Dornan T, Mann J I, Turner R
Br Med J (Clin Res Ed). 1982 Oct 16;285(6348):1073-7. doi: 10.1136/bmj.285.6348.1073.
To investigate which factors might protect against the development of retinopathy 40 insulin-dependent diabetics who had remained free from retinopathy despite diabetes of long duration (mean+/-1 SD 30+/-10 years) were compared with 40 patients who had background and 47 who had proliferative retinopathy (mean durations of disease 16+/-5 and 19+/-5 years respectively). The three groups had had similar mean ages at onset of diabetes. The mean of all postprandial blood glucose measurements at hospital clinics from diagnosis of diabetes to detection of retinopathy, or to the most recent negative eye examination, was 9.9+/-2.1 mmol/l (178+/-38 mg/100 ml) in the group with no retinopathy, 11.8+/-2.1 mmol/l (213+/-38 mg/100 ml) in those with background retinopathy, and 12.4+/-2.1 mmol/l (223+/-38 mg/100 ml) in those with proliferative retinopathy (p <0.0001). This difference was not reflected in present concentrations of haemoglobin A(1C), probably because glycaemic control had been improved after the development of retinopathy. In the groups with background and proliferative retinopathy there were significant negative correlations between mean blood glucose concentrations and the number of years that had elapsed from diagnosis of diabetes to detection of retinopathy, suggesting that the development of both grades of retinopathy depends on the degree and duration of glycaemic exposure.The patients with no retinopathy had attended clinic more frequently (p <0.025), more of them had required emergency hospital treatment for hypoglycaemia (p <0.0025), and they tended to have had a lower prevalence of hyperglycaemic coma than the other groups. Although mean percentage ideal body weight and diastolic blood pressure were lower in the patients with no retinopathy at the time of study, mean body weight, blood pressure, and the prevalence of smoking in the years before the development of retinopathy had been similar in all groups, suggesting that these did not influence the development of retinopathy.
为了研究哪些因素可能预防视网膜病变的发生,将40例长期患糖尿病(平均±1标准差,30±10年)但仍未发生视网膜病变的胰岛素依赖型糖尿病患者,与40例有背景性视网膜病变的患者以及47例有增殖性视网膜病变的患者(疾病平均病程分别为16±5年和19±5年)进行了比较。三组患者糖尿病发病时的平均年龄相似。从糖尿病诊断到视网膜病变检测或最近一次阴性眼科检查期间,医院门诊所有餐后血糖测量值的平均值,在无视网膜病变组为9.9±2.1 mmol/L(178±38 mg/100 ml),有背景性视网膜病变组为11.8±2.1 mmol/L(213±38 mg/100 ml),有增殖性视网膜病变组为12.4±2.1 mmol/L(223±38 mg/100 ml)(p<0.0001)。这种差异在目前的糖化血红蛋白A1C浓度中未得到体现,可能是因为视网膜病变发生后血糖控制得到了改善。在有背景性和增殖性视网膜病变的组中,平均血糖浓度与从糖尿病诊断到视网膜病变检测所经过的年数之间存在显著的负相关,这表明两种程度的视网膜病变的发生都取决于血糖暴露的程度和持续时间。无视网膜病变的患者门诊就诊更频繁(p<0.025),其中更多患者因低血糖需要急诊住院治疗(p<0.0025),并且他们发生高血糖昏迷的患病率往往低于其他组。尽管在研究时无视网膜病变的患者平均理想体重百分比和舒张压较低,但在视网膜病变发生前几年,所有组的平均体重、血压和吸烟患病率相似,这表明这些因素不影响视网膜病变的发生。