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Reduced fetal exposure to aspirin using a novel controlled‐release preparation in normotensive and hypertensive pregnancies

1998; Wiley; Volume: 105; Issue: 7 Linguagem: Inglês

10.1111/j.1471-0528.1998.tb10203.x

1471-0528

Carmen Regan, Brendan McAdam, Peter McParland, Peter Boylan, Garret A. FitzGerald, Desmond J. Fitzgerald,

Inflammatory mediators and NSAID effects

Objectives To examine the fetal effects of a novel controlled‐release, low dose aspirin preparation in normal and hypertensive pregnancies. Design Random double‐blind study. Participants assigned to receive conventional formulation aspirin (75 mg), controlled‐release low dose aspirin (75 mg), or matching placebo. Setting National Maternity Hospital, Dublin. Participants Eighteen women with an uncomplicated pregnancy and 18 women with preeclampsia. Main outcome measures Urine was analysed for metabolites of thromboxane and prostacyclin by gas chromatography, mass spectrometry. Serum thromboxane B 2 , was determined in maternal and cord blood. Results Both aspirin preparations reduced maternal serum thromboxane B 2 , by 95% and induced similar reductions in the urinary 11‐dehydro‐thromboxane B 2 , a major metabolite of thromboxane A 2 in vivo. In contrast, neither preparation altered urinary 2,3–dinor‐6‐keto PGF 1α , the major metabolite of prostacyclin. Despite their similar effects in the mothers, the two aspirin preparations differed in their effects on the fetus. While both suppressed cord fetal thromboxane B 2 , this was significantly ( P < 0.005 ) less for the controlled‐release preparation (210 ± 42 ng/ml for placebo vs 109 ± 22 ng/ml for controlled‐release aspirin and 44 ± 9 ng/ml for regular oral aspirin). Conclusions At equivalent maternal suppression of serum thromboxane B 2 , a controlled aspirin release preparation results in lower fetal exposure than regular oral aspirin.