Changes in Aqueous Concentrations of Various Cytokines After Intravitreal Triamcinolone Versus Bevacizumab for Diabetic Macular Edema

Sohn, Hee Jin; Han, Dae Heon; Kim, Im Tae; Oh, Il Young; Kim, Kyun Hyung; Lee, Dae Yeong; Nam, Dong Heun

doi:10.1016/j.ajo.2011.03.033

Cited by 247 publications

(211 citation statements)

References 30 publications

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“…In PDR patients, the elevation of VEGF was significantly correlated with IL-6, IL-8, and MCP-1, while no significant correlation was observed in CRVO patients. In patients with DME, the glucocorticoid triamcinolone acetate (TA) reversed edema while markedly and significantly lowering vitreous levels of IL-6, MCP-1, platelet-derived growth factor subunit A (PDGF-A), and VEGF, but not IL-8, 4 weeks after intravitreal injection [38]. Thus, TA could treat edema by virtue of its anti-inflammatory effects as well as its ability to diminish VEGF levels.…”

Section: Evidence For Inflammation In Drmentioning

confidence: 99%

Neural inflammation and the microglial response in diabetic retinopathy

Abcouwer

2011

j ocul biol dis inform

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Section: Evidence For Inflammation In Drmentioning

confidence: 99%

Neural inflammation and the microglial response in diabetic retinopathy

Abcouwer

2011

j ocul biol dis inform

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“…Other evidence suggests that anti-VEGF treatments have no effect on the cytokines other than VEGF levels in intraocular fluids. [130][131][132] The available evidence therefore implies that targeting VEGF alone or VEGF-independent pathways in isolation may not adequately block the increased permeability associated with diabetes and hyperglycaemia. A combination approach may be necessary in some cases.…”

Section: Scientific Basismentioning

confidence: 99%

A review of therapies for diabetic macular oedema and rationale for combination therapy

Amoaku

Saker

Stewart

2015

Eye

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Diabetic macular oedema (DMO) is responsible for significant visual impairment in diabetic patients. The primary cause of DMO is fluid leakage resulting from increased vascular permeability through contributory anatomical and biochemical changes. These include endothelial cell (EC) death or dysfunction, pericyte loss or dysfunction, thickened basement membrane, loss or dysfunction of glial cells, and loss/change of EC Glycocalyx. The molecular changes include increased reactive oxygen species, pro-inflammatory changes: advanced glycation end products, intracellular adhesion molecule-1, Complement 5-9 deposition and cytokines, which result in increased paracellular permeability, tight junction disruption, and increased transcellular permeability. Laser photocoagulation has been the mainstay of treatment until recently when pharmacological treatments were introduced. The current treatments for DMO target reducing vascular leak in the macula once it has occurred, they do not attempt to treat the underlying pathology. These pharmacological treatments are aimed at antagonising vascular endothelial growth factor (VEGF) or non-VEGF inflammatory pathways, and include intravitreal injections of anti-VEGFs (ranibizumab, aflibercept or bevacizumab) or steroids (fluocinolone, dexamethasone or triamcinolone) as single therapies. The available evidence suggests that each individual treatment modality in DMO does not result in a completely dry macula in most cases. The ideal treatment for DMO should improve vision and improve morphological changes in the macular (eg, reduce macular oedema) for a significant duration, reduced adverse events, reduced treatment burden and costs, and be well tolerated by patients. This review evaluates the individual treatments available as monotherapies, and discusses the rationale and potential for combination therapy in DMO.

