Platelet sensitivity to prostaglandin E1 inhibition is reduced in pre-eclampsia but not in nonproteinuric gestational hypertension

Authors

  • Pere Joan Torres,

    Consultant Obstetrician and Gyrtaecologist, Corresponding author
    1. Departament d'obstetricia i Ginecologia, Hospital Clinic, Universitat de Barcelona, Spain
      Correspondence: Dr P. J. Torres, Department of Obstetrics and Gynaecology, Hospital Clinic, Villarroel 170, 08036 Barcelona. Spain.
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  • Ginés Escolar,

    Consultant (Haematology)
    1. Departament d'Hemoteràpia i Hernostàsia, Hospital Clinic, Universitat de Barcelona, Spain
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  • Montse Palacio,

    Research Fellow
    1. Departament d'obstetricia i Ginecologia, Hospital Clinic, Universitat de Barcelona, Spain
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  • Eduard Gratacós,

    Research Fellow
    1. Departament d'obstetricia i Ginecologia, Hospital Clinic, Universitat de Barcelona, Spain
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  • Pedro L. Alonso,

    Consultant (Epidemiology)
    1. Fundació per a la Recerca Biomédica, Hospital Clinic, Universitat de Barcelona, Spain
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  • Antonio Ordinas

    Professor (Haematology)
    1. Departament d'obstetricia i Ginecologia, Hospital Clinic, Universitat de Barcelona, Spain
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Correspondence: Dr P. J. Torres, Department of Obstetrics and Gynaecology, Hospital Clinic, Villarroel 170, 08036 Barcelona. Spain.

Abstract

Objective Platelet aggregometry was used to discriminate platelet sensitivity to prostaglandin E, (PGE.) inhibition, to evaluate whether platelet behaviour in pre-eclamptic women was different in this respect than from that in nonproteinuric hypertensive women.

Methods The amount of PGE1 required to inhibit in vitro platelet aggregation induced by arachidonic acid was determined in samples from 60 women: 20 nonpregnant controls, 20 women with normal pregnancies, 10 women with gestational hypertension and 10 with pre-eclampsia.

Results The response to arachidonic acid was similar among the four groups. Amounts of PGE1 necessary to inhibit platelet aggregation were significantly higher in normal pregnant women compared with nonpregnant controls (P < 0.001). Platelets from pre-eclamptic women required significantly higher concentrations of PGE, to inhibit aggregation than the other groups studied (P < 0.001). However, there was no significant difference between normal and nonproteinuric hypertensive pregnant women.

Conclusions Our findings support the notion that increased platelet reactivity during late pregnancy is exacerbated in pre-eclamptic women but not in nonproteinuric hypertensive women. This is in agreement with the hypothesis that pre-eclampsia and gestational hypertension are different conditions. Prospective studies are required to confirm if this simple test may be useful in the early identification of pregnant women at risk for pre-eclampsia.

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