Nesteroidni protuupalni lijekovi u liječenju cistoidnog makularnog edema

Nonsteroidal antiinflammatory drugs (NSAIDs) have become a significant therapeutic adjunctive tool in the routine and complicated intraocular surgery. Topical NSAIDs prevent intraoperative miosis, reduce pain, postoperative inflammation and incidence of cystoid macular edema (CME). Although there is no established protocol for prophylaxis of pseudophakic CME, due to the relationship between proinflammatory prostaglandins and CME, using corticosteroids and NSAIDs could prevent CME. NSAIDs have a synergistic antiinflammatory effect with steroids, but can also be used alone when corticosteroid therapy could be harmful. Prospective clinical trials need to define treatment protocol for topical NSAIDs use, due to their powerful influence to prevent perioperative complications.Nesteroidni protuupalni lijekovi (NSAID, engl. nonsteroidal antiinflammatory drugs) postali su značajna dodatna terapija u rutinskim i kompliciranim intraokularnim operacijama. Topički NSAID-i sprječavaju intraoperativnu miozu, smanjuju bol, postoperativnu upalu i učestalost cistoidnog makularnog edema (CME). Iako nema uspostavljenog protokola za profilaksu pseudofakičnog CME-a, zbog veze između proupalnih prostaglandina i CME-a primjena topičkih kortikosteroida i topičkih NSAID-a može spriječiti CME. NSAID-i imaju sinergistički protuupalni učinak sa steroidima, ali se mogu upotrijebiti i sami kada bi kortikosteroidna terapija mogla biti rizična. Zbog njihovog snažnog utjecaja na prevenciju perioperativnih komplikacija potrebna su prospektivna klinička istraživanja za definiranje protokola terapijske primjene topičkih NSAID-a

Nonsteroidal antiinflammatory drugs and treatment of cystoid macular edema

Nesteroidni protuupalni lijekovi (NSAID, engl. nonsteroidal antiinflammatory drugs) postali su značajna dodatna terapija u rutinskim i kompliciranim intraokularnim operacijama. Topički NSAID-i sprječavaju intraoperativnu miozu, smanjuju bol, postoperativnu upalu i učestalost cistoidnog makularnog edema (CME). Iako nema uspostavljenog protokola za profilaksu pseudofakičnog CME-a, zbog veze između proupalnih prostaglandina i CME-a primjena topičkih kortikosteroida i topičkih NSAID-a može spriječiti CME. NSAID-i imaju sinergistički protuupalni učinak sa steroidima, ali se mogu upotrijebiti i sami kada bi kortikosteroidna terapija mogla biti rizična. Zbog njihovog snažnog utjecaja na prevenciju perioperativnih komplikacija potrebna su prospektivna klinička istraživanja za definiranje protokola terapijske primjene topičkih NSAID-a.Nonsteroidal antiinflammatory drugs (NSAIDs) have become a significant therapeutic adjunctive tool in the routine and complicated intraocular surgery. Topical NSAIDs prevent intraoperative miosis, reduce pain, postoperative inflammation and incidence of cystoid macular edema (CME). Although there is no established protocol for prophylaxis of pseudophakic CME, due to the relationship between proinflammatory prostaglandins and CME, using corticosteroids and NSAIDs could prevent CME. NSAIDs have a synergistic antiinflammatory effect with steroids, but can also be used alone when corticosteroid therapy could be harmful. Prospective clinical trials need to define treatment protocol for topical NSAIDs use, due to their powerful influence to prevent perioperative complications

