Cystoid macular edema in uveitis

Cystoid macular edema (CME) is a major complication of uveitis, which has an especially severe course in elderly patients. CME was noted in 33% of all uveitis patients, of whom 44% had low vision (visual acuity equal to or less than 20/60) in at least one eye. Of all uveitis patients with low vision, 42% was caused by CME. The aim of this thesis was to elucidate the possible role of vascular disease in the development of inflammatory CME and to explore the new treatment options for inflammatory CME. The new key insight into the pathogenesis of CME consists of an association between inflammatory CME and generalized microvascular damage. Until now, CME has been considered to represent a complication of uveitis associated with leaking ocular vessels and was believed to represent an ocular disorder only. However, our findings linked microalbuminuria, which is typical for a general vascular disorder, to inflammatory CME. If the pathological vascular conditions constitute a high risk for developing CME, we would expect that the vessel protecting drugs might have a beneficial effect on inflammatory CME. We found no effects of short-term lisinopril medication on inflammatory CME. However, other promising vascular protecting drugs are available and could be investigated in the future. Various cytokines and factors influencing the endothelial function play a role in the increased vascular permeability of patients with CME. Recent advances in the technique of the multiplex immunoassay allow us to measure a variety of cytokines in small volumes as in intraocular fluid samples. The understanding of the function that these mediators have in various uveitis entities and their effect on the vascular permeability and the vascular endothelium could lead to a better insight in the pathogenesis of these disorders. It could also lead to the development of novel therapeutic interventions for diverse uveitis entities and possibly also CME. Standard treatments for CME are frequently reported to be inefficient and associated with (systemic) side effects. We investigated the effect of systemic NSAIDs on visual acuity and inflammatory CME, but found a limited (if any) effect. Only a high drop out rate because of side effects (26%) of this medication was reported. In contrast, the use of intravitreal triamcinolone acetonide (IVTA) injections has given ophthalmologists a powerful tool in the treatment of CME with no -or very limited- systemic side effects. The role of IVTA might especially be of value in those patients with acute presentations and/or severe recurrences of non-infectious intraocular inflammation and patients with intractable inflammatory CME. IVTA might shorten the time interval needed to achieve improvement or remission in patients otherwise treated with slow acting medications. Further studies with longer follow-up and a higher number of patients of various uveitis entities are needed to determine the exact place of IVTA in the treatment of uveitis and inflammatory CME.