MedWire News: Results from an imaging study show that treating hyperglycemia does not reduce infarct growth in patients with acute stroke.
The researchers say that use of insulin to treat hyperglycemic stroke patients “requires further trials before it should be considered in routine clinical practice.”
The randomized controlled trial, published in the Annals of Neurology, included 40 patients with blood glucose levels exceeding 126 mg/dl (7 mmol/l) within 24 hours of stroke onset. Fifteen patients were given a control saline infusion, and 25 received glucose potassium insulin (GKI) infusions lasting 24, 48, or 72 hours.
Blood glucose levels rose in 68% of GKI-treated patients at the start of treatment, but were significantly lower than in the saline group after 6 hours, at 97.2 versus 124.2 mg/dl (5.4 vs 6.9 mmol/l), and after 12 hours, at 104.4 versus 126.0 mg/dl (5.8 vs 7.0 mmol/l). But blood glucose levels did not vary between active and placebo groups after 12 hours.
The primary outcome measure of infarct growth, as assessed by magnetic resonance imaging, between baseline and day 7 was not significantly different between the saline and GKI groups.
“It is possible that the duration of adequate glucose lowering in our trial was too short to observe a benefit, but it covered the period during which infarct expansion is most likely to occur,” say Keith Muir (Southern General Hospital, Glasgow, UK) and colleagues.
The researchers also examined the effect of GKI treatment in 31 patients with vessel patency data. They found that GKI treatment was associated with significant infarct growth at days 3 and 7 among patients with complete intracranial vessel occlusion, but not in those with partial or no occlusion.
Muir et al suggest that the systolic blood pressure reduction brought about by GKI treatment could cause a “critical reduction in penumbral perfusion pressure, to which a group lacking collaterals may be particularly vulnerable.”
But they stress that this subgroup analysis finding should be “regarded with caution.”
In an accompanying editorial, Karen Johnston (University of Virginia, Charlottesville, USA) and Mark Parsons (University of Newcastle, Australia) said that a larger study of glycemic control versus placebo would “be of great interest.”
Such a study should further examine the influence of vessel patency, they said, and also stratify patients by thrombolytic treatment, as this is thought to be adversely affected by hyperglycemia.
They concluded: “Overall, this work adds to the growing body of literature suggesting that there is tremendous interest in determining how best to manage hyperglycemia in the acute ischemic stroke population.”
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