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      Measuring Anterior Chamber Inflammation After Cataract Surgery: A Review of the Literature Focusing on the Correlation with Cystoid Macular Edema

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          Abstract

          Cystoid macular edema (CME) is an infrequent, though potentially visually impairing, complication after uneventful cataract surgery. Rupture of the blood-aqueous barrier, with leakage of serum proteins into the aqueous humour, is the main pathogenic factor. However, only a few studies investigated the potential correlation between anterior chamber (AC) inflammation and the risk of cystoid macular changes occurring after surgery. This review aims to identify evidence of a correlation between AC inflammation and the risk of pseudophakic CME. One hundred eighty-seven prospective trials investigating AC inflammation after uncomplicated cataract surgery were identified. Methods of analysis of AC inflammation and the frequency of macular changes were recorded. In the majority (51%) of the studies, inflammation was assessed by clinical grading, followed by laser flare and cell photometry (LFCP) (42%) and aqueous humour sample (4%). Few studies (4%) adopted a combined LFCP and aqueous sample or clinical grading analysis. Sixteen (9%) studies investigated AC inflammation and macular changes by OCT (7%) or fluorescein angiography (2%). Correlation between the amount of postoperative AC inflammation and frequency of CME was documented in 7 studies, not confirmed in 2 studies, and not examined in the other 7. LFCP, more than the other methods of analysis, correlated with the frequency of CME postoperatively. Investigation of the relationship between AC inflammation and the risk of CME changes requires the adoption of quantitative methods of analysis of the inflammatory response after surgery. For this purpose, due to the low level of inflammation in the AC after uncomplicated cataract surgery, LFCP, more than subjective clinical grading, seems a more sensitive and reproducible method of measurement. Inflammation assessment after cataract surgery has a potential role in predicting the risk of CME development and may help to titrate the duration and intensity of treatment in relation to the surgical inflammatory response.

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          Most cited references57

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          Inflammatory mediators and modulation of blood-brain barrier permeability.

          N J Abbott (2000)
          1. Unlike some interfaces between the blood and the nervous system (e.g., nerve perineurium), the brain endothelium forming the blood-brain barrier can be modulated by a range of inflammatory mediators. The mechanisms underlying this modulation are reviewed, and the implications for therapy of the brain discussed. 2. Methods for measuring blood-brain barrier permeability in situ include the use of radiolabeled tracers in parenchymal vessels and measurements of transendothelial resistance and rate of loss of fluorescent dye in single pial microvessels. In vitro studies on culture models provide details of the signal transduction mechanisms involved. 3. Routes for penetration of polar solutes across the brain endothelium include the paracellular tight junctional pathway (usually very tight) and vesicular mechanisms. Inflammatory mediators have been reported to influence both pathways, but the clearest evidence is for modulation of tight junctions. 4. In addition to the brain endothelium, cell types involved in inflammatory reactions include several closely associated cells including pericytes, astrocytes, smooth muscle, microglia, mast cells, and neurons. In situ it is often difficult to identify the site of action of a vasoactive agent. In vitro models of brain endothelium are experimentally simpler but may also lack important features generated in situ by cell:cell interaction (e.g. induction, signaling). 5. Many inflammatory agents increase both endothelial permeability and vessel diameter, together contributing to significant leak across the blood-brain barrier and cerebral edema. This review concentrates on changes in endothelial permeability by focusing on studies in which changes in vessel diameter are minimized. 6. Bradykinin (Bk) increases blood-brain barrier permeability by acting on B2 receptors. The downstream events reported include elevation of [Ca2+]i, activation of phospholipase A2, release of arachidonic acid, and production of free radicals, with evidence that IL-1 beta potentiates the actions of Bk in ischemia. 7. Serotonin (5HT) has been reported to increase blood-brain barrier permeability in some but not all studies. Where barrier opening was seen, there was evidence for activation of 5-HT2 receptors and a calcium-dependent permeability increase. 8. Histamine is one of the few central nervous system neurotransmitters found to cause consistent blood-brain barrier opening. The earlier literature was unclear, but studies of pial vessels and cultured endothelium reveal increased permeability mediated by H2 receptors and elevation of [Ca2+]i and an H1 receptor-mediated reduction in permeability coupled to an elevation of cAMP. 9. Brain endothelial cells express nucleotide receptors for ATP, UTP, and ADP, with activation causing increased blood-brain barrier permeability. The effects are mediated predominantly via a P2U (P2Y2) G-protein-coupled receptor causing an elevation of [Ca2+]i; a P2Y1 receptor acting via inhibition of adenyl cyclase has been reported in some in vitro preparations. 10. Arachidonic acid is elevated in some neural pathologies and causes gross opening of the blood-brain barrier to large molecules including proteins. There is evidence that arachidonic acid acts via generation of free radicals in the course of its metabolism by cyclooxygenase and lipoxygenase pathways. 11. The mechanisms described reveal a range of interrelated pathways by which influences from the brain side or the blood side can modulate blood-brain barrier permeability. Knowledge of the mechanisms is already being exploited for deliberate opening of the blood-brain barrier for drug delivery to the brain, and the pathways capable of reducing permeability hold promise for therapeutic treatment of inflammation and cerebral edema.
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            Cataract Surgical Rate and Socioeconomics: A Global Study.

            Cataract is the leading cause of blindness and cataract surgical rate (CSR) is used as a proxy indicator of access to cataract services in a country. The aim of this study was to explore the associations between the CSR and the economic development of countries in terms of gross domestic product per capital (GDP/P) and gross national income per capita (GNI/P).
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              Risk Factors and Incidence of Macular Edema after Cataract Surgery

              To define the incidence of pseudophakic macular edema (PME) after cataract surgery and to identify contributory risk factors.
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                Author and article information

                Journal
                Clin Ophthalmol
                Clin Ophthalmol
                OPTH
                clinop
                Clinical Ophthalmology (Auckland, N.Z.)
                Dove
                1177-5467
                1177-5483
                09 January 2020
                2020
                : 14
                : 41-52
                Affiliations
                [1 ]Ophthalmology Unit, AUSL-IRCCS of Reggio Emilia , Reggio Emilia, Italy
                [2 ]Clinical and Experimental Medicine Ph.D. Programme, University of Modena and Reggio Emilia , Modena, Italy
                [3 ]Ocular Immunology Unit, Azienda USL-IRCCS di Reggio Emilia , Reggio Emilia, Italy
                [4 ]Ophthalmology, University Campus Bio-Medico of Rome , Rome, Italy
                Author notes
                Correspondence: Luigi Fontana Ophthalmology Unit, AUSL-IRCCS of Reggio Emilia , Viale Risorgimento 80, Reggio Emilia42122, Italy Email luifonta@gmail.com
                Author information
                http://orcid.org/0000-0002-5791-4263
                http://orcid.org/0000-0003-3877-0417
                Article
                237405
                10.2147/OPTH.S237405
                6957928
                5e90241a-f50c-4435-a32c-01a1e329d2f7
                © 2020 De Maria et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 07 November 2019
                : 11 December 2019
                Page count
                Figures: 1, Tables: 1, References: 66, Pages: 12
                Categories
                Review

                Ophthalmology & Optometry
                anterior chamber inflammation,cataract surgery,clinical grading,laser flare photometry,anterior segment optical coherence tomography,aqueous humour sample,cystoid macular edema

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