Nonsteroidal antiinflammatory drugs and treatment of cystoid macular edema

Nesteroidni protuupalni lijekovi (NSAID, engl. nonsteroidal antiinflammatory drugs) postali su značajna dodatna terapija u rutinskim i kompliciranim intraokularnim operacijama. Topički NSAID-i sprječavaju intraoperativnu miozu, smanjuju bol, postoperativnu upalu i učestalost cistoidnog makularnog edema (CME). Iako nema uspostavljenog protokola za profilaksu pseudofakičnog CME-a, zbog veze između proupalnih prostaglandina i CME-a primjena topičkih kortikosteroida i topičkih NSAID-a može spriječiti CME. NSAID-i imaju sinergistički protuupalni učinak sa steroidima, ali se mogu upotrijebiti i sami kada bi kortikosteroidna terapija mogla biti rizična. Zbog njihovog snažnog utjecaja na prevenciju perioperativnih komplikacija potrebna su prospektivna klinička istraživanja za definiranje protokola terapijske primjene topičkih NSAID-a.Nonsteroidal antiinflammatory drugs (NSAIDs) have become a significant therapeutic adjunctive tool in the routine and complicated intraocular surgery. Topical NSAIDs prevent intraoperative miosis, reduce pain, postoperative inflammation and incidence of cystoid macular edema (CME). Although there is no established protocol for prophylaxis of pseudophakic CME, due to the relationship between proinflammatory prostaglandins and CME, using corticosteroids and NSAIDs could prevent CME. NSAIDs have a synergistic antiinflammatory effect with steroids, but can also be used alone when corticosteroid therapy could be harmful. Prospective clinical trials need to define treatment protocol for topical NSAIDs use, due to their powerful influence to prevent perioperative complications

Novel possibilities in treatment of dry age-related macular degeneration

Senilna makularna degeneracija (engl. age-related macular degeneration; AMD) jedan je od najvažnijih uzroka gubitka centralnog vida kod starije populacije. Dijelimo je na „vlažnu” i „suhu” formu, ovisno o prisutnosti koroidne neovaskularizacije (engl. choroidal neovascularization; CNV). Do sada nijedna terapija nije potvrđena i odobrena za liječenje geografske atrofije (engl. geographic atrophy; GA), najtežeg oblika „suhog” AMD-a, jer nije bilo moguće popraviti oštećenja retinalnog pigmentnog epitela (engl. retinal pigment epithelium; RPE) i fotoreceptora. Liječenje se svodilo na pokušaje zaustavljanja progresije oboljenja i širenja geografske atrofije. Namjera ovog članka je prikazati podatke novijih dovršenih i tekućih kliničkih ispitivanja s naglaskom na mjesto djelovanja potencijalnih lijekova. Danas su nam dostupne brojne nove dijagnostičke metode koje nam omogućavaju bolje praćenje morfoloških promjena mrežnice, RPE-a i žilnice, kao i širenja područja atrofije. Oksidativni stres, kronična upala, insuficijentni koroidalni protok krvi te depoziti lipofuscina za koje se pretpostavlja da bi imali važniju ulogu u razvoju bolesti predstavljaju potencijalne mete za djelovanje lijekova. Velik je broj tekućih studija koje istražuju moguća rješenja, kao što su protuupalni i neuroprotektivni lijekovi te matične stanice, dok će samo neki od lijekova biti dostupni na tržištu i pružiti nadu pacijentima za očuvanje centralnog vida, pa ih je potrebno dugoročno pratiti. Uključiti treba i tretman ispodpražnim i mikropulsnim laserom koji je kod nekih oboljenja mrežnice pokazao određene rezultate u revitalizaciji tkiva, a koji koristimo i na našoj Klinici, te su prvi kratkoročni rezultati skromni ali ohrabrujući i zahtijevaju daljnje tretmane i praćenje.Age-related macular degeneration (AMD) is one of the most important cause of central vision lost in elderly. AMD is “wet” or “dry”, depending on choroidal neovascularization (CNV) presence. Currently, no treatment iz approved for geographic atrophy (GA), late form of “dry” AMD because of imposibillity to restore retinal pigment epithelium (RPE) and photoreceptors. So, all earlier treatment only tried to slow down disease and spreading of GA. This review focuses on current data about potential targets for therapies evaluated in novel clinical trials. Novel diagnostic tools are available today for better monitoring of morfological changes in retina, RPE and choroid and spreading of atrophy zone. Several pathways, including oxidative stress, deposits of lipofuscin, chronic inflammation andchoroidal blood flow insufficiency, seem to play an important role in the pathogenesis of “dry” AMD and represent possible targets for new therapies. A great number of treatment for GA such as anti-inflammatory agents, neuroprotective agents and stem cells are under investigation with promising results in preliminary study, and only few will enter the market. Besides them we need to mention subtreshold and micropulse laser treatment with ability to revitalize tissue. We, also, used them on our Eye clinic with “short-term” follow-up and modest but encouraging results, so we need other studies with “long-term” follow-up

