Effects of autonomic neuropathy on counterregulation and awareness at hypoglycemia in type 1 diabetic patients
Effects of autonomic neuropathy on counterregulation and awareness at hypoglycemia in type 1 diabetic patients
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DOI：
10.2337/diacare.21.11.1960
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发表时间：
1998-11-01
期刊：
影响因子：
16.2
通讯作者：
Bretzel, RG
中科院分区：
文献类型：
--
作者：
Meyer, C;Grossmann, R;Bretzel, RG
目的-最近的EURODIAB研究已经确定自主神经病变是1型糖尿病患者严重低血糖的独立危险因素。我们检验了这样一种假设，即在伴有自主神经病变（AN（+））的1型糖尿病患者中，与那些没有自主神经病变（AN（-））的1型糖尿病患者相比，反调节性儿茶酚胺反应和低血糖意识受到更大程度的损害。和低血糖发作史我们还研究了33名非糖尿病对照受试者使用阶梯式低血糖钳夹技术和确定血糖阈值和反调节激素反应和低血糖症状的幅度。两组糖尿病患者对低血糖的意识降低，表现为自主神经症状的血糖阈值升高大于或等于正常值2 SD，但症状的幅度和阈值均无差异AN（+）和AN（-）患者。两组患者对低血糖的胰高血糖素、肾上腺素、去甲肾上腺素、格鲁激素和皮质醇反应均受损。然而，与AN（-）患者相比，AN（+）患者的肾上腺素和去甲肾上腺素反应的幅度（194 +/- 49 vs. 784 1 206 pmol/l，P < 0.007，316 +/- 56 vs. 610 +/- 87 pmol/l，P < 0.02，肾上腺素和去甲肾上腺素血糖阈值（分别为2.33 +/- 0.10 vs. 2.82 - 0.10 mmol/l，P < 0.009和2.34 +/- 0.06 vs. 2.79 +/- 0.10 mmol/l，P < 0.008）受损程度更大。这与在2.3 mmol/l血糖平台期需要50%以上的外源性葡萄糖来防止更严重的低血糖有关（P < 0.002）。AN（+）和AN（-）patients.CONCLUSIONS -我们的结论是，在1型糖尿病患者中，自主神经病变进一步降低了反调节儿茶酚胺反应之间没有差异。由于这会增加严重低血糖的风险，因此可以考虑在这些患者中实现更安全的治疗目标。
OBJECTIVE - The recent EURODIAB Study has identified autonomic neuropathy as an independent risk factor for severe hypoglycemia in patients with type 1 diabetes. We tested the hypothesis that counterregulatory catecholamine responses and awareness of hypoglycemia are impaired to a greater extent in type 1 diabetic patients with autonomic neuropathy (AN(+)) than in those without autonomic neuropathy (AN(-)).RESEARCH DESIGN AND METHODS - We studied 22 type 1 diabetic patients (8 AN(+), 14 AN(-)) matched for age, duration of diabetes, glycemic control, and history of hypoglycemic episodes. We also studied 33 nondiabetic control subjects using the stepped hypoglycemic clamp technique and determined glycemic thresholds and magnitudes of counterregulatory hormone responses and of hypoglycemia symptoms.RESULTS - Both groups of diabetic patients had reduced awareness of hypoglycemia as evidenced by an elevated glycemic threshold for autonomic symptoms greater than or equal to 2 SD above normal but neither the magnitude nor thresholds for symptoms differed in AN(+) patients and AN(-) patients. Both groups also had impaired glucagon, epinephrine, norepinephrine, grou th hormone and cortisol responses to hypoglycemia. However, in AN(+) patients compared with AN(-) patients, magnitudes of epinephrine and norepinephrine responses (194 +/- 49 vs. 784 1 206 pmol/l, P < 0.007, and 316 +/- 56 vs. 610 +/- 87 pmol/l, P < 0.02, respectively) and epinephrine and norepinephrine glycemic thresholds (2.33 +/- 0.10 vs. 2.82 - 0.10 mmol/l, P < 0.009 and 2.34 +/- 0.06 vs. 2.79 +/- 0.10 mmol/l, P < 0.008, respectively) were impaired to a greater extent. This was associated with a 50% greater requirement of exogenous glucose to prevent more severe hypoglycemia during the 2.3 mmol/l glycemic plateau (P < 0.002). No differences were observed between other counterregulatory hormone responses in AN(+) and AN(-) patients.CONCLUSIONS - We conclude that in patients with type 1 diabetes, autonomic neuropathy further reduces counterregulatory catecholamine responses. Since this should increase the risk for severe hypoglycemia, one might consider safer therapeutic goals in these patients.