Avni P Finn1, Akshay S Thomas1, Sandra S Stinnett1, Robert T Keenan2, Dilraj S Grewal1, Glenn J Jaffe3. 1. Department of Ophthalmology, Duke University Medical Center, Durham, NC, USA. 2. Department of Medicine, Division of Rheumatology and Immunology, Duke University School of Medicine, Durham, NC, USA. 3. Department of Ophthalmology, Duke University Medical Center, Durham, NC, USA. Glenn.jaffe@duke.edu.
Abstract
PURPOSE: To determine the relationship between cystoid macular edema (CME) and disease severity and progression in non-paraneoplastic autoimmune retinopathy (npAIR). METHODS: A retrospective study was conducted on patients seen between 2008 and 2016 with npAIR as defined by electroretinogram (ERG) dysfunction, visual field changes, presence of antiretinal antibodies, a negative malignancy workup, and no other apparent cause for visual dysfunction. Optical coherence tomography (OCT) scans were reviewed for each patient. A minimum follow-up of 1 year was necessary for study inclusion. The presence or absence of CME and the length of the preserved EZ on the centermost line scan of the SD-OCT images was recorded at each visit. The main outcome measure assessed was the rate of EZ loss (EZ final - EZ initial / days follow-up) over time, a marker for disease progression. RESULTS: Thirty-two eyes (16 patients) were included with an average follow-up of 42 months. Twenty-one eyes (66%) had CME on initial presentation and final follow-up (group 1), eight eyes (25%) did not have CME on presentation or final follow-up (group 2), and three eyes (9%) did not have CME on presentation but developed CME during follow-up (group 3). Group 1 eyes had a lower maximal a-wave amplitude (59.0 vs. 220.9 mV, p = 0.012) and lower maximal b-wave amplitude (88.1 vs 256.9 mV, p = 0.017) on baseline ERG compared to Group 2 eyes. The rate of EZ loss over time was significantly greater for group 1 with CME compared to group 2 without CME both at 12 months (- 1.26 μm/day vs. - 0.26 μm/day, p = 0.022) and at final follow-up (- 1.03 μm/day vs. - 0.08 μm/day, p = 0.012). CONCLUSIONS: CME was associated with decreased ERG amplitudes and greater velocity of EZ loss, suggesting that CME is a useful biomarker of more severe and more progressive disease in npAIR.
PURPOSE: To determine the relationship between cystoid macular edema (CME) and disease severity and progression in non-paraneoplastic autoimmune retinopathy (npAIR). METHODS: A retrospective study was conducted on patients seen between 2008 and 2016 with npAIR as defined by electroretinogram (ERG) dysfunction, visual field changes, presence of antiretinal antibodies, a negative malignancy workup, and no other apparent cause for visual dysfunction. Optical coherence tomography (OCT) scans were reviewed for each patient. A minimum follow-up of 1 year was necessary for study inclusion. The presence or absence of CME and the length of the preserved EZ on the centermost line scan of the SD-OCT images was recorded at each visit. The main outcome measure assessed was the rate of EZ loss (EZ final - EZ initial / days follow-up) over time, a marker for disease progression. RESULTS: Thirty-two eyes (16 patients) were included with an average follow-up of 42 months. Twenty-one eyes (66%) had CME on initial presentation and final follow-up (group 1), eight eyes (25%) did not have CME on presentation or final follow-up (group 2), and three eyes (9%) did not have CME on presentation but developed CME during follow-up (group 3). Group 1 eyes had a lower maximal a-wave amplitude (59.0 vs. 220.9 mV, p = 0.012) and lower maximal b-wave amplitude (88.1 vs 256.9 mV, p = 0.017) on baseline ERG compared to Group 2 eyes. The rate of EZ loss over time was significantly greater for group 1 with CME compared to group 2 without CME both at 12 months (- 1.26 μm/day vs. - 0.26 μm/day, p = 0.022) and at final follow-up (- 1.03 μm/day vs. - 0.08 μm/day, p = 0.012). CONCLUSIONS: CME was associated with decreased ERG amplitudes and greater velocity of EZ loss, suggesting that CME is a useful biomarker of more severe and more progressive disease in npAIR.
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