Novel possibilities in treatment of dry age-related macular degeneration

Senilna makularna degeneracija (engl. age-related macular degeneration; AMD) jedan je od najvažnijih uzroka gubitka centralnog vida kod starije populacije. Dijelimo je na „vlažnu” i „suhu” formu, ovisno o prisutnosti koroidne neovaskularizacije (engl. choroidal neovascularization; CNV). Do sada nijedna terapija nije potvrđena i odobrena za liječenje geografske atrofije (engl. geographic atrophy; GA), najtežeg oblika „suhog” AMD-a, jer nije bilo moguće popraviti oštećenja retinalnog pigmentnog epitela (engl. retinal pigment epithelium; RPE) i fotoreceptora. Liječenje se svodilo na pokušaje zaustavljanja progresije oboljenja i širenja geografske atrofije. Namjera ovog članka je prikazati podatke novijih dovršenih i tekućih kliničkih ispitivanja s naglaskom na mjesto djelovanja potencijalnih lijekova. Danas su nam dostupne brojne nove dijagnostičke metode koje nam omogućavaju bolje praćenje morfoloških promjena mrežnice, RPE-a i žilnice, kao i širenja područja atrofije. Oksidativni stres, kronična upala, insuficijentni koroidalni protok krvi te depoziti lipofuscina za koje se pretpostavlja da bi imali važniju ulogu u razvoju bolesti predstavljaju potencijalne mete za djelovanje lijekova. Velik je broj tekućih studija koje istražuju moguća rješenja, kao što su protuupalni i neuroprotektivni lijekovi te matične stanice, dok će samo neki od lijekova biti dostupni na tržištu i pružiti nadu pacijentima za očuvanje centralnog vida, pa ih je potrebno dugoročno pratiti. Uključiti treba i tretman ispodpražnim i mikropulsnim laserom koji je kod nekih oboljenja mrežnice pokazao određene rezultate u revitalizaciji tkiva, a koji koristimo i na našoj Klinici, te su prvi kratkoročni rezultati skromni ali ohrabrujući i zahtijevaju daljnje tretmane i praćenje.Age-related macular degeneration (AMD) is one of the most important cause of central vision lost in elderly. AMD is “wet” or “dry”, depending on choroidal neovascularization (CNV) presence. Currently, no treatment iz approved for geographic atrophy (GA), late form of “dry” AMD because of imposibillity to restore retinal pigment epithelium (RPE) and photoreceptors. So, all earlier treatment only tried to slow down disease and spreading of GA. This review focuses on current data about potential targets for therapies evaluated in novel clinical trials. Novel diagnostic tools are available today for better monitoring of morfological changes in retina, RPE and choroid and spreading of atrophy zone. Several pathways, including oxidative stress, deposits of lipofuscin, chronic inflammation andchoroidal blood flow insufficiency, seem to play an important role in the pathogenesis of “dry” AMD and represent possible targets for new therapies. A great number of treatment for GA such as anti-inflammatory agents, neuroprotective agents and stem cells are under investigation with promising results in preliminary study, and only few will enter the market. Besides them we need to mention subtreshold and micropulse laser treatment with ability to revitalize tissue. We, also, used them on our Eye clinic with “short-term” follow-up and modest but encouraging results, so we need other studies with “long-term” follow-up

Cistoidni makularni edem nakon operacije katarakte

Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery and is one of the possible causes of low visual acuity after cataract surgery. Various factors are implicated in its development but the core mechanism is likely surgically induced anterior segment inflammation that results in the release of endogenous inflammatory mediators. Anti-inflammatory medicines, including steroid and nonsteroid anti-inflammatory drugs, are postulated as having a role in both the prophylaxis and treatment of PCME. This article presents an updated review on the pathogenesis, risk factors, prophylaxis and treatment in PCME that reflect current research and practice.Cistoidni makularni edem komplikacija je nakon operacije katarakte i najčešći je uzrok loše vidne oštrine nakon operacije katarakte. Različiti su patofiziološki mehanizmi nastanka makularnog edema, ali najčešće se dovodi u vezu s postoperativnom upalom pri kojoj se oslobađaju medijatori upale i dovode do nakupljanja tekućine u području makule. Protuupalni lijekovi, uključujući steroide i nesteroidne antireumatike, imaju veliku ulogu u profilaksi i terapiji cistoidnog makularnog edema. U ovom preglednom članku prikazani su najnoviji stavovi o patogenetskom mehanizmu nastanka edema, rizičnim faktorima, profilaksi i terapiji, proizišli iz istraživanja i kliničke prakse

