ABSTRACT
The weight of evidence favors a modest reduction in platelet count in pregnancy towards term8-12. Burrows and Kelton11studied over 1300 subjects and found a mean platelet count at term of 225 x 109/l (95% confidence interval 109-341 x 109/l), which is below accepted nonpregnant normal values. The reports of increased mean platelet volume and volume distribution width13,14 are consistent with a compensated state of progressive platelet destruction, particularly during the third trimester. However, a cytofluorimetry study15, using an antibody directed against a platelet α granule membrane protein to identify activated platelets ex vivo, observed no platelet volume change or activation. In vitro, an increase in platelet reactivity is seen in normal pregnancy in response to a variety of agonists that stimulate aggregation, but
particularly those that are thromboxane-dependent16-20. This may reflect increased platelet sensitivity to thromboxane A221, and a relative failure of increased cyclic adenosine monophosphate (cAMP) production in response to agents such as prostacyclin, which inhibit platelet function through cAMP21. An increase in circulating platelet aggregates also suggests a degree of in vivo platelet activation in normal pregnancy22, in keeping with enhanced reactivity, while ex vivo platelet reactivity is simultaneously reduced. This apparent paradox may reflect a degree of platelet exhaustion consequent upon enhanced activation in levels of β-thromboglobulin, a protein reflecting in vivo platelet activation and degranulation23. Thus, the available evidence is consistent with vivo. In vivo platelet activation is also supported by increased plasma a degree of enhanced platelet activation and/or destruction in normal pregnancy, which is partly compensated by increased production, thus resulting in a reduction in platelet count. Following delivery, the platelet count increases9 in reaction to, and in compensation for, platelet consumption.
