Diedrich Laura, Sandoval Darleen, Davis Stephen N
715 PRB II, Division of Diabetes & Endocrinology, Vanderbilt University Medical School, Nashville, TN 37232-6303, USA.
Clin Auton Res. 2002 Oct;12(5):358-65. doi: 10.1007/s10286-002-0035-9.
Intensively treated patients with diabetes have a three-fold increased risk of severe hypoglycemic episodes with an attendant four percent mortality. These findings, unfortunately undermine attempts to achieve normoglycemia in diabetic patients. It has been proven that antecedent hypoglycemia is a major factor responsible for blunting metabolic, neuroendocrine and also autonomic responses to subsequent hypoglycemia. Diabetic patients with good glycemic control become unable to recognize symptoms of hypoglycemia. Lack of symptoms, or hypoglycemia unawareness, is part of the syndrome called hypoglycemia associated autonomic failure. This syndrome also includes inadequate neuroendocrine hormonal responses and reduced glycemic thresholds for counterregulatory hormonal secretion. Factors regulating the magnitude of hypoglycemia associated autonomic failure include antecedent duration and frequency of hypoglycemia, prior episodes of exercise, and autonomic neuropathy. Understanding the pathophysiology of this syndrome will provide a foundation for therapy aimed at preventing severe hypoglycemia during intensive metabolic control. This article will review our current understanding of the mechanisms responsible for hypoglycemia associated autonomic failure.
强化治疗的糖尿病患者发生严重低血糖事件的风险增加了两倍，随之而来的死亡率为4%。不幸的是，这些发现削弱了在糖尿病患者中实现血糖正常的努力。已经证明，先前的低血糖是导致对随后低血糖的代谢、神经内分泌以及自主神经反应迟钝的主要因素。血糖控制良好的糖尿病患者无法识别低血糖症状。缺乏症状，即低血糖无察觉，是称为低血糖相关自主神经衰竭综合征的一部分。该综合征还包括神经内分泌激素反应不足以及对抗调节激素分泌的血糖阈值降低。调节低血糖相关自主神经衰竭严重程度的因素包括先前低血糖的持续时间和频率、先前的运动发作以及自主神经病变。了解该综合征的病理生理学将为旨在预防强化代谢控制期间严重低血糖的治疗提供基础。本文将综述我们目前对低血糖相关自主神经衰竭机制的理解。
