Myopia and inflammation

The correlation between myopia and intraocular inflammation has rarely been explored. The aim of this article is to review myopic changes induced by inflammatory diseases and inflammatory diseases related to myopia, followed by a discussion on inflammatory choroidal neovascularization. Clinical cases are used to illustrate these conditions. The review does not include inflammatory conditions caused by surgical interventions employed for treatment of myopia. Uveitic conditions that can induce a myopic shift include sclero-choroidal inflammation, lens induced myopia due to steroid cataracts, juvenile idiopathic arthritis [JIA] induced myopia, and transient drug induced myopia due to sulfonamides and acetazolamide used for treatment of ocular toxoplasmosis and inflammatory cystoid macular edema, respectively. Most inflammatory conditions related to myopia are conditions involving the choriocapillaris. These include multifocal choroiditis and/or punctate inner choroiditis, multiple evanescent white dot syndrome and acute idiopathic blind spot enlargement. It can be hypothesized that fragility of the choriocapillaris due to particular anatomic changes due to myopia, together with unknown immunogenetic factors predispose myopic eyes to primary inflammatory choriocapillaropathies

Central serous chorioretinopathy mistaken for tuberculous choroiditis

To report a patient erroneously diagnosed with tuberculous choroiditis who was accordingly treated with long term steroids which in turn, worsened the actual disease process that turned out to be central serous chorioretinopathy [CSC]. A 59-year-old Caucasian man developed a chorioretinal disease in his right eye in 1997. Having a positive tuberculin skin test, tuberculous chorioretinitis was suspected and antituberculous therapy was administered for 4 months. In 2005, visual symptoms in the same eye recurred and despite negative interferon gamma release assay, tuberculous choroiditis was considered as the diagnosis and the patient further received massive corticosteroid therapy along with antituberculous agents. Despite a deteriorating clinical picture, therapy was continued. Upon initial examination at our center, no sign of inflammation was observed and a diagnosis of CSC was made, consequently steroid therapy was terminated. In some chorioretinopathies, it is difficult to differentiate inflammatory from non-inflammatory causes. One should observe the course of the disease and question the initial diagnosis when no improvement or deterioration occurs despite therapy

Antiglaucoma drugs: the role of preservative-free formulations

Hypersensitive reactions to eyedrops are a common finding in clinical practice and represent a frequent cause of discontinuation of the therapy. Moreover, experimental and clinical studies show that long term use of topical drugs may induce ocular surface changes causing discomfort and potentially negatively affecting the compliance to the treatment as well as the success rate of filtering procedures. The exact mechanism involved and the roles of the active compound and the preservatives in inducing such detrimental effects of ophthalmic solutions are unclear. During the last years several antiglaucoma agents have been marketed as either preservative-free or benzalkonium chloride-free formulations in an attempt to reduce the adverse effects related to preservatives. This paper summarizes the body of evidence from existing studies about preservatives in antiglaucoma eyedrops, focusing on the latest compounds commercially available. A systematic review of the literature was performed. Current research is focusing not only on the efficacy of the drugs but also on their tolerability. Based on the existing data, there is a rationale to support the use of benzalkonium-free solutions whenever possible, especially in patients suffering from concomitant ocular surface diseases, experiencing local side effects and in those expected to need multiple and prolonged topical treatments

Idiopathic choroidal neovascularisation as the inaugural sign of multiple evanescent white dot syndrome

We report a case of multiple evanescent white dot syndrome [MEWDS] that presented with putative idiopathic choroidal neovascularisation [ICNV] before showing angiographic signs typical of MEWDS. A 16-year-old male presented with unilateral metamorphopsias and visual loss in his left eye. ICNV with subretinal hemorrhage was diagnosed and treated with intravitreal Avastin [trade mark]. Fifteen days later, regression of choriodal neovascularization [CNV] was documented together with the appearance of fluorescein angiography [FA] and indocyanine green angiography [ICGA] signs typical for MEWDS, that included faint mottled FA hyperfluorescence in the mid-peripheral fundus, irregularly shaped mid-peripheral ICGA dark areas in the intermediate angiographic phase that were clearly delineated in the late phase as well as peripapillary hypofluorescence. Fundus examination appeared completely normal during the follow-up except for the CNV hemorrhage noted at the initial visit. This case demonstrates the need to consider ICNV as a diagnosis of exclusion until inflammatory causes have been eliminated. In this case, the underlying occult inflammatory condition would have been missed without the ICGA data that clearly showed signs of MEWDS that was supported by FA findings