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To the Editor: Dr Mills and colleagues¹ reported reduced prostacyclin (PGI₂) production in the face of unchanged thromboxane A₂ (TxA₂) generation in pregnant women 3.5 to 4 months before clinical onset of preeclampsia. This is exactly what we described 10 years ago in a longitudinal study aimed at systematically measuring TxA₂ and PGI₂ urinary metabolites in healthy pregnant women and in subjects at risk of developing pregnancy-induced hypertension.² We showed that urinary excretion of 6-keto (PGF₁) was significantly reduced (by 42%) in women at risk of developing preeclampsia compared with healthy pregnant women as early as 12 weeks of gestation and remained lower at 16 weeks (by 48%), 24 weeks (by 30%), and until term (by 43%). By contrast, urinary thromboxane B₂ (TxB₂) excretion was fairly similar in women at risk of preeclampsia and in those with normal pregnancy. Consequently, the ratio of TxB₂ and 6-keto . . . [Full Text of this Article]

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RELATED ARTICLE

Prostacyclin and Thromboxane Changes Predating Clinical Onset of Preeclampsia: A Multicenter Prospective Study
James L. Mills, Rebecca DerSimonian, Elizabeth Raymond, Jason D. Morrow, L. Jackson Roberts II, John D. Clemens, John C. Hauth, Patrick Catalano, Baha Sibai, L. B. Curet, and Richard J. Levine
JAMA. 1999;282(4):356-362.
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