherence tomography showed a disruption of the retinal layers. The visual acuity was counting fingers in both eyes. Nine months later, optical coherence tomography angiography showed a rarefaction in the choriocapillaris vascular flow in the area of the laser injuries. DISCUSSION: The retinal layer mainly damaged by the laser injury was the retinal pigment epithelium. However, it is suggested that the laser injury could involve tissues beyond the retinal pigment epithelium, since a rarefaction of the choriocapillaris was found after exposure to the laser.

Choroidal γδ T cells in protection against retinal pigment epithelium and retinal injury.

γδ T cells located near the epithelial barrier are integral components of local inflammatory and innate immune responses. We have previously reported the presence of choroidal γδ T cells in a model of chronic degeneration of the retinal pigment epithelium (RPE). The goals of the current study were to further define the functions of choroidal γδ T cells and to explore the underlying mechanisms of their action. Our data demonstrate that choroidal γδ T cells are activated by RPE injury in response to NaIO3 treatment, and that they express genes that encode immunosuppressive cytokines, such as IL-4 and IL-10. γδ-T-cell-deficient mice developed profound RPE and retinal damage at doses that caused minimal effects in wild-type mice, and adoptive transfer of γδ T cells prevented sensitization. Intravitreal injection of IL-4 and IL-10 ameliorated RPE toxicity that was induced by NaIO3Ex vivo coculture of γδ T cells with RPE explants activated the production of anti-inflammatory cytokines via an aryl hydrocarbon receptor (AhR)-dependent mechanism. AhR deficiency abolished the protective effects of γδ T cells after adoptive transfer. Collectively, these findings define important roles for choroid γδ T cells in maintaining tissue homeostasis in the outer retina.-Zhao, Z., Liang, Y., Liu, Y., Xu, P., Flamme-Wiese, M. J., Sun, D., Sun, J., Mullins, R. F., Chen, Y., Cai, J. Choroidal γδ T cells in protection against retinal pigment epithelium and retinal injury.

Retinal pigment epithelium wound healing after traumatic choroidal rupture.

PURPOSE: The aim of this study was to investigate wound healing in the retinal pigment epithelium (RPE) after traumatic indirect choroidal rupture using fundus autofluorescence (FAF) and spectral-domain optical coherence tomography (SD-OCT). METHODS: A total of 14 eyes of 14 patients with traumatic indirect choroidal rupture were included. Baseline and last follow-up FAF images were compared to evaluate the extent of RPE healing after choroidal rupture, and associated morphologic characteristics were examined by SD-OCT. RESULTS: The size of the RPE lesion was reduced in five eyes. The change occurred in the fovea in four eyes and in the macula in three eyes. The change was noted in both the fovea and the macula in two eyes; in these cases, the changes were more prominent in the fovea than in the macula. Extra-macular lesions and lesions with deep choroidal involvement did not show any reduction in size. Choroidal neovascularization (CNV) developed in seven eyes. There was no extra-macular CNV. CONCLUSION: Retinal pigment epithelium (RPE) wound healing after traumatic choroidal rupture is affected by location and extent of the lesion.

Anti-VEGF y sus consecuencias sobre la retina externa: rotura del epitelio pigmentario tras inyección de aflibercept en ojo contralateral / Anti-VEGF and its impact on the outer retina: retinal pigment epithelium tear after an injection of aflibercept in contralateral eye

CASO CLÍNICO: Mujer de 62 años con antecedentes personales de desprendimiento del epitelio pigmentario (DEP) de la retina bilateral, secundario a degeneración macular, que presenta una rotura del mismo en su ojo izquierdo (OI) tras inyección de aflibercept en el ojo contralateral un mes antes. DISCUSIÓN: La rotura del epitelio pigmentario de la retina (EPR) es la principal complicación cuando se utiliza la terapia anti-VEGF para el manejo de los DEP. Por otro lado, se debe tener en cuenta que la absorción sistémica del fármaco puede inducir algún efecto en el ojo no tratado

CASE REPORT: A 62-year-old woman with a history of bilateral retinal pigment epithelium detachment (PED), secondary of age-related macular degeneration (AMD), who presented with a retinal pigment epithelium (RPE) tear on her left eye after an aflibercept injection in the contralateral eye one month earlier. DISCUSSION: A RPE tear is the main complication when the anti-VEGF therapy is used for the management of the PED. Furthermore, it should be noted that systemic absorption of the drug can induce an effect on the untreated eye

RETINAL PIGMENT EPITHELIAL TEAR AFTER INTRAVITREAL RANIBIZUMAB TREATMENT FOR NEOVASCULAR AGE-RELATED MACULAR DEGENERATION.

