Heller S R
Clinical Sciences Centre, Northern General Hospital, Sheffield, UK.
Baillieres Best Pract Res Clin Endocrinol Metab. 1999 Jul;13(2):279-94. doi: 10.1053/beem.1999.0020.
Hypoglycaemia is a major factor preventing insulin-treated patients from achieving normoglycaemia. This reflects the inadequacy of current insulin treatment, which causes high insulin concentrations in the post-absorptive period. Physiological defences to hypoglycaemia include autonomic activation, which limits the fall in glucose level and causes symptoms, alerting patients to an impending episode. Many patients develop defective responses and hypoglycaemia unawareness after longstanding disease or with tight glycaemic control and are then prone to severe attacks. This may be the result of repeated hypoglycaemic episodes, which by altering cerebral glucose uptake, disturb the mechanisms that activate the central response to hypoglycaemia. Preventing further hypoglycaemia can partially reverse these defects and restore symptomatic awareness. Clinical hypoglycaemia has also been implicated in the 'dead in bed' syndrome and in chronic cognitive impairment. The problem of hypoglycaemia will eventually be solved by better insulin delivery and non-invasive glucose meters, but until then, more focused education may have a more substantial impact.
低血糖是妨碍接受胰岛素治疗的患者实现血糖正常的一个主要因素。这反映出当前胰岛素治疗存在不足,导致吸收后期胰岛素浓度过高。对低血糖的生理防御机制包括自主神经激活,它能限制血糖水平下降并引发症状,提醒患者即将发生低血糖事件。许多患者在长期患病或血糖控制严格后会出现反应缺陷和低血糖无意识现象,进而容易发生严重低血糖发作。这可能是反复发生低血糖事件的结果,反复低血糖事件通过改变大脑葡萄糖摄取,扰乱了激活对低血糖中枢反应的机制。预防进一步的低血糖可部分逆转这些缺陷并恢复症状感知。临床低血糖还与“睡梦中死亡”综合征以及慢性认知障碍有关。低血糖问题最终将通过更好的胰岛素给药方式和无创血糖仪得到解决,但在此之前,更有针对性的教育可能会产生更大影响。