Introduction of management protocol for early-onset severe pre-eclampsia.

AIM: This quality Improvement study evaluated the applicability of our protocol for early-onset severe pre-eclampsia, prepared in April 2013. METHODS: We collected data from all women with early-onset severe pre-eclampsia treated at our hospital between March 2008 and August 2015. Neonatal and maternal outcomes were compared between protocol-based (n = 17) and non-protocol-based management groups (n = 28). RESULTS: The latency period was significantly longer in the protocol-based than in the non-protocol-based group (21.9 ± 3.7 vs 11.0 ± 2.9 days). Gestational age at delivery was significantly more advanced in the protocol-based than in the non-protocol-based group (31.4 ± 0.6 vs 29.8 ± 0.4 weeks). Serious neonatal complications were significantly less prevalent in the protocol-based than in the non-protocol-based group (26% vs 79%). Among the protocol components, magnesium sulfate use was the only independent factor contributing to the absence of serious neonatal complications. The percentages of women exhibiting persistent proteinuria or hypertension at one, two and three months post-partum were similar between the groups. CONCLUSIONS: Strict adherence to our protocol improved neonatal outcomes without affecting maternal prognosis. Routine use of magnesium sulfate could be the most important component of the protocol.

Planned vaginal delivery versus planned cesarean delivery in cases of low-lying placenta.

OBJECTIVE: To assess the applicability of trial of labor in cases of low-lying placenta. METHODS: In this observational cohort study, we collected data from the women with low-lying placenta delivered at our hospital between April 2012 and December 2015. Low-lying placenta was diagnosed when the length from the placental lowest edge to the internal cervical os (placenta-os distance) was 0-20 mm at 36 gestational weeks. Planned mode of delivery for each case was determined by patient's preference. Maternal and neonatal outcomes were compared between the planned vaginal delivery group (N = 11) and the planned cesarean delivery group (N = 7). RESULTS: All the women in the planned cesarean delivery group underwent scheduled cesarean section at 37-38 gestational weeks. Three cases in the planned vaginal delivery group required emergency cesarean section for uncontrollable antepartum bleeding. The intrapartum blood loss was significantly smaller in the planned vaginal delivery group than in the planned cesarean delivery group (946 ± 204 g vs. 1649 ± 256 g, p = 0.047). Umbilical arterial blood pH was similar between the two groups. All the women requiring emergency cesarean section were accompanied by marginal sinus. CONCLUSIONS: Trial of labor can be offered to all the women with low-lying placenta except for those accompanied by marginal sinus.

Diffusion-Weighted MRI and FDG-PET in Diagnosis of Endometrial Stromal Nodule.

Preoperative differentiation of benign endometrial stromal nodule (ESN) from malignant low-grade endometrial sarcoma (LGESS) is challenging, because it requires histological evaluation of the tumor-myometrium interface, which is difficult to obtain in conventional endometrial curettage. A 72-year-old postmenopausal woman presented with 5-year history of persistent vaginal bleeding. Histological examination of the endometrial curettage specimen revealed hyperplasia of apparently normal endometrial stromal cells. T2-weighted magnetic resonance imaging (T2W-MRI) showed polypoid tumor occupying the entire uterine cavity. The tumor exhibited high signal intensity in diffusion-weighted MRI (DW-MRI) and intense accumulation of (18)F-fluorodeoxyglucose (FDG) in positron emission tomography (PET). Intense FDG accumulation was also observed in the left internal iliac region. Total abdominal hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymphadenectomy were performed under the diagnosis of LGESS with lymph node metastasis. However, postoperative histological examination proved that the tumor was ESN without lymph node metastasis. Since mitotic figure is no longer included in the diagnostic criteria of ESN or LGESS, ESN could exhibit high cellularity and high proliferative activity as observed in this case. Therefore, DW-MRI or FDG-PET is not useful in the differentiation of ESN from LGESS.

The relationship between maternal plasma leptin levels and fetal growth restriction.

