Principles of therapy for subretinal hemorrhage

2021 ◽  
pp. 135-139
Author(s):  
D.V. Petrachkov ◽  
◽  
E.N. Korobov ◽  
◽  
Keyword(s):  
Minimally Invasive ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Age Related Macular Degeneration ◽  
Surgical Approaches ◽  
Submacular Hemorrhage ◽  
Vegf Inhibitors ◽  
Surgical Interventions ◽  
Age Related ◽  
Minimally Invasive Methods

Purpose. To study approaches to the treatment of submacular hemorrhage in age-related macular degeneration based on the literature data. Material and methods. The search for publications on the treatment of submacular hemorrhage (SMH) was carried out in the PubMed, SCOPUS, Umedp databases, as well as manually in journals and publications of conference materials until January 2021. Results and discussion. SMH treatment is represented by a variety of methods, from minimally invasive methods, such as intravitreal injection of drugs, gas tamponade and their combinations, to complex surgical approaches with pigment epithelium transplantation. Conclusions. The successful treatment of massive SMH is possible with minimally invasive methods. However, with significant prominating SMH, vitreoretinal surgical interventions are more appropriate. It is advisable to treat SMH as soon as possible from the moment of hemorrhage. Key words: submacular hemorrhage, age-related macular degeneration, pneumodislocation, vitrectomy, anti-VEGF inhibitors, tissue plasminogen activator.

scholarly journals Structural and Functional Reorganization of the Retina in an Experimental Simulation of Age-Related Macular Degeneration and the Melatonin Effect

2019 ◽  
Vol 8 (3) ◽  
pp. 66-71
Author(s):  
A. A. Stadnikov ◽  
N. S. Khodzhaev ◽  
A. D. Chuprov ◽  
S. M. Kim
Keyword(s):  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Age Related Macular Degeneration ◽  
Experimental Simulation ◽  
Surgical Interventions ◽  
Functional Reorganization ◽  
Uveal Tract ◽  
Age Related ◽  
Group 2 ◽  
Group 1

The aim of the study was to evaluate regularities of morphological and functional reorganization of the rabbit retina in the experimental simulation of age-related macular degeneration (AMD) and the use of melatonin.Material and methods. The study included 21 sexually mature male rabbits (42 eyes) weighed 2800– 3300 g, chinchilla breed. All the animals included in the study were divided into 3 groups: group 1 (experimental) (n=9), group 2 (control) included animals that were simulated AMD (n=9), and group 3 (intact) (n=3). Surgical interventions were performed in sterile conditions using an Opton operating microscope (Germany). Massage of the retina was performed under visual control through fixed caliber ports with a 25 G silicone-tip cannula at 10 and 2 hours in 4 mm from the limb, retreating from the optic nerve disk at a distance equal its one diameter, until the pigment epithelium was destroyed (dispersion). The size of the injury was 3 mm (RF Patent for the invention No. 2480844, 2011). Group 1 (experimental) was orally administered a suspended solution of the drug “Melaxen” (the active substance is melatonin), dosage 10 ml/kg daily once a day from 21.00 to 22.00 h for 3 months. Animals of group 2 did not receive treatment. Experimental animals were removed from the experiment on the 30th, 60th and 90th days. A histological and immunocytochemical study of the retina of experimental, control, and intact (without AMD simulation) animals was performed, including two-stage reactions to identify proteins p-53 and bcl-2.Results. Experimental histological studies allowed us to obtain a model of AMD, which corresponded to the morphological manifestations of the exudative form of chorioretinal dystrophy and destruction with a primary lesion of the choriocapillaris layer of the uveal tract. The use of melatonin for therapeutic purposes resulted in the resistant adaptation of pigment epithelium and retina gliocytes, reduction of pigment dystrophy and hemorrhage, destruction, reduction of apoptotic dominant and plexiform layers of the retina.

scholarly journals Role of amyloid β-peptide in the pathogenesis of age-related macular degeneration

2021 ◽  
Vol 6 (1) ◽  
pp. e000774
Author(s):  
Minwei Wang ◽  
Shiqi Su ◽  
Shaoyun Jiang ◽  
Xinghuai Sun ◽  
Jiantao Wang
Keyword(s):  
Mitochondrial Dysfunction ◽  
Macular Degeneration ◽  
Vision Loss ◽  
Cell Structure ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Amyloid Β ◽  
Age Related Macular Degeneration ◽  
Amyloid Β Peptide ◽  
Age Related

