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Updated: Jun 14, 2026

Monitoring Dynamic Growth of Retinal Vessels in Oxygen-Induced Retinopathy Mouse Model
Published on: April 2, 2021
Nocturnal intermittent serious hypoxia and reoxygenation in proliferative diabetic retinopathy cases
Tomoaki Shiba1, Takatoshi Maeno, Yoshitsugu Saishin
1Department of Ophthalmology, Toho University Sakura Medical Center, Sakura, Chiba, Japan. tomoaki-s@sakura.med.toho-u.ac.jp
Purpose:
To clarify the relationship between evaluation items of sleep-disordered breathing and diabetic retinopathy in detail.
Design:
Cross-sectional comparative study.
Methods:
Sixty-eight consecutive nonproliferative diabetic retinopathy and 151 proliferative diabetic retinopathy (PDR) cases who had undergone surgeries in our department were included in this study. Pulse oximetry was conducted overnight and mean oxygen saturation by pulse oximeter (SpO(2); %), the sleeping 4% oxygen desaturation index (4% ODI times/hour), lowest SpO(2) (%), and the cumulative percent time spent at SpO(2) < 90% (CT 90%) were calculated. The results were evaluated and compared between the 2 groups. In addition, these results and preoperative patient background factors were analyzed using logistic regression analysis to clarify risk factor of PDR.
Results:
4% ODI and CT 90% in the PDR group were significantly higher than in the nonproliferative diabetic retinopathy group (4% ODI, 7.8 vs. 4.9; P = .007; CT 90%, 2.2 vs 0.8; P = .0006). Lowest SpO(2) was significantly lower in the PDR group than in the nonproliferative diabetic retinopathy groups (82.4 vs 87.0; P = .0006). Logistic regression analysis identified being younger, having a lower value for the lowest SpO(2), and a high hemoglobin A1c value to be risk factors for PDR (age: odds ratio, 0.90; 95% confidence interval, -0.86 to -0.94; P < .0001; lowest SpO(2): odds ratio, 0.93; 95% confidence interval, 0.88 to 0.99; P = .02; hemoglobin A1c: odds ratio, 1.00 to 1.69; P = .047).
Conclusions:
This study indicated that PDR cases had episodes of nocturnal intermittent hypoxia and reoxygenation as a result of sleep-disordered breathing and that low-value lowest SpO(2) were the risk factors for PDR development.