Leptin is a satiety hormone secreted from the adipose tissue and human placenta. We previously demonstrated that severe preeclampsia up-regulated leptin mRNA expression in the placenta and elevated maternal plasma leptin concentrations. Preeclampsia is frequently related to generation of small for gestational age (SGA) infant especially in cases with severe preeclampsia. However, it is still controversial whether the increase in maternal plasma leptin levels is associated with fetal growth restriction without complication of preeclampsia. Therefore, the aim of the present study was to explore the relationship between maternal plasma leptin levels and fetal growth in non-preeclamptic (n = 98) and preeclamptic (n = 40) women. In non-preeclamptic pregnant women, plasma leptin levels in SGA group (n = 11) were significantly higher than those in appropriate for gestational age (AGA) group (n = 87, P<0.05). In pregnant women with preeclampsia, likewise, plasma leptin levels in SGA group (n = 15) were significantly higher than those in AGA group (n = 25, P<0.05). In multiple linear regression analysis, maternal BMI, mean arterial blood pressure and Delta SD of neonatal body weight were significant factors for determining maternal plasma leptin levels in all population studied. Maternal BMI and Delta SD of neonatal body weight showed positive correlation with maternal plasma leptin levels when analysis was performed in non-preeclamptic subjects alone. In conclusion, maternal plasma leptin levels reflect, at least partly, deterioration in fetal growth.

Significant increase in maternal plasma leptin concentration in induced delivery: a possible contribution of pro-inflammatory cytokines to placental leptin secretion.

Maternal plasma leptin concentration is significantly increased during pregnancy. However, its roles in pregnancy, especially in labor, have not been fully clarified. We measured plasma leptin concentrations in pregnant women during the course of induced labor, just after spontaneous vaginal delivery and Cesarean section at term. We also studied the regulation of leptin secretion from term placental tissue and BeWo cells, a trophoblastic cell-line. Plasma leptin concentrations increased significantly during labor (58.9 +/- 9.2 ng/ml) compared to those before labor induction (37.5 +/- 5.8 ng/ml, P<0.05), then decreased 3-6 days postpartum (14 +/- 3 ng/ml, n = 6, P<0.0001) to the levels of normal nonpregnant women. Leptin concentrations within an hour and 24 hours after spontaneous vaginal delivery were significantly higher than those after Cesarean section (P<0.05 for both comparisons). Similarly, leptin mRNA expression in placental tissues obtained after spontaneous vaginal delivery was significantly greater than that in those obtained after Cesarean section without labor (P<0.05). IL-1alpha and TNF-alpha treatment significantly stimulated leptin secretion and leptin mRNA expression in explant culture of human term placental tissue and in BeWo cells as compared with those in vehicle controls (P<0.05, for all comparisons). By contrast, oxytocin and prostaglandin F(2alpha) treatment had no effects on leptin secretion from explant culture of human term placental tissue or from BeWo cells. These data indicate that pro-inflammatory cytokines might stimulate placental leptin secretion, thus finally contributing to the increase in plasma leptin concentration during labor.

Free-to-total leptin ratio in maternal plasma is constant throughout human pregnancy.

To clarify the mechanism of leptin resistance during pregnancy, we measured plasma leptin concentrations, free to total leptin ratio (percent free leptin) and soluble leptin receptor concentrations in pregnant women, and compared the results with those in non-pregnant women. We collected plasma samples from 23 non-pregnant and 31 pregnant women in the third trimester. Plasma samples from 5 pregnant women were collected longitudinally in each trimester. Plasma leptin concentrations in pregnant women in the second trimester (17.4 +/- 3.2 ng/ml) were higher than those in the first trimester of pregnancy (11.0 +/- 2.8 ng/ml, n = 5), as previously reported. However, percent free leptin did not change significantly throughout pregnancy. Percent free leptin correlated with total leptin concentrations (ng/ml) in non-pregnant women (r = 0.727, P < 0.0001), but not in women in the third trimester of pregnancy (r = 0.006). Constant percent free leptin during pregnancy despite increased leptin concentrations indicates increased leptin binding capacity in pregnant women, that might partly contribute to the establishment of leptin resistance. On the other hand, soluble leptin receptor concentrations showed significant negative correlation with BMI and plasma leptin concentrations in pregnant women (r = -0.470, P < 0.01 and r = -0.493, P < 0.01, respectively) but not in non-pregnant women. These data suggest the possibility that soluble leptin receptor is a minor component of leptin binding capacity in the plasma of pregnant women.