Prostacyclin and Thromboxane Changes Predating Clinical Onset of Preeclampsia

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Abstract
The etiology of preeclampsia is one of the major unsolved mysteries in obstetrics. Because vascular changes are a prominent feature of this condition, numerous investigations during the past decade have studied the possibility that preeclampsia is causally linked to an imbalance in the formation of prostacyclin (PGI2), a vasodilator, and thromboxane A2 (TxA2), a vasoconstrictor.1-8 The results of these studies, however, have been conflicting and confusing. One problem is that assessment of eicosanoid formation was usually performed after the onset of symptoms and, in some instances, after initiation of treatment. Thus, it is difficult, if not impossible, to determine whether changes in PGI2 or TxA2 are the cause or the result of the disease (or even its therapy). Prospective studies have been carried out in an attempt to circumvent the problem, but the number of women who developed preeclampsia was small, limiting the power of these studies to detect differences.