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    Latest concepts in steroid therapy for diabetic macular oedema

    Take-home: Steroids are an important second-line treatment for the treatment of diabetic macular oedema. While side effects remain a concern, modern formulations of intravitreal steroid allow the treatment to be tailored to the individual patient.

    Introduction

    Diabetic macular oedema (DME) is the leading cause of visual impairment in patients with diabetes. It has been estimated that approximately 93 million people in developed nations are affected with diabetic retinopathy, 21 million of whom have DME. A study showed that the prevalence of DME in the US is 3.8%, with risk factors being elevated haemoglobin A1c levels and longer duration of diabetes.1 The increasing number of patients with diabetes worldwide suggests that the impact of DME on vision loss as well as functional impairment will continue to grow over the coming years.

    DME results from breakdown of the blood–retinal barrier and increased vascular permeability mediated by inflammatory cells, cytokines and other inflammatory mediators including vascular endothelial growth factor (VEGF). This increased permeability results in accumulation of intraretinal fluid and macular thickening.

    The most commonly used treatments for DME target the VEGF molecule; however, we have recently become more aware of other mediators of this condition to target, especially in cases refractory to anti-VEGF therapy.

    The efficacy of corticosteroids in DME has been shown in multiple clinical trials. The effectiveness of steroids in the treatment of DME results from multiple mechanisms. Recruitment of leukocytes, production of adhesion molecules, up-regulation of prostaglandins and accumulation of macrophages within the retina occur in diabetes, and steroids are nonspecific anti-inflammatory agents that inhibit these processes.

    Steroids also stabilise the blood–retinal barrier and reduce capillary permeability by inhibiting leukocyte recruitment and enhancing the activity of endothelial cell tight junctions.2,3 Furthermore, steroids inhibit the action of VEGF and regulate its expression, thereby directly affecting permeability and angiogenesis,4,5 in addition to regulating a number of other peptides involved in the inflammatory processes leading to DME.

    The side effects of steroids are a concern, especially in the era of anti-VEGF medications that have few ocular side effects. The main side effects of intravitreal corticosteroids for DME are cataract progression and glaucoma. For this reason, steroids are typically considered relatively contraindicated in patients with glaucoma or ocular hypertension.

    The question remains: How do today’s steroid options fit into the treatment of patients with DME?

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