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Hyperglycaemia and the Ischaemic Brain: Continuous Glucose Monitoring and Implications for Therapy

机译:高血糖症与缺血性脑:连续血糖监测及其对治疗的意义

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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.nnStroke 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 [1]. Importantly, a significant proportion of hyperglycaemic acute stroke patients (∼50%) have undiagnosed disorders of glucose metabolism, including diabetes [2,3]. 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.
机译:无论糖尿病状态如何,急性中风后的高血糖都是常见的和长期的。来自动物和人类文献的大量证据表明,中风后高血糖症对临床和放射学中风结局具有有害作用。强化的血糖控制是否会积极影响缺血组织的命运仍有待观察。本文概述了中风后高血糖导致的组织损伤的患病率,病因和机制,并探讨了迄今为止降低血糖治疗试验的证据。此外,还讨论了从连续血糖监测中得出的对中风后高血糖症的新颖见解。nn中风是全球死亡的主要原因,也是成年人长期残疾的最常见原因。越来越多的证据表明,急性缺血性中风后的生理紊乱会对结果产生不利影响。其中,中风后高血糖症(PSH)是最常见的异常现象,在中风发作时有多达50%的患者被记录[1]。重要的是,大量高血糖的急性中风患者(约50%)患有未诊断的糖代谢异常,包括糖尿病[2,3]。动物和人类数据已反复证明,PSH对缺血性脑组织的命运具有负面影响,在高血糖卒中患者中,一致的发现是梗死面积更大,死亡率更高,残疾更严重。由于这些原因,PSH代表了急性中风治疗的有吸引力的生理学靶标,并可能在广泛的时间范围,中风亚型和中风严重程度中应用。除了概述急性缺血性卒中后高血糖的不良反应外,本文还旨在总结当前降低血糖治疗试验的证据,并探讨持续的血糖监测及其对未来血糖控制的意义。

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