Inflammation in Dry Age-Related Macular Degeneration

Rodrigues, Eduardo B

doi:10.1159/000099293

Cited by 65 publications

(45 citation statements)

References 95 publications

(76 reference statements)

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“…14 The inflammation is an important component of other ocular diseases such as age-related macular degeneration (AMD) and vascular diseases of retina. [15][16][17] The relationship between NLR and diabetic retinopathy was shown. 11 The assessment of NLR in patients with AMD was studied by Ilhan N et al 17 In their study, patients with AMD have higher NLR compared with controls and NLR correlates with age and disease severity.…”

Section: Discussionmentioning

confidence: 99%

Elevated neutrophil-to-lymphocyte ratio in pseudoexfoliation syndrome

Kurtul

Özer

Kabataş

2016

Eye

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Section: Discussionmentioning

confidence: 99%

Elevated neutrophil-to-lymphocyte ratio in pseudoexfoliation syndrome

Kurtul

Özer

Kabataş

2016

Eye

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“…Evidence indicates that the major pathogenic factors in the formation of AMD include ischemia, oxidative stress, local production of angiogenic factors, altered cholesterol metabolism, and immunological and inflammatory factors [3]. Knowledge of AMD-promoting factors has accumulating evidence that immunological factors including inflammatory events play an important role in the pathogenesis of AMD [4].…”

Section: Introductionmentioning

confidence: 99%

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

Liu¹,

Liu

Cao

et al. 2011

Inflammation

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Age-related macular degeneration (AMD) is the predominant cause of irreversible blindness in the elderly population. Despite intensive basic and clinical research, its pathogenesis remains unclear. However, evidence suggests that immunological and inflammatory factors contribute to the pathogenesis of AMD. A newly identified cytokine, IL-33, appears to be an important pro-inflammatory cytokine promoting tissue inflammation. In this study, IL-33 was increased through amyloid-beta(1-40) (Aβ(1-40)) stimulation and regulated inflammatory cytokines including IL-6, IL-8, IL-1β, and TNF-α secretion using different signaling pathways in retinal pigment epithelium (RPE) cells. Furthermore, ST2L, the important component of the IL-33 receptor, was significantly increased following recombinant human IL-33 stimulation in RPE cells. These findings suggest that IL-33-mediated inflammatory responses in RPE cells are involved in the pathogenesis of AMD. Greater understanding of the inflammatory effect of IL-33 and its role in RPE cells should aid the development of future clinical therapeutics and enable novel pharmacological approaches towards the prevention of AMD.

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“…Although the pathogenesis of CNV is complex and multifactorial, a growing body of scientific evidence indicates that inflammation plays a central role. [1][2][3] In support of this, intraocular corticosteroids have shown anatomical and visual benefit in patients with CNV. [4][5][6][7] However, their routine use is limited by their adverse effects; thus, safer alternative anti-inflammatory agents would be beneficial.…”

mentioning

confidence: 77%

Inhibition of Choroidal Neovascularization by Intravitreal Ketorolac

Kim

Toma²

2010

Arch Ophthalmol

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To determine the inhibitory effect of intravitreal nonsteroidal anti-inflammatory drugs on choroidal neovascularization (CNV) in an animal model of age-related macular degeneration.Methods: Six laser burns of sufficient power to rupture the Bruch membrane were induced in the peripapillary area of each eye of 18 adult Brown Norway rats. Both eyes of each animal received the same 5-µL intravitreal injection of 30 mg/mL of ketorolac tromethamine, 40 mg/mL of triamcinolone acetonide, or balanced salt solution. Fluorescein angiography was performed on days 14 and 21 after injection, animals were euthanized, and retinal pigment epithelium-choroidsclera (choroidal) flat mounts were prepared. Areas of abnormal vascular leakage on fluorescein angiography and vascular budding on choroidal mounts were measured and quantified using an image analysis program.Results: Intravitreal ketorolac significantly reduced CNV leakage on fluorescein angiography at 2 (P Ͻ.001) and 3 (P=.006) weeks compared with eyes injected with balanced salt solution, but intravitreal triamcinolone was a more potent inhibitor of CNV leakage than ketorolac (P Ͻ.001). Vascular budding on choroidal mounts was almost entirely suppressed with triamcinolone (PϽ.001) and significantly inhibited with ketorolac (P =.009). Conclusion:Intravitreal ketorolac significantly reduced laser-induced CNV leakage and vascular budding as determined by fluorescein angiography and choroidal flat mounts, respectively, although this effect was less than that of triamcinolone.Clinical Relevance: Intravitreal nonsteroidal antiinflammatory drugs may be useful in the treatment of CNV owing to age-related macular degeneration or other causes and offer distinct clinical advantages over corticosteroids because of their lack of association with cataract formation or glaucoma.

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Inflammation in Dry Age-Related Macular Degeneration

Cited by 65 publications

References 95 publications

Elevated neutrophil-to-lymphocyte ratio in pseudoexfoliation syndrome

Elevated neutrophil-to-lymphocyte ratio in pseudoexfoliation syndrome

IL-33 Is Induced by Amyloid-β Stimulation and Regulates Inflammatory Cytokine Production in Retinal Pigment Epithelium Cells

Inhibition of Choroidal Neovascularization by Intravitreal Ketorolac

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