Tordjman K M, Havlin C E, Levandoski L A, White N H, Santiago J V, Cryer P E
Metabolism Division, Washington University School of Medicine, St. Louis, MO 63110.
N Engl J Med. 1987 Dec 17;317(25):1552-9. doi: 10.1056/NEJM198712173172502.
To test the hypothesis that nocturnal hypoglycemia causes fasting hyperglycemia (the Somogyi phenomenon) in patients with insulin-dependent diabetes mellitus, we studied 10 patients, who were on their usual therapeutic regimens, from 10 p.m. through 8 a.m. on three nights. On the first night, only a control procedure was performed (blood sampling only); on the second night, hypoglycemia was prevented (by intravenous glucose infusion, if necessary, to keep plasma glucose levels above 100 mg per deciliter [5.6 mmol per liter]); and on the third night, hypoglycemia was induced (by stepped intravenous insulin infusions between midnight and 4 a.m. to keep plasma glucose levels below 50 mg per deciliter [2.8 mmol per liter]). After nocturnal hypoglycemia was induced (36 +/- 2 mg per deciliter [2.0 +/- 0.1 mmol per liter] [mean +/- SE] from 2 to 4:30 a.m.), 8 a.m. plasma glucose concentrations (113 +/- 18 mg per deciliter [6.3 +/- 1.0 mmol per liter]) were not higher than values obtained after hypoglycemia was prevented (182 +/- 14 mg per deciliter [10.1 +/- 0.8 mmol per liter]) or those obtained after blood sampling only (149 +/- 20 mg per deciliter [8.3 +/- 1.1 mmol per liter]). Indeed, regression analysis of data obtained on the control night indicated that the 8 a.m. plasma glucose concentration was directly related to the nocturnal glucose nadir (r = 0.761, P = 0.011). None of the patients was awakened by hypoglycemia. Scores for symptoms of hypoglycemia, which were determined at 8 a.m., did not differ significantly among the three studies. We conclude that asymptomatic nocturnal hypoglycemia does not appear to cause clinically important fasting hyperglycemia in patients with insulin-dependent diabetes mellitus on their usual therapeutic regimens.
为了验证夜间低血糖会导致胰岛素依赖型糖尿病患者空腹血糖升高(即苏木杰现象)这一假说,我们对10例采用常规治疗方案的患者进行了研究,在三个晚上从晚上10点至次日上午8点进行观察。第一个晚上,仅进行对照操作(仅采血);第二个晚上,预防低血糖(必要时通过静脉输注葡萄糖使血浆葡萄糖水平保持在每分升100毫克[每升5.6毫摩尔]以上);第三个晚上,诱发低血糖(在午夜至凌晨4点之间逐步静脉输注胰岛素使血浆葡萄糖水平保持在每分升50毫克[每升2.8毫摩尔]以下)。在诱发夜间低血糖后(凌晨2点至4点30分血浆葡萄糖浓度为36±2毫克每分升[2.0±0.1毫摩尔每升][均值±标准误]),上午8点的血浆葡萄糖浓度(113±18毫克每分升[6.3±1.0毫摩尔每升])并不高于预防低血糖后测得的值(182±14毫克每分升[10.1±0.8毫摩尔每升])或仅采血后测得的值(149±20毫克每分升[8.3±1.1毫摩尔每升])。实际上,对照晚上所获数据的回归分析表明,上午8点的血浆葡萄糖浓度与夜间葡萄糖最低点直接相关(r = 0.761,P = 0.011)。没有患者因低血糖而醒来。上午8点测定的低血糖症状评分在三项研究中无显著差异。我们得出结论,对于采用常规治疗方案的胰岛素依赖型糖尿病患者,无症状性夜间低血糖似乎不会导致具有临床意义的空腹血糖升高。