Inhibition of agonist-induced platelet aggregation by magnesium sulfate warrants its use as an alternative in vitro anticoagulant in pseudothrombocytopenia

MgSO4 anticoagulant prevents pseudothrombocytopenia by preserving the integrity of the platelet GPIIb‐IIIa complex

“…First of all, we confirmed that MgSO 4 , when used instead of EDTA, effectively prevents the development of PTP: 5,12 The platelet counts of three PTP patients decreased with time in EDTA blood samples kept at room temperature, while they remained stable in MgSO 4 samples (Fig 1A). However, the results of additional experiments were not compatible with the suggestion that the effect of MgSO 4 is mediated by inhibition of platelet aggregation 5,12 .…”

“…First of all, we confirmed that MgSO 4 , when used instead of EDTA, effectively prevents the development of PTP: 5,12 The platelet counts of three PTP patients decreased with time in EDTA blood samples kept at room temperature, while they remained stable in MgSO 4 samples (Fig 1A). However, the results of additional experiments were not compatible with the suggestion that the effect of MgSO 4 is mediated by inhibition of platelet aggregation 5,12 . Indeed, we showed that platelet aggregation, compared to that observed in citrate platelet‐rich plasma (PRP), was abolished in EDTA‐PRP with any tested agonist [adenosine diphosphate (ADP), collagen and arachidonic acid], while it was abolished with ADP and only partially inhibited with collagen and arachidonic acid in MgSO 4 ‐PRP (Fig 1B).…”

“…It has been proposed to substitute EDTA with magnesium sulfate (MgSO 4 ) which prevents the development of PTP 5–7 . Excess Mg 2+ inhibits platelet aggregation, 8,9 likely interfering with the essential role of Ca 2+ , 10,11 and this property has been advocated as the mechanism by which it prevents PTP 5,12 . However, this suggestion appears incongruous, because EDTA is a very potent inhibitor of platelet aggregation, as it is a strong Ca 2+ chelator: 11 if PTP is prevented by inhibitors of platelet aggregation, then EDTA would prevent, rather than cause it.…”

Influence of different methods and anticoagulants on platelet parameter measurement

“…This observation suggests that MgSO 4 anticoagulation has more far-reaching effects on platelets than citrate anticoagulation, which works primarily via Ca 2+ withdrawal. Hwang and Ravn's observation that Mg 2+ inhibits platelet aggregation in a dose-dependent manner [40,172] was confirmed by Mannuß et al, who focused on the effects of increasing MgSO 4 concentrations in hirudin anti-coagulated blood sampling devices on impedance aggregometry [171]. The activated fibrinogen receptor Gp IIb/IIIa plays an important role in the formation of a stable platelet aggregate by recruiting further platelets via fibrinogen binding and ensuring the formation of a stable aggregate.…”

“…When Mannuß and colleagues investigated platelet activation in MgSO 4 anti-coagulated blood, they demonstrated that the stimulation with ADP and arachidonic acid leads to a similarly high state of platelet activation (proportion of CD62p-and CD63-positive platelets) as in citrate anti-coagulated blood, but the aggregation as induced by several agonists (ADP, arachidonic acid, ristocetin, collagen and TRAP) was lower in MgSO 4 anti-coagulated blood than in the respective citrate or hirudin anticoagulated samples [171]. This observation suggests that MgSO 4 anticoagulation has more far-reaching effects on platelets than citrate anticoagulation, which works primarily via Ca 2+ withdrawal.…”