Abstract
Background. The aim of this study was to investigate the prostanoid production in pregnancies at high risk for hypertensive disorders, and the effect of low-dose acetylsalicylic acid (ASA) on prostanoids. Material and methods. Ninety women with a bilateral notching in uterine arteries screened by Doppler ultrasound at 12-14 gestational weeks were randomized to the ASA (0.5 mg/kg/day) or placebo group. Forty-three women in both groups were followed up throughout the pregnancy. Urine samples were taken at baseline, and at 24-26 and 32-34 weeks of gestation to determine the urinary 11-dehydrothromboxane B 2 (u-11-dehydro-TxB 2 ) and 2,3-dinor-6-keto-prostaglandin F 1α (u-2,3-dinor-6-keto-PGF 1α ), the metabolites of thromboxane A 2 and prostacyclin, respectively. Results. In the pregnancies with pregnancy-induced hypertension (PIH) before 37 gestational weeks, the 2,3-dinor-6-keto-PGF 1α /11-dehydro-TxB 2 ratio did not increase as much as in other pregnancies ( P = 0.028). In the placebo group pregnancies with preeclampsia had significantly lower 2,3-dinor-6-keto-PGF 1α ( P = 0.019) at 12-14 weeks of gestation compared to other pregnancies. In the placebo group the 2,3-dinor-6-keto-PGF 1α /11-dehydroTxB 2 ratio remained unchanged throughout the pregnancy, with no significant difference between pregnancies with a normal or an adverse outcome. In the ASA group the 2,3-dinor-6-keto-PGF 1α /11-dehydro-TxB 2 ratio increased ( P < 0.001, early vs. midpregnancy). Again, the changes were similar in pregnancies with a normal or an adverse outcome. Conclusion. The balance of prostacyclin and thromboxane A 2 shifted in an unfavorable direction in pregnancies complicated by PIH. ASA had a favorable effect on the prostanoids.