Effects of Salvia miltiorrhiza active compounds on placenta-mediated pregnancy complications

The population-based incidence of early-onset (<34 weeks) and late-onset preeclampsia (≥34 weeks) has not been adequately studied. We examined the gestational age-specific incidence of preeclampsia onset and identified the associated risk factors and birth outcomes. All singleton deliveries in Washington State, 2003-2008 (n = 456,668), were included, and preeclampsia onset was determined from hospital records linked to birth certificates. Cox and logistic regression models were used to obtain adjusted hazard ratios and odds ratios (AORs) for risk factors and birth outcomes, respectively. The overall preeclampsia rate was 3.1% and the incidence increased sharply with gestation; early- and late-onset preeclampsia rates were 0.38% and 2.72%, respectively. Among women with early-onset preeclampsia, 12% delivered at a gestation of 34 weeks or longer. Risk/protective factors common to both diseases included older maternal age, Hispanic and Native-American race, smoking, unmarried status, and male fetus. African-American race, chronic hypertension, and congenital anomalies were more strongly associated with early-onset preeclampsia, whereas younger maternal age, nulliparity, and diabetes mellitus were more strongly associated with late-onset disease. Early- but not late-onset preeclampsia conferred a high risk of fetal death (AOR, 5.8; 95% confidence interval [CI], 4.0-8.3 vs AOR, 1.3; 95% CI, 0.8-2.0, respectively). The AOR for perinatal death/severe neonatal morbidity was 16.4 (95% CI, 14.5-18.6) in early-onset and 2.0 (95% CI, 1.8-2.3) in late-onset preeclampsia. Early- and late-onset preeclampsia shares some etiological features, differ with regard to several risk factors, and lead to different outcomes. The 2 preeclampsia types should be treated as distinct entities from an etiological and prognostic standpoint. Copyright © 2013 Mosby, Inc. All rights reserved.

Pre-eclampsia is a multisystem pregnancy disorder characterised by variable degrees of placental malperfusion, with release of soluble factors into the circulation. These factors cause maternal vascular endothelial injury, which leads to hypertension and multi-organ injury. The placental disease can cause fetal growth restriction and stillbirth. Pre-eclampsia is a major cause of maternal and perinatal mortality and morbidity, especially in low-income and middle-income countries. Prophylactic low-dose aspirin can reduce the risk of preterm pre-eclampsia, but once pre-eclampsia has been diagnosed there are no curative treatments except for delivery, and no drugs have been shown to influence disease progression. Timing of delivery is planned to optimise fetal and maternal outcomes. Clinical trials have reported diagnostic and prognostic strategies that could improve fetal and maternal outcomes and have evaluated the optimal timing of birth in women with late preterm pre-eclampsia. Ongoing studies are evaluating the efficacy, dose, and timing of aspirin and calcium to prevent pre-eclampsia and are evaluating other drugs to control hypertension or ameliorate disease progression.