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Randomized, controlled trial of insulin for acute poststroke hyperglycemia
Michael McCormick1, Donald Hadley, John R McLean
1Division of Clinical Neurosciences, University of Glasgow, Glasgow, Scotland, UK.
Annals of Neurology
|May 4, 2010
Summary
Glucose potassium insulin (GKI) infusion in acute ischemic stroke did not reduce infarct growth. While GKI lowered blood glucose and brain lactate, it increased infarct size in patients with arterial occlusion and caused hypoglycemia.
Area of Science:
- Neuroscience
- Neurology
- Clinical Trials
Background:
- Poststroke hyperglycemia is common and linked to poor outcomes.
- The role of glucose management, like glucose potassium insulin (GKI) infusion, in ischemic stroke remains unclear.
- Hyperglycemia may increase infarct size by promoting lactic acidosis and ischemic tissue recruitment.
Purpose of the Study:
- To evaluate the efficacy of GKI infusion in reducing infarct growth in patients with acute ischemic stroke.
- To assess the impact of GKI on brain lactate concentrations and infarct progression.
Main Methods:
- A randomized, placebo-controlled trial involving 40 patients with ischemic stroke and blood glucose >126mg/dl within 24 hours.
- Primary endpoint: infarct growth measured by MRI between baseline and day 7.
- Secondary analysis: brain lactate levels measured by magnetic resonance spectroscopy.
Main Results:
- GKI infusion significantly lowered blood glucose levels but did not affect overall infarct growth compared to saline.
- A secondary analysis indicated GKI was associated with greater infarct growth in patients with complete intracranial vessel occlusion.
- Brain lactate levels were attenuated with GKI, but asymptomatic hypoglycemia occurred in 76% of GKI-treated subjects.
Conclusions:
- GKI infusion in acute ischemic stroke lowers blood glucose and brain lactate but does not reduce infarct growth.
- GKI may worsen outcomes in patients with persistent arterial occlusion and carries a high risk of hypoglycemia.
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