Diabetic retinopathy: Difference between revisions

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==Pathogenesis==
[[File:Blausen 0312 DiabeticRetinopathy.png|thumb|Illustration depicting diabetic retinopathy]]
Diabetic retinopathy is the result of damage to the small blood vessels and neurons of the retina. The earliest changes leading to diabetic retinopathy include narrowing of the retinal arteries associated with [[Ischemia|reduced retinal blood flow]]; dysfunction of the neurons of the inner retina, followed in later stages by changes in the function of the outer retina, associated with subtle changes in visual function; dysfunction of the [[blood-retinal barrier]], which protects the retina from many substances in the blood (including toxins and [[immune cells]]), leading to the leaking of blood constituents into the retinal [[neuropile]].<ref name="XuCurtisStitt">{{cite journal| vauthors = Xu H, Curtis T, Stitt A |title=Pathophysiology and Pathogenesis of Diabetic Retinopathy [internet] |journal= Diapedia|date=13 August 2013 |volume=7104343513 |issue=14 |doi=10.14496/dia.7104343513.14|doi-broken-date=2024-0209-0518 |url=http://www.diapedia.org/acute-and-chronic-complications-of-diabetes/7104343513/pathophysiology-of-diabetic-retinopathy|access-date=26 August 2016}}</ref> Later, the basement membrane of the retinal blood vessels thickens, [[capillaries]] degenerate and lose cells, particularly [[pericytes]] and vascular [[smooth muscle cells]]. This leads to loss of blood flow and progressive [[ischemia]], and microscopic [[aneurysm]]s which appear as balloon-like structures jutting out from the capillary walls, which recruit inflammatory cells; and advanced dysfunction and degeneration of the [[neurons]] and [[glia]]l cells of the retina.<ref name="XuCurtisStitt"/><ref>{{Cite journal|title=Understanding diabetic retinopathy | vauthors = Pardianto G |journal=Mimbar Ilmiah Oftalmologi Indonesia |year=2005 |volume=2 |pages=65–6}}</ref> The condition typically develops about 10–15 years after receiving the diagnosis of diabetes mellitus.
 
An experimental study suggests that pericyte death is caused by blood glucose persistently activating [[protein kinase C]] and [[mitogen-activated protein kinase]] (MAPK), which, through a series of intermediates, inhibits signaling through [[platelet-derived growth factor receptor]]s—signaling that supports cellular survival, proliferation, and growth. The resulting withdrawal of this signaling leads to the programmed cell death ([[apoptosis]]) of the cells in this experimental model.<ref>{{cite journal | vauthors = Geraldes P, Hiraoka-Yamamoto J, Matsumoto M, Clermont A, Leitges M, Marette A, Aiello LP, Kern TS, King GL | display-authors = 6 | title = Activation of PKC-delta and SHP-1 by hyperglycemia causes vascular cell apoptosis and diabetic retinopathy | journal = Nature Medicine | volume = 15 | issue = 11 | pages = 1298–1306 | date = November 2009 | pmid = 19881493 | pmc = 3290906 | doi = 10.1038/nm.2052 }}</ref>
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===Mild or moderate NPDR===
For those with mild to moderate non-proliferative diabetic retinopathy, the American Academy of Ophthalmology recommends only more frequent retinal exams—every six to twelve months—as these people are at an increased risk of developing proliferative retinopathy or macular edema.{{sfn|Flaxel|Adelman|Bailey|Fawzi|2020|loc="Mild to moderate NPDR without macular edema"}} InInjection a randomized trial in Scotland,of [[fenofibrateanti-VEGF]] reduceddrugs progressionor ofsteroids can reduce diabetic retinopathy toprogression referablein diseasearound (retinopathyhalf orof eyes treated; however, whether this results in improved vision long term is not yet known.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loc="Treatment of nonproliferative diabetic retinopathy”}} The lipid-lowering drug [[maculopathyfenofibrate]]) oralso needreduces forprogression treatmentof vsdisease placeboin among participantspeople with earlymild retinalto changesmoderate disease.<ref>{{Cite journal |lastlast1=PreissNgah |firstfirst1=DavidNor Fariza |last2=LogueMuhamad |first2=JenniferNor Asiah |last3=SammonsAbdul Aziz |first3=EmilyRoslin Azni |last4=ZayedMohamed |first4=MohammedShelina Oli |last5=EmbersonAhmad Tarmizi |first5=JonathanNor Azita |last6=WadeAdnan |first6=RachelAzian |last7=WallendszusAsnir |first7=KarlZalifah Zakiah |last8=StevensHussein |first8=WillZanariah |last9=CretneySiew |first9=RosannaHui Foo |last10=HardingMohamed |first10=SimonMasni |last11=LeeseLodz |first11=GrahamNoor Aliza |last12=CurrieValayatham |first12=Gemma |last13=Armitage |first13=JaneVijayamala |date=20242022-0712-2318 |title=EffectFenofibrate offor Fenofibratethe onprevention Progressionof progression of Diabeticnon-proliferative Retinopathydiabetic |url=httpsretinopathy://evidence.nejm.org/doi/10.1056/EVIDoa2400179 review, consensus recommendations and guidance for clinical practice |journal=NEJMInternational EvidenceJournal |language=enof Ophthalmology |volume=315 |issue=812 |pages=2001–2008 |doi=10.105618240/EVIDoa2400179ijo.2022.12.16 |issn=27662222-55263959 |pmc=9729076 |pmid=36536974}}</ref><ref>{{Cite Injectionweb of|title=Trial: [[anti-VEGF]]Fenofibrate drugsSlows orDiabetic steroidsRetinopathy can reduceProgression |url=https://www.medscape.com/viewarticle/trial-fenofibrate-slows-diabetic -retinopathy -progression-2024a1000bm8 in|access-date=2024-07-29 around half of eyes treated; however, whether this results in improved vision|website=Medscape long term is not yet known.{{sfn|Brownlee|Aiello|Sun|Cooper|2020|loclanguage="Treatment of nonproliferative diabetic retinopathy"en}}</ref>
 
===Diabetic macular edema===