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“…By inhibiting prostaglandin production, IVTA also suppresses VEGF along with various other cytokines suspected to be involved in the pathogenesis of DME, proving to be a more effective treatment than strictly anti-VEGF agents. [47][48][49] Most recent studies are now suggesting a neuroprotective function of corticosteroids as well, specifically by demonstrating antiapoptotic effects in retinal neurons under diabetic conditions. 50 The restorative effects of IVTA are also notably longer lasting than anti-VEGF therapies, thus requiring less frequent treatment and lowering the risk for injection-associated complications such as endophthalmitis and retinal detachment over time.…”

Section: 36mentioning

confidence: 99%

Diabetic RetinopathyUpdate on Prevention Techniques, Present Therapies, and New Leads

Marozas

Fort

2014

US Endocrinology

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Diabetes is a metabolic disease resulting from the body's insufficient production or use of insulin, a peptide hormone responsible for regulating glucose levels in the blood and tissues. Especially when improperly managed, diabetes results in a number of complications over time, affecting nearly every organ system, including the ocular tissue. In addition to increased risk for glaucoma and cataracts, the most threatening ocular implication of diabetes is diabetic retinopathy, an aggressive disorder historically clinically associated with a variety of retinal microvascular abnormalities. Disease severity is typically classified into two types: nonproliferative diabetic retinopathy (NPDR), marked by microaneurysms, intraretinal hemorrhaging, and other microvascular aberrations, and proliferative diabetic retinopathy (PDR), characterized by the onset of neovascularization and vitreal hemorrhaging.1 Diabetic macular edema (DME), another manifestation of diabetic retinopathy involving macular thickening due to fluid accumulation, is accountable for a great proportion of diabetes-related vision loss. 2 While advanced stages of PDR have classically been regarded as the most threatening to sight, visual dysfunction at all stages, even those deemed mild by clinical evaluation, is now apparent. As the leading cause of blindness in US working-age adults, 3 diabetic retinopathy has many economic implications for healthcare systems and the overall population, 4 as well as a variety of personal consequences on patient quality of life. 5,6 However, if addressed early and proactively, the incidence of severe vision loss from diabetic retinopathy can be significantly reduced. This review will discuss the systemic measures necessary for diabetic retinopathy prevention, as well as interventions currently available to delay or stop retinopathy progression once diagnosed. The limitations of present treatment options will also be addressed, as well as current developments in the search for new endpoints and technologies that may allow for earlier detection.Finally, investigations of some of the new therapies and future approaches to diabetic retinopathy research will be reviewed. Systemic Control and Preventive InterventionAs the prevalence of diabetes worldwide continuously increases, incidence of vision-threatening diabetic retinopathy is projected to nearly triple in the next 40 years. 7 For patients diagnosed with diabetes, the most important method of preventing visual complications, such as retinopathy, is to control the diabetes at a systemic level. Tight regulation of glycemia via intensive insulin therapy significantly reduces the risk for retinopathy prevalence and progression. 8 In addition to its effect on glycemic and circulating insulin levels, systemic insulin therapy has been shown to have a local impact on ocular tissue as well, including restoration of retinal insulin receptor signaling cascade and rod photoreceptor function. 9,10We recently demonstrated that both components of systemic insulin treatment-normaliza...

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Changes in Aqueous Concentrations of Various Cytokines After Intravitreal Triamcinolone Versus Bevacizumab for Diabetic Macular Edema

Cited by 247 publications

References 30 publications

Neural inflammation and the microglial response in diabetic retinopathy

Neural inflammation and the microglial response in diabetic retinopathy

A review of therapies for diabetic macular oedema and rationale for combination therapy

Diabetic RetinopathyUpdate on Prevention Techniques, Present Therapies, and New Leads

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Changes in Aqueous Concentrations of Various Cytokines After Intravitreal Triamcinolone Versus Bevacizumab for Diabetic Macular Edema

Cited by 247 publications

References 30 publications

Neural inflammation and the microglial response in diabetic retinopathy

Neural inflammation and the microglial response in diabetic retinopathy

A review of therapies for diabetic macular oedema and rationale for combination therapy

Diabetic RetinopathyUpdate on Prevention Techniques, Present Therapies, and New Leads

Contact Info

Product

Resources

About

Diabetic RetinopathyUpdate on Prevention Techniques, Present Therapies, and New Leads