Mokán M
Metabolická jednotka I. internej kliniky MFN v Martine, Slovakia.
Bratisl Lek Listy. 1995 Jun;96(6):311-6.
The occurrence of hypoglycemia is common in patients with insulin-dependent diabetes mellitus. They experience an average of one to two episodes of symptomatic hypoglycemia per week; 10-20% suffer at least one episode of severe hypoglycemia in a given year. The incidence of severe hypoglycemia in diabetic patients treated with intensive insulin therapy is threefold higher than in patients on conventional insulin therapy and 55% of all episodes occurred in sleep. Prevention of hypoglycemia or the restoring of euglycemia involve the dissipation of metabolic insulin effects and activation of counterregulatory hormone responses (glucagon, catecholamines, growth hormone, cortisol). Among counterregulatory mechanisms there exists hierarchy. The glycemic threshold for release of glucoregulatory hormones in normal people is about 3.8 mmol/l. The glucose counterregulatory system is often impaired in patients with diabetes mellitus with the onset early after diagnosis of diabetes mellitus. Impaired glucagon response is almost universally present after 5 years of diabetes. The defect is selective and the mechanism is not fully explained. Most often it is considered a defect in signal perception of alfa-cells, a rearrangement of islets of Langerhans with predominance of delta-cells or mechanism of central adaptation. After 5-10 years of diabetes glucose counterregulation becomes further impaired with a defect in epinephrine secretion. A possible mechanism is the abnormality at the CNS level. Autonomic neuropathy is a contributory factor. Defective hormonal counterregulation correlates well with duration of diabetes and strict glycemic control. If the glucagon response is intact the hormonal counterregulation is sufficient even in the presence of the impairment of other glucoregulatory factors.(ABSTRACT TRUNCATED AT 250 WORDS)
低血糖在胰岛素依赖型糖尿病患者中很常见。他们平均每周经历一到两次有症状的低血糖发作;10%至20%的患者在特定年份至少经历一次严重低血糖发作。接受强化胰岛素治疗的糖尿病患者发生严重低血糖的发生率比接受传统胰岛素治疗的患者高三倍,且所有发作中有55%发生在睡眠中。预防低血糖或恢复正常血糖需要消除胰岛素的代谢作用并激活反调节激素反应(胰高血糖素、儿茶酚胺、生长激素、皮质醇)。在反调节机制中存在层级关系。正常人中释放血糖调节激素的血糖阈值约为3.8 mmol/l。糖尿病患者的葡萄糖反调节系统常在糖尿病诊断后早期就受损。糖尿病5年后几乎普遍存在胰高血糖素反应受损。这种缺陷具有选择性,其机制尚未完全阐明。最常被认为是α细胞信号感知缺陷、以δ细胞为主的胰岛细胞重排或中枢适应机制。糖尿病5至10年后,葡萄糖反调节会因肾上腺素分泌缺陷而进一步受损。一种可能的机制是中枢神经系统层面的异常。自主神经病变是一个促成因素。激素反调节缺陷与糖尿病病程和严格的血糖控制密切相关。如果胰高血糖素反应完好,即使存在其他血糖调节因子受损,激素反调节也足够。(摘要截断于250字)