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Hypothesis of preeclampsia requires inclusion of the role ofplatelets

        To the Editors: We read with interest the important article by Ness and Roberts (Ness RB, Roberts JM. Heterogeneous causes constituting the single syndrome of preeclampsia: A hypothesis and its implications. Am J Obstet Gynecol 1996;175:1365-70) in which they described their hypothesis of preeclampsia. They suggest that there are distinct origins of preeclampsia, each with its own pathologic characteristics and natural history. One genesis is the result of reduced placental perfusion and another results from maternal disorders that preexist pregnancy. "Oxidative stress" may be a key for the common explanation for all the clinical and pathologic signs associated with preeclampsia; however, we are afraid that the role of platelets in the pathogenesis of that disease needs to be taken into consideration.
        Platelet-activating factor has an important role in the female genital tract during human reproduction, including ovulation, fertilization, implantation, embryo development, and initiation of parturition. An increased consumption of platelets, resulting in a mild, transient thrombocytopenia in the mother, was observed as a first maternal response to pregnancy. Wallenburg et al.
        • Wallenburg HCS
        • Dekker GA
        • Markovitz JW
        • Rotmans P.
        Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae.
        (1986) has suggested that activated platelets are involved in the pathogenesis of preeclampsia. Louden et al.
        • Louden KA
        • Broughton Pipkin F
        • Heptinstall S
        • Fox SC
        • Mitcell JRA
        • Symonds EM.
        Platelet reactivity and serum thromboxane B2 production in whole blood in gestational hypertension and pre-eclampsia.
        (1991) demonstrated a decreased platelet reactivity in women with preeclampsia. In the context of platelet activation in preeclampsia, the authors interpreted their observations as reflecting platelet exhaustion.
        We propose the following schematic explanation. The controlled activation of platelets is required in physiologic pregnancy because of implantation, placental development, maintenance of placental blood flow, induction of labor, etc. If the organism loses the equilibrium of the thromboxane A2 and prostacyclin, a hyperactivation of the platelet occurs. The effects of this activation caused the symptoms of the preeclampsia. In pregnancy-induced hypertension and preeclampsia there is a controlled hyperactivation of platelets (controlled by other regulatory mechanisms and by therapy). This hyperactivation of platelets, at least in part, may be physiologic and contributes to the maintenance of placental blood supply but has some pathophysiologic consequences (e.g., high blood pressure, increased coagulability). In HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome there is an uncontrolled hyperactivation of platelets with concomitant hemolysis, elevated liver enzymes, and low platelet count. With use of our terminology the results of Louden et al.
        • Louden KA
        • Broughton Pipkin F
        • Heptinstall S
        • Fox SC
        • Mitcell JRA
        • Symonds EM.
        Platelet reactivity and serum thromboxane B2 production in whole blood in gestational hypertension and pre-eclampsia.
        (1991) can be explained as the low reactivity of platelets is the consequence of their hyperfunction in preeclampsia; furthermore, platelet exhaustion is the well-documented sign of their hyperfunction.
        The article by Ness and Roberts is a well-documented review of preeclampsia in epidemiologic and in part of pathophysiologic relation. We might suggest that our comment complemented it with the generally accepted platelet hyperfunction associated with preeclampsia.
        József Bódis, MD, PhD, Attila Török, MD, PhD, Department of Obstetrics and Gynecology, County Teaching Hospital, H-7621 Pécs, Dischka Gy.u.7., Hungary, Hans-Rudolf Tinneberg, MD, PhD, Department of Obstetrics and Gynecology, Bielefeld,
        6/8/82911
        NO LABEL6/8/82911

        References

          • Wallenburg HCS
          • Dekker GA
          • Markovitz JW
          • Rotmans P.
          Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae.
          Lancet. 1986; 1: 1-3
          • Louden KA
          • Broughton Pipkin F
          • Heptinstall S
          • Fox SC
          • Mitcell JRA
          • Symonds EM.
          Platelet reactivity and serum thromboxane B2 production in whole blood in gestational hypertension and pre-eclampsia.
          Br J Obstet Gynaecol. 1991; 98: 1239-1244