Cystoid macular edema after cataract surgery

Cistoidni makularni edem komplikacija je nakon operacije katarakte i najčešći je uzrok loše vidne oštrine nakon operacije katarakte. Različiti su patofiziološki mehanizmi nastanka makularnog edema, ali najčešće se dovodi u vezu s postoperativnom upalom pri kojoj se oslobađaju medijatori upale i dovode do nakupljanja tekućine u području makule. Protuupalni lijekovi, uključujući steroide i nesteroidne antireumatike, imaju veliku ulogu u profilaksi i terapiji cistoidnog makularnog edema. U ovom preglednom članku prikazani su najnoviji stavovi o patogenetskom mehanizmu nastanka edema, rizičnim faktorima, profilaksi i terapiji, proizišli iz istraživanja i kliničke prakse.Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery and is one of the possible causes of low visual acuity after cataract surgery. Various factors are implicated in its development but the core mechanism is likely surgically induced anterior segment inflammation that results in the release of endogenous inflammatory mediators. Anti-inflammatory medicines, including steroid and nonsteroid anti-inflammatory drugs, are postulated as having a role in both the prophylaxis and treatment of PCME. This article presents an updated review on the pathogenesis, risk factors, prophylaxis and treatment in PCME that reflect current research and practice

Cystoid macular edema after cataract surgery

Cistoidni makularni edem komplikacija je nakon operacije katarakte i najčešći je uzrok loše vidne oštrine nakon operacije katarakte. Različiti su patofiziološki mehanizmi nastanka makularnog edema, ali najčešće se dovodi u vezu s postoperativnom upalom pri kojoj se oslobađaju medijatori upale i dovode do nakupljanja tekućine u području makule. Protuupalni lijekovi, uključujući steroide i nesteroidne antireumatike, imaju veliku ulogu u profilaksi i terapiji cistoidnog makularnog edema. U ovom preglednom članku prikazani su najnoviji stavovi o patogenetskom mehanizmu nastanka edema, rizičnim faktorima, profilaksi i terapiji, proizišli iz istraživanja i kliničke prakse.Pseudophakic cystoid macular edema (PCME) is the most common complication of cataract surgery and is one of the possible causes of low visual acuity after cataract surgery. Various factors are implicated in its development but the core mechanism is likely surgically induced anterior segment inflammation that results in the release of endogenous inflammatory mediators. Anti-inflammatory medicines, including steroid and nonsteroid anti-inflammatory drugs, are postulated as having a role in both the prophylaxis and treatment of PCME. This article presents an updated review on the pathogenesis, risk factors, prophylaxis and treatment in PCME that reflect current research and practice

The Expression of Interleukin-1 alpha, TNF and VEGF in Corneal Cells of Patients with Bullous Keratopathy

Bullous keratopathy (BK) is a chronic corneal edema with or without subepithelial bullae as a result of a loss of the endothelial cells. 15 patients with BK after cataract surgery with intraocular lens implantation, due to Fuchs dystrophy (n=3) or corneal endothelial trauma (n=12) were included in the study. All patients were treated by amniotic membrane transplantation (AMT). Corneal epithelial cells in patients suffering from BK secreted 3.91±3.09 pg/mL of IL-1 alpha, 4446±16.8 pg/mL of TNF and 81.43±37.81 pg/mL of VEGF-I. Levels of all 3 investigated cytokines were significantly higher as compared to controls (p<0.005). Amniotic membranes that were used to treat investigated patients contained 638.98±613.98 pg/mL of IL-1ra, 0.026±0.009 pg/mL of sTNF and 81.39±21.01 pg/mL of VEGF-R. Beneficial clinical effect of the AMT in treating BK could be explained by its natural production of pro-inflammatory cytokine antagonists such as IL-ra, sTNF antagonist and VEGF-R