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Tomer Batash, Hadas Newman, Adiel Barak, Shiri Zayit-Soudry, Eran Pras, Eyal Banin, Michael Politis, Anat Loewenstein, Meira Neudorfer; Retinitis pigmentosa-associated cystoid macular edema has inflammatory optical density characteristics. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3236. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Cystoid macular edema (CME) is reported in 10-15% of patients with retinitis pigmentosa (RP). The pathogenesis of CME in RP is not entirely understood, and both inflammatory and tractional mechanisms have been suggested. The purpose of this study was to evaluate intraretinal/intracystic fluid optical density (OD) of eyes with RP-associated CME in order to determine the more likely pathogenesis.
A retrospective multicenter study was conducted. Spectralis SD-OCT (Heidelberg, Germany) was used to evaluate intraretinal-intracystic OD in 12 treatment-naive eyes with RP as the sole ophthalmic pathology. OD in the vitreous and the CME cystic spaces was measured using imageJ software (NIH) from exported raw scan data. OD ratios (ODR) were calculated by dividing the mean pixel intensity of the CME by the mean pixel intensity of the vitreous. An ODR cutoff value (1.0489, p=0.0001) was used to differentiate between an inflammatory (>1.0489) versus a tractional etiology (<1.0489), as determined in an earlier study by our group (93.6% sensitivity and 62.5% specificity). Level P < 0.05 was assumed to denote significance in all tests.
The mean ODR value of the RP patients was 1.32, suggestive of a dominant inflammatory process (i.e., >1.0489). No significant difference was found between the RP eyes and the inflammatory ODR values (p=0.5), whereas RP ODR values differed significantly from the tractional ODR values (p=0.02), revealing a dominant inflammatory process in the pathogenesis of CME secondary to RP.
Our findings indicate a dominance of inflammatory processes in the CME of RP eyes. The higher reflectivity of the intraretinal fluid might reflect the presence of inflammatory proteins and acute-phase serum reactants. Understanding the pathogenesis of CME in RP may support a potential anti-inflammatory therapeutic approach for this ailment.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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