Phil B.FontanarosaMD, Deputy EditorStephen J.LurieMD, PhD, Fishbein Fellow
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. doi:10.1001/jama.283.12.1568-JLT0322-15-1
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