A randomized clinical trial was performed to test the hypothesis that if suspected intrauterine growth retardation (IUGR) is associated with normal umbilical artery Doppler ultrasound findings, hospitalization can safely be avoided. One hundred and fifty women with singleton pregnancies and suspected IUGR were randomized between an intervention (n = 74) and a control group (n = 76). In the intervention group, clinicians were strongly requested not to hospitalize for suspected IUGR if the Doppler findings were normal. In the control group, the Doppler results were not revealed and the participants received the standard management for suspected IUGR. Endpoints of the trial were: costs in terms of hospitalization, perinatal outcome, neurological development, and postnatal growth. Duration of hospitalization was significantly shorter in the intervention group than in the control group. Contrary to expectations, the hospitalization rate during pregnancy in the intervention group was not below that of the control group. This negative finding was partly due to the admission of patients in the intervention group despite their normal Doppler results. Moreover, the trial might have induced a more critical attitude towards hospitalization in suspected IUGR, decreasing admission in the control group. No clear differences were found in perinatal outcome, neurological development, or postnatal growth. The results suggest that normal umbilical artery Doppler findings in suspected cases of IUGR justify outpatient management.

Summary. Thirty-three women who were planned for an in vitro fertilization (IVF) cycle donated blood at four time points during treatment: at baseline, after downregulation, hyperstimulation and luteal support. Levels of progesterone, 17b-oestradiol and indicators of the protein C pathway, i.e. activated protein C sensitivity ratios (APCsr), protein C, protein C inhibitor and protein S were measured. Compared with baseline, oestradiol decreased twofold at downregulation and increased 40-fold at hyperstimulation. Progesterone was elevated 2´5-fold at hyperstimulation and 40-fold at luteal support. The APCsr increased slightly at downregulation, significantly increased during hyperstimulation and remained high during luteal support. The plasma levels of the anticoagulant proteins did not change or changed moderately during treatment. During downregulation, progesterone correlated negatively with APCsr (r 20´398, P 0´024). At hyperstimulation oestradiol correlated with the APCsr (r 0´615, P , 0´0005). Moreover, there was a significant correlation (r 0´599, P , 0´0005) between the difference in baseline and hyperstimulation values of oestradiol (DE2 6´6 nmol/l) and the APCsr (DAPCsr 0´30). Six women who participated in this study became pregnant. Compared with baseline, the APCsr was increased 1´9-fold (DAPCsr 1´48) and free protein S free level decreased 30% at 7 weeks of pregnancy. This study demonstrates that despite the considerable changes in endogenous oestradiol and progesterone during an IVF cycle, changes in plasma levels of anticoagulant proteins are moderate. The significant increase in the APCsr during hyperstimulation indicates that acquired APC resistance observed during sex steroid hormone changes in women is at least partially caused by high oestrogen levels. Our findings demonstrate that IVF treatment is accompanied by the development of a mild prothrombotic condition.

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