Urinary Excretion of 6-Keto-Pgf1α, TxB2, and PGE2 in Pregnancy-Induced Hypertension and Preeclampsia

Objective: Our intention was to investigate whether, in pregnancy-induced hypertension (PIH), preeclampsia is accompanied by an altered urinary excretion of 6-keto-PGF1α (a metabolite of prostacyclin PGI2), TxB2 (a metabolite of thromboxane A2) and PGE2. Methods: Our study included 59 PIH patients with a blood pressure > 140/90 mm Hg. Of them, 18 displayed a proteinuria > 300 mg/L and were classified as preeclamptic. As controls, 53 normotensive pregnancies were investigated. Urine samples were purified by solid-phase extraction and reversed-phase HPLC, and 6-keto-PGF1α TxB2, and PGE2 were quantified by radioimmunoassays. Results: Urinary excretion of vasodilatory prostaglandins in the third trimester was significantly reduced in hypertensive pregnancies compared to controls. Further reductions were observed in preeclamptic patients. Mean values > SEM are: 6-keto-PGFα: controls 926 ± 49 pg/mg creatinine (crea), PIH 694 ± 49 pg/mg crea, 0.01 < P < 0.001, preeclampsia 424 ± 65 pg/mg crea, P < 0.001; PGE2: controls 635 ± 34 pg/mg crea, PIH 489 ± 34 pg/mg crea, 0.01 < P < 0.001, preeclampsia 374 ± 28 pg/mg crea, P < 0.001). No significant differences were found in TxB2 output (controls 300 ± 17 pg/mg crea, PIH 243 ± 14 pg/mg crea, preeclampsia 213 ± 17 pg/mg crea). Conclusions: We conclude that hypertensive pregnancy disorders do reduce the production of vasodilatory PGI2 and PGE2. Thus, the balance between vasodilating and vasoconstrictive prostaglandins was disturbed by a smaller production of PGI2 and PGE2 rather than an overproduction of TxA2. The degree of imbalance correlated with the severity of the disease.