Matyka K A, Crowne E C, Havel P J, Macdonald I A, Matthews D, Dunger D B
Department of Paediatrics, John Radcliffe Hospital, Oxford, U.K.
Diabetes Care. 1999 Jul;22(7):1144-50. doi: 10.2337/diacare.22.7.1144.
To examine counterregulatory responses during spontaneous nocturnal hypoglycemia in prepubertal children with type 1 diabetes.
A total of 29 prepubertal patients with type 1 diabetes underwent two overnight profiles. Data were analyzed from 16 children (median [range] 8.7 [5.9-12.9] years of age) with a night of hypoglycemia and a nonhypoglycemic night. Children hypoglycemic (< 3.5 mmol/l) on night 1 were given 25% extra carbohydrate as uncooked cornstarch with their usual evening snack on night 2 to avoid hypoglycemia. Glucose, growth hormone, and cortisol were measured every 15 min, catecholamines every 30 min, and glucagon, pancreatic polypeptide, insulin, and ketones every 60 min. A group of 15 healthy control subjects, aged 9.5 (5.6-12.1) years, underwent one overnight profile.
Median duration of hypoglycemia was 225 (30-630) min, and glucose nadir was 2.0 (1.2-3.3) mmol/l. Insulin levels were not different on the two nights (P = 0.9, analysis of variance), but children with diabetes had higher insulin levels than normal control subjects between 2300 and 0300, maximal at 0200 (mean +/- SEM 57.4 +/- 5.7 vs. 31.6 +/- 5.0 pmol/l, P = 0.002). Peak epinephrine was higher on the night of hypoglycemia (0.98 [0.52-2.09] nmol/l) versus nonhypoglycemia (0.32 [0.21-0.62] nmol/l), P = 0.001, but norepinephrine (1.29 [1.07-2.64] vs. 1.26 [1.04-1.88] nmol/l, P = 0.5), glucagon (93 [64.2-125.6] vs. 100.5 [54.6-158] ng/l, P = 0.6), pancreatic polypeptide (410.2 [191-643.2] vs. 270.8 [158.2-777.8] ng/l, P = 0.5), and cortisol (513 [300-679] vs. 475 [235-739] nmol/l, P = 0.6) were not different. Glucose threshold for epinephrine release was very low, 1.9 +/- 0.2 mmol/l. There was a short-lived rise in growth hormone from 75-105 min after onset of hypoglycemia, maximal at 90 min (7.8 +/- 1.2 vs. 3.5 +/- 0.9 ng/ml, P = 0.02).
The prolonged nature of nocturnal hypoglycemic episodes may be explained in part by defective counterregulation. The risk of nocturnal hypoglycemia needs to be reduced before intensification of insulin therapy can be contemplated in this age-group.
研究1型糖尿病青春期前儿童夜间自发性低血糖期间的对抗调节反应。
29例1型糖尿病青春期前患者进行了两次夜间血糖监测。对16例儿童（年龄中位数[范围]8.7[5.9 - 12.9]岁）的数据进行分析，这些儿童经历了一个低血糖夜间和一个非低血糖夜间。第1晚发生低血糖（<3.5 mmol/l）的儿童在第2晚的常规晚餐时额外给予25%的碳水化合物，以生玉米淀粉形式提供，以避免低血糖。每15分钟测量一次血糖、生长激素和皮质醇，每30分钟测量一次儿茶酚胺，每60分钟测量一次胰高血糖素、胰多肽、胰岛素和酮体。15名年龄为9.5（5.6 - 12.1）岁的健康对照者进行了一次夜间血糖监测。
低血糖的中位持续时间为225（30 - 630）分钟，血糖最低点为2.0（1.2 - 3.3）mmol/l。两晚的胰岛素水平无差异（P = 0.9，方差分析），但糖尿病儿童在23:00至03:00之间的胰岛素水平高于正常对照者，在02:00时达到最高（平均±标准误57.4±5.7 vs. 31.6±5.0 pmol/l，P = 0.002）。低血糖夜间的肾上腺素峰值（0.98[0.52 - 2.09]nmol/l）高于非低血糖夜间（0.32[0.21 - 0.62]nmol/l），P = 0.001，但去甲肾上腺素（1.29[1.07 - 2.64] vs. 1.26[1.04 - 1.88]nmol/l，P = 0.5）、胰高血糖素（93[64.2 - 125.6] vs. 100.5[54.6 - 158]ng/l，P = 0.6）、胰多肽（410.2[191 - 643.2] vs. 270.8[158.2 - 777.8]ng/l，P = 0.5）和皮质醇（513[300 - 679] vs. 475[235 - 739]nmol/l，P = 0.6）无差异。肾上腺素释放的血糖阈值非常低，为1.9±0.2 mmol/l。低血糖发作后75 - 105分钟生长激素有短暂升高，在90分钟时达到最高（7.8±1.2 vs. 3.5±0.9 ng/ml，P = 0.02）。
夜间低血糖发作时间延长可能部分归因于对抗调节缺陷。在考虑加强该年龄组胰岛素治疗之前，需要降低夜间低血糖的风险。
