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A 24-year-old man presented with substantial loss of visual acuity in the left eye. He had been diagnosed with type 1 diabetes 5 years prior and had never been examined for diabetic retinopathy. At the initial examination, his hemoglobin A1c level was 11.0% (to convert to the proportion of total hemoglobin, multiply by 0.01), suggesting a lack of compliance with his diabetic treatment regimen. His best-corrected visual acuity (BCVA) was 20/100 OS and 20/60 OD. On examination of the left eye, the anterior segments were unremarkable, with no neovascularization of the angle or iris. However, there was considerable retinal thickening, substantial capillary nonperfusion in the macular area, and a large area of disc neovascularization (in more than one-third of the disc area), with leakage on the disc associated with prepapillary neovascularization, as confirmed by fluorescein angiography (Figure 1A). Optical coherence tomography confirmed retinal thickening in the macular area (central subfield thickness [CST], 805 μm), with cystoid abnormalities throughout the retinal layers as well as subretinal fluid (Figure 1B).
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Center-involved diabetic macular edema and proliferative diabetic retinopathy
C. Intravitreal anti–vascular endothelial growth factor injections and laser panretinal photocoagulation
The patient presented with proliferative diabetic retinopathy (PDR) and center-involved diabetic macular edema (CI-DME), as confirmed by disc neovascularization, increased macular thickness, and subretinal fluid. He had high-risk characteristics associated with poor diabetes control. While evidence from clinical trials supports the treatment of PDR with1 and without2 CI-DME with either anti–vascular endothelial growth factor (anti-VEGF) or panretinal photocoagulation (PRP), 1 trial3 in which a subgroup had PDR and DME demonstrated that patients benefited from anti-VEGF monotherapy (compared with PRP combined with anti-VEGF) over 2 years.
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Corresponding Author: Anat Loewenstein, MD, MHA, Tel Aviv Medical Center, Tel Aviv University, 6 Weizmann St, Tel Aviv 64239, Israel (firstname.lastname@example.org).
Published Online: July 18, 2019. doi:10.1001/jamaophthalmol.2019.2137
Conflict of Interest Disclosures: Dr Loewenstein reports grants and personal fees from Allergan plc and Bayer Healthcare AG; personal fees from Alcon, Alimera, Beyeonics, ForSight Labs, and NotalVision; and grants from Novartis and Sensor, all outside of the submitted work. Dr Korobelnik reports personal fees and nonfinancial support from Bayer Healthcare AG during the conduct of this study and personal fees from Alcon, Allergan plc, Alimera, Bayer, Chengdu Kanghong Pharmaceuticals, Novartis, Roche, Thea, and Zeiss outside of the submitted work. Dr Okada reports personal fees from Bayer Healthcare Pharmaceuticals during the conduct of this study; personal fees from AbbVie, Astellas Japan, Daiichi-Sankyo, and Senju Pharmaceutical, outside the submitted work; grants and personal fees from Bayer Yakuhin Ltd, Novartis Pharma Japan, Santen Pharmaceutical Co Ltd, and Alcon Pharma KK, during the conduct of this study; and grants and personal fees from Mitsubishi-Tanabe Pharma, outside the submitted work.
Additional Contributions: We thank the patient for granting permission to publish this information and Patricia Udaondo, MBBS, Hospital Universitario y Politécnico La Fe, for providing the case study (uncompensated). Medical writing assistance was provided by Katie L. Beski, PhD, Complete HealthVizion Ltd, who was funded by Bayer Consumer Care AG.
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