PURPOSE: To evaluate the risk factors for retinal pigment epithelium (RPE) tears after intravitreal ranibizumab injections in neovascular age-related macular degeneration (nAMD) and to determine the efficacy of continued ranibizumab treatment after RPE tears. METHODS: A total of 407 treatment-naïve eyes (377 patients) with nAMD were retrospectively included. All patients were treated with an initial series of 3 monthly loading injections, followed by further injections as required. Baseline characteristics and pigment epithelial detachment (PED) lesion features were evaluated as potential risk factors for RPE tear. The visual and anatomical outcomes after treatment during 12 months were also evaluated. RESULTS: By 12 months, RPE tears developed in 32 eyes (7.9%). Pigment epithelial detachment height was associated with a higher risk of RPE tear (odds ratio [OR], 1.318; 95% confidence interval [CI], 1.217-2.031, P = 0.018). Fibrovascular PED compared with serous PED had a higher risk of developing tears (OR, 9.129; 95% CI, 6.228-32.124, P = 0.039), and typical nAMD (OR, 4.166; 95% CI, 2.030-14.913, P = 0.031) and retinal angiomatous proliferation (OR, 3.778; 95% CI, 2.185-9.277, P = 0.040) had a higher risk of developing tears compared with polypoidal choroidal vasculopathy. Mean best-corrected visual acuity (BCVA) of RPE tear patients showed no significant improvement after treatment at 12 months; however, patients with RPE tears without foveal involvement (19 eyes) showed significant BCVA improvement at 12 months (P = 0.034). CONCLUSION: PED type and nAMD subtype are associated with the development of RPE tears after intravitreal ranibizumab injections. Continued ranibizumab therapy after RPE tear development can maintain visual acuity when the fovea is not involved.

Anti-VEGF and its impact on the outer retina: retinal pigment epithelium tear after an injection of aflibercept in contralateral eye. / Anti-VEGF y sus consecuencias sobre la retina externa: rotura del epitelio pigmentario tras inyección de aflibercept en ojo contralateral.

CASE REPORT: A 62-year-old woman with a history of bilateral retinal pigment epithelium detachment (PED), secondary of age-related macular degeneration (AMD), who presented with a retinal pigment epithelium (RPE) tear on her left eye after an aflibercept injection in the contralateral eye one month earlier. DISCUSSION: A RPE tear is the main complication when the anti-VEGF therapy is used for the management of the PED. Furthermore, it should be noted that systemic absorption of the drug can induce an effect on the untreated eye.

Change in vision after retinal pigment epithelium tear following the use of anti-VEGF therapy for age-related macular degeneration.

PURPOSE: We investigated visual acuity outcomes and their associations in the setting of retinal pigment epithelium tear (RPET) following the use of anti-vascular endothelial growth factor (anti-VEGF) agents. METHODS: This retrospective review included all patients treated for neovascular age-related macular degeneration (AMD) with an anti-VEGF agent who subsequently developed an RPET. All patients who developed an RPET were identified and outcome measures data were recorded and analysed. The main outcome measures were best corrected visual acuity (BCVA) and spectral domain optical coherence tomography characteristics. RESULTS: Among the 14 participants identified, a subfoveal RPET was associated with the loss of one or more lines of vision from baseline (p = 0.03). There was no association between the size of the RPET and BCVA at the time of the RPET or final BCVA. The development of a disciform scar was associated both with a BCVA at the time of the RPET of < 6/24 (p = 0.02) and a final BCVA of < 6/24 (p = 0.02). Ongoing treatment with an anti-VEGF agent following an RPET saw five patients (35.7 %) have an improvement in their BCVA and all patients maintained their BCVA following the RPET with ongoing anti-VEGF treatment. CONCLUSIONS: Visual decline following an RPET is associated with subfoveal location of the RPET (p = 0.03) and later development of a disciform scar. These data also suggest that the ongoing use of an anti-VEGF agent may stabilise vision in some patients following an RPET and for some patients there may be an improvement in visual acuity despite the RPET, depending on its location.