Routine weighing to reduce excessive antenatal weight gain: a randomised controlled trial.

OBJECTIVE: To assess whether routinely weighing women at each antenatal visit leads to a difference in gestational weight gain and weight gain within the Institute of Medicine (IOM) recommendation. DESIGN: A randomised controlled trial. SETTING: Antenatal clinics in a tertiary obstetric hospital in Melbourne, Australia. POPULATION: Healthy women were enrolled during their antenatal booking visit if they were between 18 and 45 years of age, were <21 weeks' gestation with a singleton pregnancy. METHODS: The intervention was weighing at each antenatal clinic appointment followed by counselling by their treating clinician according to IOM gestational weight gain guidelines. The control group had standard antenatal care comprising recording weight at booking and then at 36 weeks. Primary analysis was by intention-to-treat. OUTCOME: The primary outcome was difference in mean weight gain between groups. An important secondary outcome was gestational weight gain within IOM recommendations. Secondary outcomes also included maternal or neonatal morbidity. RESULTS: Seven hundred and eighty two women consented to take part and 386 were randomised to the intervention group and 396 to the control group. There was no significant difference in weight gain between the intervention group (0.54 kg/week) compared with the control group (0.53 kg/week) (P = 0.63). A similar proportion of women gained more weight than the IOM recommended range: 75% in the intervention group and 71% in the control group (P = 0.21). There were no significant differences in secondary outcomes between the two groups. CONCLUSION: We found no evidence that regular weighing in antenatal clinics changed weight gain or was effective at reducing excessive gestational weight gain.

Women's opinions on being weighed at routine antenatal visits.

OBJECTIVE: To assess the opinions of pregnant women regarding their weight gain and to assess the level of satisfaction and anxiety provoked by being weighed in clinic. DESIGN: Questionnaires were given to women participating in a randomised controlled trial comparing routine weighing in the antenatal clinic with standard care. SETTING: A tertiary hospital antenatal clinic in Melbourne, Australia. POPULATION: In all, 782 healthy pregnant women participated in the randomised controlled trial and 586 responded to the questionnaire. METHODS: A questionnaire was offered to all participants at 36 weeks of gestation gauging their satisfaction with their weight gain during pregnancy. The intervention group was asked about their level of satisfaction and anxiety provoked by being weighed in clinic. The control group was asked whether they would have liked to be weighed in clinic. Both groups were questioned about the influences on their weight gain. RESULTS: Women in both groups were satisfied with their weight gain during pregnancy. Seventy-three percent of women in the intervention group were very comfortable with being weighed in clinic. Approximately half of those in the control group would have favoured being weighed. Twenty-one percent of women said other people influenced their weight gain; mostly family members and two-thirds of them encouraged weight gain. Less than half of the women in the study used weighing scales at home. CONCLUSION: Women were satisfied with being weighed antenatally and it did not cause anxiety. Pregnant women accepted the re-introduction of weighing in the antenatal clinic.

Persistent reversed end diastolic flow in the fetal middle cerebral artery: an ominous finding.

Fetal persistent middle cerebral artery reversed end diastolic flow is a rare and ominous finding. Previous cases have been associated with intracranial hemorrhage, growth restriction, anaemia, and hepatic anomaly. Intrauterine demise or early neonatal death is a common outcome. We report the case of persistent middle cerebral artery reversed end diastolic flow in a well-grown fetus at 32 weeks' gestation resulting from acute, severe anaemia due to a large feto-maternal hemorrhage. An emergency cesarean section was performed and the neonate required advanced resuscitation and immediate blood transfusion. Postnatal magnetic resonance imaging confirmed a hemorrhagic parietal infarct and bilateral ischaemic changes in the basal ganglia. This provides further evidence that persistent middle cerebral artery reversed end diastolic flow in any fetus is an ominous finding warranting urgent diagnostic evaluation and/or delivery.

Soluble endoglin production is upregulated by oxysterols but not quenched by pravastatin in primary placental and endothelial cells.

INTRODUCTION: Preeclampsia is a serious pregnancy complication. Soluble endoglin (sEng) is released from the placenta and contributes to the maternal endothelial dysfunction seen in preeclampsia. Recently oxysterols, which activate the Liver X Receptor (LXR), have been implicated in producing sEng, by upregulating matrix metalloproteinase-14 (MMP14; cleaves endoglin to produce sEng) and down-regulating tissue inhibitor of metalloproteinase-3 (TIMP-3; inhibitor of MMP14). The functional experiments in that study were performed on JAR cells (human choriocarcinoma cell line) and placental explants. METHODS: We characterized LXR in severe preeclamptic placentas, and assessed whether oxysterols increase release of sEng from primary human umbilical vein endothelial cells (HUVECs), primary trophoblasts and placental explants. Given pravastatin is thought to block oxysterol production and inhibit the LXR, we examined whether pravastatin reduces sEng release. RESULTS: LXRα and ß were localized to the syncytiotrophoblast and villous tips and were significantly up-regulated in preeclamptic placenta. Oxysterols upregulated sEng production in HUVECs and placental explants although the increases were far more modest than that recently reported. Oxysterols did not upregulate sEng in primary trophoblasts. Furthermore, mRNA expression of MMP14 and TIMP-3 were not altered by oxysterols in any tissue. Surprisingly, pravastatin did not decrease oxysterol-induced upregulation of sEng. DISCUSSION: LXR is up-regulated in preeclamptic placenta. Oxysterols upregulate sEng production from human tissues, but the increase is modest, suggesting this may not be the main mechanism for the very significant elevations in sEng seen in preeclampsia. Pravastatin does not decrease sEng production. CONCLUSION: Oxysterols modestly up-regulate sEng production which is not quenched by pravastatin.