Key result
Maintaining physiological calcium prevents artifactual increases in diabetic platelet TxB2 production seen with citrated plasma.
Why the study?
Platelets of diabetic patients show increased thromboxane B2 production in vitro under low ionized calcium conditions, contrasting with normal in vivo production, suggesting a need to clarify the effect of physiological ionized calcium on thromboxane B2 production.
Does maintaining physiological ionized calcium concentrations in vitro normalize thromboxane B2 production by platelets from diabetic patients compared to controls?
Comparison
PPACK anticoagulation (physiological ionized calcium) vs citrate anticoagulation (low ionized calcium) in vitro
Design
Case-control study
Authors
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Cautions against citrated plasma assays for diabetic platelet studies; challenges prior hyperreactivity reports and leaves open physiological calcium effects on clinical risk.
Case-Control (n=77)
Does maintaining physiological ionized calcium concentrations in vitro normalize thromboxane B2 production by platelets from diabetic patients compared to controls?
p-value: p=<0.01
The apparent in vitro hyperreactivity and increased thromboxane B2 production of diabetic platelets is an artifact caused by low ionized calcium in citrated plasma, and normalizes at physiological calcium concentrations.
Falcón et al. (1993) conducted a case-control in Diabetes mellitus (n=77). Diabetes mellitus vs. Matched controls was evaluated on Arachidonic acid induced aggregation and TxB2 production (p=<0.01). Platelets from diabetic patients produced normal amounts of thromboxane B2 in vitro when physiological ionized calcium concentrations were maintained, unlike the artifactual increases seen in citrated plasma.
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