Rosenlund E F, Haakens K, Brinchmann-Hansen O, Dahl-Jørgensen K, Hanssen K F
Eye Department, Ullevål Hospital, Oslo, Norway.
Am J Ophthalmol. 1988 Jun 15;105(6):618-25. doi: 10.1016/0002-9394(88)90054-2.
Two women aged 22 and 19 years who had had diabetes for 11 and four years, respectively, developed proliferative retinopathy after five to seven months of significantly improved metabolic control. They were participants in two separate prospective studies including 97 insulin-dependent patients. At inclusion, one patient showed minimal background retinopathy and the other showed no retinopathy. Their level of glycosylated hemoglobin was initially high (14.3% and 17.5%) but within five to six months had fallen by 5.7% and 7.5%. The improved metabolic control was obtained by home blood glucose monitoring and insulin pump in the older patient and by home blood glucose monitoring only in the other. By maintaining near normoglycemia, regression of the proliferative retinopathy was achieved. Photocoagulation was not performed. After five and two years of follow-up, respectively, only mild background retinopathy has been noted in both patients. We concluded that a significant lowering of blood glucose may provoke proliferative retinopathy and that sustained good metabolic control may reverse this retinopathy without photocoagulation.
两名分别为22岁和19岁的女性，她们患糖尿病的时间分别为11年和4年，在代谢控制显著改善五到七个月后出现了增殖性视网膜病变。她们是两项独立前瞻性研究的参与者，这两项研究共纳入了97名胰岛素依赖型患者。入组时，一名患者有轻微的背景性视网膜病变，另一名患者没有视网膜病变。她们最初的糖化血红蛋白水平较高（分别为14.3%和17.5%），但在五到六个月内分别下降了5.7%和7.5%。年长患者通过家庭血糖监测和胰岛素泵实现了代谢控制的改善，另一名患者仅通过家庭血糖监测实现了改善。通过维持血糖接近正常水平，增殖性视网膜病变得到了消退，未进行光凝治疗。分别经过五年和两年的随访，两名患者均仅出现了轻度背景性视网膜病变。我们得出结论，血糖的显著降低可能会引发增殖性视网膜病变，而持续良好的代谢控制可能会使这种视网膜病变在无光凝治疗的情况下逆转。
