Phil B.FontanarosaMD, Deputy EditorIndividualAuthorStephen J.LurieMD, PhD, Fishbein FellowIndividualAuthor
Copyright 2000 American Medical Association. All Rights Reserved.
Applicable FARS/DFARS Restrictions Apply to Government Use.2000
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 (PGF1α) 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 PGF1α was higher as early as
12 weeks in women at risk of pregnancy-induced hypertension over normal pregnancy
(TxB2/6-keto PGF1α: 0.75 vs 0.4 g) and remained
as such at term.
Benigni A, Remuzzi G. Prostacyclin and Thromboxane and the Development of Preeclampsia. JAMA. 2000;283(12):1568-1569. doi:10.1001/jama.283.12.1563