Age-related macular degeneration (AMD) is the most common eye disease in elderly patients, which could lead to irreversible vision loss and blindness. Increasing evidence indicates that amyloid β-peptide (Aβ) might be associated with the pathogenesis of AMD. In this review, we would like to summarise the current findings in this field. The literature search was done from 1995 to Feb, 2021 with following keywords, ‘Amyloid β-peptide and age-related macular degeneration’, ‘Inflammation and age-related macular degeneration’, ‘Angiogenesis and age-related macular degeneration’, ‘Actin cytoskeleton and amyloid β-peptide’, ‘Mitochondrial dysfunction and amyloid β-peptide’, ‘Ribosomal dysregulation and amyloid β-peptide’ using search engines Pubmed, Google Scholar and Web of Science. Aβ congregates in subretinal drusen of patients with AMD and participates in the pathogenesis of AMD through enhancing inflammatory activity, inducing mitochondrial dysfunction, altering ribosomal function, regulating the lysosomal pathway, affecting RNA splicing, modulating angiogenesis and modifying cell structure in AMD. The methods targeting Aβ are shown to inhibit inflammatory signalling pathway and restore the function of retinal pigment epithelium cells and photoreceptor cells in the subretinal region. Targeting Aβ may provide a novel therapeutic strategy for AMD.

scholarly journals Retinal Pigment Epithelium Expressed Toll-like Receptors and Their Potential Role in Age-Related Macular Degeneration

2021 ◽  
Vol 22 (16) ◽  
pp. 8387
Author(s):  
Alexa Klettner ◽  
Johann Roider
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Current Status ◽  
Toll Like Receptors ◽  
Cell Degeneration ◽  
Age Related

(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.

scholarly journals The Impact of Oxidative Stress on Blood-Retinal Barrier Physiology in Age-Related Macular Degeneration

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 64
Author(s):  
Annamaria Tisi ◽  
Marco Feligioni ◽  
Maurizio Passacantando ◽  
Marco Ciancaglini ◽  
Rita Maccarone
Keyword(s):  
Oxidative Stress ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Blood Retinal Barrier ◽  
Functional Changes ◽  
Beneficial Effects ◽  
Age Related ◽  
The Impact

The blood retinal barrier (BRB) is a fundamental eye component, whose function is to select the flow of molecules from the blood to the retina and vice-versa, and its integrity allows the maintenance of a finely regulated microenvironment. The outer BRB, composed by the choriocapillaris, the Bruch’s membrane, and the retinal pigment epithelium, undergoes structural and functional changes in age-related macular degeneration (AMD), the leading cause of blindness worldwide. BRB alterations lead to retinal dysfunction and neurodegeneration. Several risk factors have been associated with AMD onset in the past decades and oxidative stress is widely recognized as a key factor, even if the exact AMD pathophysiology has not been exactly elucidated yet. The present review describes the BRB physiology, the BRB changes occurring in AMD, the role of oxidative stress in AMD with a focus on the outer BRB structures. Moreover, we propose the use of cerium oxide nanoparticles as a new powerful anti-oxidant agent to combat AMD, based on the relevant existing data which demonstrated their beneficial effects in protecting the outer BRB in animal models of AMD.

scholarly journals Pachychoroid Neovasculopathy Disguising as Age-Related Macular Degeneration Treated by Spironolactone and Anti-VEGF Combination Therapy

2021 ◽  
pp. 116-123
Author(s):  
Leonie F. Keidel ◽  
Benedikt Schworm ◽  
Siegfried G. Priglinger ◽  
Jakob Siedlecki
Keyword(s):  
Combination Therapy ◽  
Macular Degeneration ◽  
Pigment Epithelium ◽  
Subretinal Fluid ◽  
Age Related Macular Degeneration ◽  
Chronic Central Serous Chorioretinopathy ◽  
Anti Vegf ◽  
Age Related ◽  
Therapeutic Concepts ◽  
Pachychoroid Neovasculopathy

Nonresponse of neovascular age-related macular degeneration (nAMD) to anti-vascular endothelial growth factor (anti-VEGF) therapy can often be attributed to misdiagnosis, and pathologies mimicking AMD might require different therapeutic concepts. In the following, we want to outline a case of presumed nAMD which revealed to be pachychoroid neovasculopathy (PNV) and was successfully treated by the addition of spironolactone. A 67-year-old female patient was referred for nonresponse of nAMD on her left eye after 29 intravitreal injections of aflibercept with no complete resolution of subretinal fluid. On fundoscopy, both maculae presented with pigment epithelium alterations, while the left eye showed subretinal fluid on optical coherence tomography (OCT) with an associated pigment epithelium detachment, which revealed to contain a neovascular network on OCT angiography. There was faint leakage on fluorescence (FAG) and indocyanine green angiography (ICGA) and some focal vascular dilation of the neovascular network on ICGA. Due to the absence of Drusen on any eye, a thick choroid, and the presence of a gravitational tract on blue autofluorescence (BAF), chronic central serous chorioretinopathy with a choroidal neovascularization, defined as PNV in the pachychoroid disease was diagnosed. Upon the addition of spironolactone to anti-VEGF treatment, choroidal thickness significantly decreased, and subretinal fluid resolution was observed and maintained for the first time. In conclusion, PNV should be ruled out in cases of presumed nAMD nonresponding to anti-VEGF. In these cases, a combination therapy of anti-VEGF and mineralocorticoid antagonists can facilitate fluid resorption.

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