Hypertensive disorder of pregnancy is associated with increased risk of maternal-perinatal adverse outcome. The complications of severe preeclampsia and eclampsia could be prevented by more widespread use of prenatal care, education of primary medical care personnel, prompt diagnosis of high-risk patients and timely referral to tertiary medical centers.

Objective: To compare the efficacy of misoprostol 50 µg vaginally and 50 µg sublingually for labor induction at term. Materials and Methods: One hundred and sixty women were randomized to receive misoprostol 50 µg vaginally (n = 80) or 50 µg sublingually misoprostol (n = 80). The doses were given every 4 h (maximum 6 doses). Primary outcome measure was number of cesarean deliveries. Induction to delivery time, delivery within 24 h, the number of misoprostol doses given; the need for oxytocin augmentation, tachysystole and uterine hyperstimulation rates and neonatal outcomes were secondary outcome measures. Results: The mean induction to delivery time was 748 ± 379 min in the vaginal group and 711 ± 425 in the sublingual group (p = 0.56). The number of women delivering within 24 h was 73 (91.3%) in the vaginal group and 74 (92.5%) in the sublingual group (p = 0.78). The mean number of misoprostol doses required was significantly higher in the sublingual group (1.9 ± 1.2) compared with the vaginal group (1.1 ± 0.4; p < 0.001). More women in the sublingual group experienced tachysystole (n = 14, 17.5%) compared with the vaginal group (n = 3, 3.8%; p = 0.005). Seven cases (8.8%) in the vaginal group and 12 cases in the sublingual group (15%) required emergent cesarean delivery for fetal heart rate abnormalities (p = 0.22). Other neonatal outcomes including umbilical artery pH, Apgar scores and intensive care unit admission were similar in the two groups. Conclusion: Sublingual misoprostol is as efficacious as vaginal misoprostol for induction of labor. More frequent tachysystole is observed with misoprostol 50 µg sublingually, but neonatal outcomes are similar.

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Doppler sonography of the utero-ovarian circulation may contribute to the evaluation of PCOS patients and a better understanding of the pathophysiology of this syndrome.

PSA is a well-established tumor marker of prostatic adenocarcinoma. It is also shown to be produced by extraprostatic tissues and fluids. As the gene expression of PSA is upregulated by the androgens and progestins in hormonally responsive tissues, hyperandrogenic syndromes such as PCOS may be associated with elevated serum PSA levels. PSA appears to be a promising marker of endogenous androgen excess in females suffering from PCOS.