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Low-dose aspirin in pregnancy: maternal and neonatal aspirin concentrations and neonatal prostanoid formation
Andreas Leonhardt1, Stefanie Bernert, Bernhard Watzer
1Department of Pediatrics, Philipp's University, Marburg, Germany. andreas.leonhardt@mailer.uni-marburg.de
Insights
Low-dose aspirin prophylaxis (LDA) in pregnant women leads to fetal exposure to salicylic acid, suppressing neonatal platelet function. However, neonatal renal prostanoid formation remains unaffected by maternal LDA.
Area of Science:
- Obstetrics and Gynecology
- Neonatal Pharmacology
- Maternal-Fetal Medicine
Background:
- Low-dose aspirin prophylaxis (LDA) is commonly used during pregnancy.
- Understanding the pharmacokinetic and pharmacodynamic effects of LDA on both mother and fetus is crucial.
Purpose of the Study:
- To evaluate maternal and neonatal plasma concentrations of acetylsalicylic acid and salicylic acid.
- To assess neonatal endogenous prostanoid formation during maternal LDA.
Main Methods:
- Gas chromatography-mass spectrometry was used to determine drug concentrations in maternal and umbilical cord plasma.
- In vivo evaluation of neonatal prostanoid formation (thromboxane A2, prostaglandin E2, prostacyclin) and their metabolites.
Main Results:
- Maternal plasma showed rapid increases in acetylsalicylic acid and salicylic acid with LDA.
- Neonatal platelet thromboxane A2 formation was significantly suppressed by maternal LDA.
- Neonatal renal prostanoid formation and prostaglandin E2/prostacyclin levels were unaffected.
Conclusions:
- Maternal LDA leads to fetal exposure to salicylic acid.
- Acetylsalicylic acid exerts antiplatelet effects in the fetus and newborn.
- Neonatal platelet function recovers post-discontinuation of maternal LDA.
Objective:
To evaluate maternal and neonatal plasma concentrations of acetylsalicylic acid and salicylic acid and the neonatal endogenous prostanoid formation during low-dose aspirin prophylaxis (LDA; 100 mg daily) in pregnant women.
Methods:
Concentrations of acetylsalicylic acid and salicylic acid in maternal plasma after at least 4 weeks of LDA (n = 14) and in umbilical cord plasma of newborns after maternal LDA (n = 7) were determined by gas chromatography-mass spectrometry. Platelet and renal formation of thromboxane A2 and the formation of prostaglandin E2 and prostacyclin were evaluated in vivo by quantification of index metabolites in plasma and urine by gas chromatography-mass spectrometry in neonates after maternal LDA (n = 14) and in a control group.
Results:
In the pregnant women, acetylsalicylic acid and salicylic acid concentrations rapidly increased after ingestion of LDA. Acetylsalicylic acid was completely eliminated within 4 hours, whereas salicylic acid was detected with low concentrations at 18 and 21 hours after dosing. In the neonates, acetylsalicylic acid was not detected. Salicylic acid was detected in 1 infant only. Platelet thromboxane A2 formation in the newborn infants was significantly suppressed but recovered within 2 to 3 days after discontinuation of LDA. Renal thromboxane A2 formation and the formation of prostaglandin E2 and prostacyclin were not affected by LDA.
Conclusion:
In pregnant women who are treated with LDA, acetylsalicylic acid is not completely inactivated in the portal circulation but reaches the uteroplacental circulation and exerts antiplatelet effects in the fetus and newborn.
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