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Evidence underlying the clinical management of diabetic macular oedema.

ABSTRACT: Diabetic retinopathy (DR) is the leading cause of visual loss in the developed world in those of working age, and its prevalence is predicted to double by 2025. The management of diabetic retinopathy has traditionally relied on screening, on laser treatment delivered by ophthalmologists, and on optimising blood glucose and blood pressure. Recent evidence suggests that the role of systemic factors is more complex than originally thought, and that drugs such as ACE inhibitors, fibrates and glitazones may all influence the course of diabetic macular oedema. Antagonism of vascular endothelial growth factor offers a new therapeutic avenue that may transform the management of diabetic macular oedema. Several other therapeutic options are under investigation and development, including aminoguanidine, sorbinol, ruboxistaurin and autologous stem cell transfusion.

SUBMITTER: Williams MA

PROVIDER: S-EPMC4954300 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

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Evidence underlying the clinical management of diabetic macular oedema.

Williams Michael Andrew MA Chakravarthy Usha U

Clinical medicine (London, England) 20130801 4

Diabetic retinopathy (DR) is the leading cause of visual loss in the developed world in those of working age, and its prevalence is predicted to double by 2025. The management of diabetic retinopathy has traditionally relied on screening, on laser treatment delivered by ophthalmologists, and on optimising blood glucose and blood pressure. Recent evidence suggests that the role of systemic factors is more complex than originally thought, and that drugs such as ACE inhibitors, fibrates and glitazo ...[more]

PMID: 23908503

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Project description:ObjectivesThe aim of this systematic review is to appraise the evidence for the use of anti-VEGF drugs and steroids in diabetic macular oedema (DMO) as assessed by change in best corrected visual acuity (BCVA), central macular thickness and adverse eventsData sourceMEDLINE, EMBASE, Web of Science with Conference Proceedings and the Cochrane Library (inception to July 2012). Certain conference abstracts and drug regulatory web sites were also searched.Study eligibility criteria, participants and interventionsRandomised controlled trials were used to assess clinical effectiveness and observational trials were used for safety. Trials which assessed triamcinolone, dexamethasone, fluocinolone, bevacizumab, ranibizumab, pegaptanib or aflibercept in patients with DMO were included.Study appraisal and synthesis methodsRisk of bias was assessed using the Cochrane risk of bias tool. Study results are narratively described and, where appropriate, data were pooled using random effects meta-analysis.ResultsAnti-VEGF drugs are effective compared to both laser and placebo and seem to be more effective than steroids in improving BCVA. They have been shown to be safe in the short term but require frequent injections. Studies assessing steroids (triamcinolone, dexamethasone and fluocinolone) have reported mixed results when compared with laser or placebo. Steroids have been associated with increased incidence of cataracts and intraocular pressure rise but require fewer injections, especially when steroid implants are used.LimitationsThe quality of included studies varied considerably. Five of 14 meta-analyses had moderate or high statistical heterogeneity.Conclusions and implications of key findingsThe anti-VEGFs ranibizumab and bevacizumab have consistently shown good clinical effectiveness without major unwanted side effects. Steroid results have been mixed and are usually associated with cataract formation and intraocular pressure increase. Despite the current wider spectrum of treatments for DMO, only a small proportion of patients recover good vision (?20/40), and thus the search for new therapies needs to continue.

Dataset Information

Evidence underlying the clinical management of diabetic macular oedema.

Publications

Evidence underlying the clinical management of diabetic macular oedema.

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