Key result
Acute hyperglycemia increases platelet activation and thrombogenic markers vs euglycemia in T2DM.
Why the study?
Hyperglycemic spikes are thought to precipitate ischemic events in T2DM, and although in vivo platelet activation had been shown in diabetes, no studies had assessed whether acute in vivo hyperglycemia induces further platelet activation.
Does acute, short-term hyperglycemia (13.9 mmol/l for 4 hours) increase shear stress-induced platelet activation and vWF levels compared to euglycemia (5.5 mmol/l) in patients with Type II diabetes mellitus?
RCT (n=12)
Double-blind
Cross-over, randomized
Does acute, short-term hyperglycemia (13.9 mmol/l for 4 hours) increase shear stress-induced platelet activation and vWF levels compared to euglycemia (5.5 mmol/l) in patients with Type II diabetes mellitus?
Acute, short-term hyperglycemic spikes in patients with Type II diabetes mellitus significantly enhance shear stress-induced platelet activation and von Willebrand factor levels, providing a potential mechanism for precipitated ischemic vascular events.
Answers are grounded in this paper and cite their sources.
Acute hyperglycemia warrants caution in type 2 diabetes for thrombotic risk; confirms causal platelet activation in RCT.
Objectives The aim of our study was to assess whether acute, short-term hyperglycemia affects platelet reactivity in patients with Type II diabetes mellitus (T2DM). Background Hyperglycemic spikes are thought to precipitate ischemic events in T2DM. Previous studies have shown in vivo platelet activation in diabetes; however, no studies have assessed whether acute in vivo hyperglycemia induces further activation of platelets. Methods In a cross-over, randomized, double-blind study, 12 patients with T2DM underwent 4 h of either acute hyperglycemia (13.9 mmol/l, 250 mg/dl) or euglycemia (5.5 mmol/l, 100 mg/dl). Shear stress-induced platelet activation, P-selectin and lysosomal integral membrane protein (LIMP) expression on platelets in the bleeding-time blood, urinary 11-dehydro-thromboxane B(2) (TxB(2)) excretion, von Willebrand factor:antigen (vWF:Ag), and von Willebrand factor:activity (vWF:activity) were measured before and after hyperglycemia or euglycemia. Results Shear stress-induced platelet activation, P-selectin and LIMP expression on platelets in the bleeding-time blood, and urinary 11-dehydro-TxB(2) excretion increased significantly after hyperglycemic clamping, whereas no changes were observed after euglycemic clamping. Plasma vWF:Ag and vWF:activity increased strikingly in parallel fashion after hyperglycemic clamping, whereas no changes were observed after euglycemic clamping. Conclusions Our data demonstrate that acute, short-term hyperglycemia induces an increased activation of platelets exposed to high shear stress conditions in vitro (filtration method) or in vivo (bleeding time). In vivo platelet activation is reflected by an increased urinary excretion of 11-dehydro-TxB(2). The increased levels of vWF in the circulation correlate with the increase in platelet activation markers and may indicate some degree of causation. Acute, short-term hyperglycemia in T2DM may precipitate vascular occlusions by facilitating platelet activation.
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Gresele et al. (2003) conducted an RCT in Type II diabetes mellitus (T2DM) (n=12). Acute hyperglycemic clamping vs. Euglycemic clamping (5.5 mmol/l, 100 mg/dl) was evaluated on Shear stress-induced platelet activation, P-selectin and LIMP expression on platelets in bleeding-time blood, urinary 11-dehydro-thromboxane B2 excretion, and plasma vWF:Ag and vWF:activity. Acute 4-h hyperglycemia (13.9 mmol/l) significantly increased shear stress-induced platelet activation, P-selectin, LIMP, urinary 11-dehydro-TxB2, and vWF vs euglycemia (5.5 mmol/l) in 12 T2DM patients.
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