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Purpose: To report the efficacy and safety of interferon (IFN) α-2a in patients with cystoid macular edema (CME) associated with presumed ocular tuberculosis (TB).Methods: We reviewed the clinical records of 5 patients with presumed ocular TB who had been treated with IFN α-2a for recurrent CME during or after completion of anti-tubercular therapy. IFN α-2a was administered at an initial dose of 3 million IU per day and then tapered after the initial response. Treatment efficacy was assessed by central macular thickness (CMT) measurement using spectral-domain optical coherence tomography and visual acuity.Results: Three patients were men, and 2 were women. Patients were aged between 38 and 66 years. Mean CMT was 483 ± 178.6 μm at baseline, 302.3 ± 56 μm at 1 week, 312.3 ± 49.5 μm at 1 month, and 286.2 ± 31.9 μm at 3 months. Mean LogMAR visual acuity was 0.6 ± 0.4 at baseline, 0.4 ± 0.3 μm at 1 week, 0.3 ± 0.3 at 1 month, and 0.3 ± 0.3 at 3 months. The treatment was interrupted for 10 days because of neutropenia after 2 weeks in 1 patient and discontinued in another after 10 days because of intolerance. Total treatment duration was 3-24 months in the remaining 4 patients.Conclusion: The present small case series suggests that IFN α-2a may be an effective and safe therapeutic option for CME that is associated with presumed ocular TB. [ABSTRACT FROM AUTHOR]

Uveitis is one of the fields in ophthalmology where a tremendous evolution took place in the past 25 years. Not only did we gain access to more efficient, more targeted, and better tolerated therapies, but also in parallel precise and quantitative measurement methods developed allowing the clinician to evaluate these therapies and adjust therapeutic intervention with a high degree of precision. Objective and quantitative measurement of the global level of intraocular inflammation became possible for most inflammatory diseases with direct or spill-over anterior chamber inflammation, thanks to laser flare photometry. The amount of retinal inflammation could be quantified by using fluorescein angiography to score retinal angiographic signs. Indocyanine green angiography gave imaging insight into the hitherto inaccessible choroidal compartment, rendering possible the quantification of choroiditis by scoring indocyanine green angiographic signs. Optical coherence tomography has enabled measurement and objective monitoring of retinal and choroidal thickness. This multimodal quantitative appraisal of intraocular inflammation represents an exquisite security in monitoring uveitis. What is enigmatic, however, is the slow pace with which these improvements are integrated in some areas. What is even more difficult to understand is the fact that clinical trials to assess new therapeutic agents still mostly rely on subjective parameters such as clinical evaluation of vitreous haze as a main endpoint; whereas a whole array of precise, quantitative, and objective modalities are available for the design of clinical studies. The scope of this work was to review the quantitative investigations that improved the management of uveitis in the past 2-3 decades. [ABSTRACT FROM AUTHOR]

Behçet disease is a chronic relapsing multisystem inflammatory disorder. Ocular involvement is characterized by a bilateral recurrent non-granulomatous panuveitis and retinal vasculitis. Posterior segment findings vary during the course of the disease, in parallel with the relapsing and remitting intraocular inflammation. Structural alterations occur with increased disease duration. Fluorescein angiography is the gold standard in revealing the extent and severity as well as the leaky and/or occlusive nature of retinal vasculitis. Multimodal imaging using color fundus photography, fluorescein angiography, and optical coherence tomography is essential in visualizing diagnostic features, detecting structural changes, and monitoring disease activity and response to treatment in patients with Behçet uveitis. [ABSTRACT FROM PUBLISHER]

PURPOSE: To describe nonglaucomatous retinal nerve fiber layer (RNFL) defects in patients with Behcet uveitis. DESIGN: Cross-sectional study and observational case series. METHODS: We reviewed the clinical photographs of patients with Behcet uveitis (n = 259), ocular toxoplasmosis (n = 120), and multiple sclerosis (MS)-associated uveitis (n = 40) for the presence of localized RNFL defects. Behcet patients with localized RNFL defects were invited to participate in a prospective evaluation including standard automated perimetry, spectraldomain optical coherence tomography (SD OCT), and RNFL thickness analysis. Main outcome measures were the prevalence of localized RNFL defects, perimetric and SD OCT findings, and RNFL thickness analysis. RESULTS: Sixty-two patients with Behcet uveitis (24%) had localized RNFL defect(s) without any visible scar. Twenty patients (17%) with ocular toxoplasmosis had a localized RNFL defect associated with a retinochoroidal scar in all. None of the MS patients had a localized RNFL defect. Of the 19 patients (24 eyes) with RNFL defect associated with Behcet uveitis who returned for follow-up, there was a corollary thinning on SD OCT B-scan in all and a corresponding visual field defect in 83%. RNFL thickness analysis was within normal limits in 54%, but revealed thinning in the thickness profile scale in 46% and in the pie chart in 21%. CONCLUSION: In Behcet uveitis, localized RNFL defects may be caused by microvascular ischemia at the optic nerve head and/or at the posterior pole and may serve as a helpful ocular diagnostic clue and an indicator of posterior pole involvement, a risk factor for poor visual prognosis. [ABSTRACT FROM AUTHOR]

Purpose: To describe 3 representative cases of autoimmune retinopathy (AIR). Methods: Clinical records of patients with a diagnosis of AIR were analyzed for demographic data, clinical findings, ancillary and laboratory tests, and treatment employed. Results: Three female patients diagnosed with AIR had bilateral reduction of electroretinogram amplitudes and elevation of visual field threshold within the central 30 degrees of the visual field that was disproportionately more severe than the clinical findings of retinal degeneration. The diagnoses were cancer-associated retinopathy, non-neoplastic AIR, and hereditary retinal dystrophy with secondary inflammation. Optic nerve involvement was also present in all cases. The patient with non-neoplastic AIR was successfully treated with systemic corticosteroids and immunomodulatory agents. Conclusion: High index of suspicion is essential for an early diagnosis of AIR. Visual function and electrophysiological tests should be included in the initial workup of patients who present with suggestive clinical signs and symptoms of AIR. [ABSTRACT FROM AUTHOR]