Allport Louise E, Baird Tracey A, Davis Stephen M
Department of Neurology, Royal Melbourne Hospital, Parkville, Vic 3050, Australia.
Curr Diabetes Rev. 2008 Aug;4(3):245-57. doi: 10.2174/157339908785294433.
Hyperglycaemia following acute stroke is both common and prolonged, regardless of diabetes status. A substantial body of evidence, derived from animal and human literature, has demonstrated that post-stroke hyperglycaemia has a deleterious effect upon clinical and radiological stroke outcomes. Whether intensive glycaemic manipulation positively influences the fate of ischaemic tissue remains to be shown. This article provides an overview of the prevalence, aetiology, and mechanisms of tissue injury arising as a result of post-stroke hyperglycaemia, as well as exploring the evidence from glucose-lowering treatment trials to date. Additionally, novel insights into post-stroke hyperglycaemia derived from continuous glucose monitoring are discussed. Stroke is a leading cause of death worldwide and the commonest cause of long-term disability amongst adults. Increasing evidence suggests that disordered physiological variables following acute ischaemic stroke adversely affect outcomes. Of these, post-stroke hyperglycaemia (PSH) is the most frequently recognised abnormality and is documented in up to 50% of patients at the time of stroke presentation. Importantly, a significant proportion of hyperglycaemic acute stroke patients (approximately 50%) have undiagnosed disorders of glucose metabolism, including diabetes. Animal and human data have repeatedly demonstrated that PSH negatively impacts upon the fate of ischaemic brain tissue, with greater infarct growth, higher mortality and more severe disability being consistent findings amongst hyperglycaemic stroke subjects. For these reasons, PSH represents an attractive physiological target for acute stroke therapies with potential application across broad time windows, stroke subtypes and stroke severity. In addition to providing an overview of the adverse effects of hyperglycaemia following acute ischaemic stroke, this article aims to summarise the evidence from current glucose-lowering treatment trials as well as exploring continuous glucose monitoring and the implications for future glycaemic manipulation.
无论糖尿病状态如何，急性中风后高血糖都很常见且持续时间较长。来自动物和人类文献的大量证据表明，中风后高血糖对临床和影像学中风结局具有有害影响。强化血糖控制是否对缺血组织的转归产生积极影响仍有待证实。本文概述了中风后高血糖导致组织损伤的患病率、病因和机制，并探讨了迄今为止降糖治疗试验的证据。此外，还讨论了连续血糖监测对中风后高血糖的新见解。中风是全球主要的死亡原因，也是成年人长期残疾的最常见原因。越来越多的证据表明，急性缺血性中风后生理变量紊乱会对结局产生不利影响。其中，中风后高血糖（PSH）是最常被识别的异常情况，在中风就诊时高达50%的患者中都有记录。重要的是，相当一部分高血糖急性中风患者（约50%）患有未被诊断的糖代谢紊乱，包括糖尿病。动物和人类数据反复表明，PSH对缺血性脑组织的转归产生负面影响，在高血糖中风患者中，梗死灶扩大、死亡率升高和残疾更严重是一致的发现。由于这些原因，PSH是急性中风治疗中一个有吸引力的生理靶点，可能适用于广泛的时间窗、中风亚型和中风严重程度。除了概述急性缺血性中风后高血糖的不良影响外，本文旨在总结当前降糖治疗试验的证据，并探讨连续血糖监测及其对未来血糖控制的影响。
