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The role of cystoid macular edema as a marker in the progression of non-paraneoplastic autoimmune retinopathy

  • Retinal Disorders
  • Published:
Graefe's Archive for Clinical and Experimental Ophthalmology Aims and scope Submit manuscript

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.

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Authors and Affiliations

  1. Department of Ophthalmology, Duke University Medical Center, Durham, NC, USA

    Avni P. Finn, Akshay S. Thomas, Sandra S. Stinnett, Dilraj S. Grewal & Glenn J. Jaffe

  2. Department of Medicine, Division of Rheumatology and Immunology, Duke University School of Medicine, Durham, NC, USA

    Robert T. Keenan

Authors
  1. Avni P. Finn
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  2. Akshay S. Thomas
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  3. Sandra S. Stinnett
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  4. Robert T. Keenan
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  5. Dilraj S. Grewal
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  6. Glenn J. Jaffe
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Corresponding author

Correspondence to Glenn J. Jaffe.

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Financial support/disclosures

Glenn J. Jaffe is a consultant for Heidelberg Engineering.

The authors have no other financial disclosures to report.

Conflict of interest

All authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest (such as honoraria; educational grants; participation in speakers’ bureaus; membership, employment, consultancies, stock ownership, or other equity interests; and expert testimony or patent-licensing arrangements), or non-financial interest (such as personal or professional relationships, affiliations, knowledge, or beliefs) in the subject matter or materials discussed in this manuscript.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

For this type of retrospective study, formal consent is not required.

Additional information

Meeting presentation

This was presented as a paper at the Retina Society Meeting, 2017 in Boston.

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Finn, A.P., Thomas, A.S., Stinnett, S.S. et al. The role of cystoid macular edema as a marker in the progression of non-paraneoplastic autoimmune retinopathy. Graefes Arch Clin Exp Ophthalmol 256, 1867–1873 (2018). https://doi.org/10.1007/s00417-018-4084-8

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  • DOI: https://doi.org/10.1007/s00417-018-4084-8

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