A placental polyp arising from an exaggerated placental site

There are very few reported cases of the clinical course of exaggerated placental site, and a case of a placental polyp arising from an exaggerated placental site has not been reported previously. Here, we report a case of a 43-year-old woman whose chief complaint was of massive genital bleeding. She had undergone an operation for induced abortion in the first trimester 41 days previously. A placental polyp measuring 45 mm with an abundant blood flow could be detected by transvaginal color Doppler ultrasonography and enhanced magnetic resonance imaging. We performed a transabdominal simple total hysterectomy. At the anterior wall of the uterus, a protruding lesion into the uterine cavity was observed and a placental polyp was attached to the protruding lesion. The histological specimen of the protruding lesion, which was considered to be the implantation site, showed intermediate trophoblastic cells infiltrated into the myometrium. An exaggerated placental site was diagnosed, which might lead to a placental polyp.     

The correlation of reduced amniotic fluid volume, placental maturity and morphologic placental changes in placental insufficiency

A reduced quantity of amniotic fluid is diagnosed semiquantitatively in 41 pregnant women in the 38th to 40th week of gestation. In 21 cases, the birth of a mature hypotrophic child below the 10th weight percentile is registered. Sonographically, the placentas of the mature eutrophic children significantly more frequently show a grade III maturity and the placentas of the mature hypotrophic children a grade II maturity. In contrast to the values found in the placentas of eutrophic children and in the placentas with grade III maturity, a significantly decreased villous vascularization is determined in the placentas of hypotrophic children and in placentas with grade II maturity. The area of attachment of the placenta is 301 cm2 for the eutrophic children and 222 cm2 for the hypotrophic children. All findings are discussed and compared with the relevant data of the pertinent literature.     

Concentration of placental protein 19 in body fluid and placental tissues

Summary Placental protein 19 (PP19) is one of the new placental tissue proteins identified in extracts from human term placenta by Bohn and Winkler [1]. We measured the PP19 concentration in body fluids and placental tissue by radioimmunoassay; the minimum detectable dose of standard was 1.5 ng/ml. Although ethylene diamine tetraacetic acid (EDTA-2K) inhibited the immunoreaction between PP19 (225/242) and anti-PP19 antibody (632 ZA), the PP19 concentration did not differ between serum and heparin and sodium citrate plasmas. The serum PP19 concentration was increased by hemolysis. In blood cell fractions separated by the Ficoll-Paque/Macrodex method, polymorphonuclear leukocyte fraction contained the highest PP19 concentration. The circulating serum PP19 concentration was 4.5±1.1 ng/ml (mean ± standard deviation) in the proliferative phase (n=8) and 5.1±1.6 ng/ml in the secretory phase (n=7) for nonpregnant women, and 4.6±2.2 ng/ml from men (n=12). Seminal plasma (n=8) contained 212.2±99.7 ng/ml. The maternal serum PP19 concentration in 291 normal pregnancies increased from 6.2 ng/ml (median) at 6–7 weeks of gestation to 34.1 ng/ml at 38–39 weeks. The mean PP19 concentration was higher in amniotic fluid and retroplacental blood, but lower in umbilical cord blood than that in circulating maternal serum. In hydatidiform mole, vesicular fluid contained high PP19 concentration (1154.6±659.5 ng/ml), although these maternal serum concentration was not statistically higher than normal range. The chorionic villous trophoblast contained more PP19 than decidua, chorion, and amnion. These results suggest that PP19 has an extraplacental source, even though the chorionic villous trophoblast may be the main source throughout pregnancy.     

Serial human placental lactogen estimations in serum and placental weight-for-dates.

The relation between serial HPL assays in serum and placental weight-for-dates was studied in 70 randomly chosen pregnant women. Out of five different aspects of the HPL curve only a fall below the 2-3d centile without subsequent recovery was related to low placental weight. When a small-for-dates (SFD) placenta was associated with normal HPL levels, maternal body weight tended to be lower than if both placental weight and HPL levels were abnormal. This suggests that physiologically small placentae are discernible from pathologically small placentae by a normal HPL curve.     

Glucocorticoids inhibit placental cytokines from cultured normal and preeclamptic placental explants

Glucocorticoids are used in pregnancy to enhance fetal lung maturity as well as to ameliorate antepartum and postpartum HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome, but it is not clear if glucocorticoids can modulate placental cytokine production. The aim of this study is to examine the effect of glucocorticoids at equivalent doses used for fetal lung maturity on placental tissue production of cytokines (IL-10, IL-6 and TNF-alpha). Placental biopsies were taken from the decidual surface of term placentas of normal pregnancy (n = 5) and preeclampsia (n = 5). Villous explants were cultured with increasing concentrations of glucocorticoids (betamethasone and methyl-prednisolone, 0.0025 microM, 0.25 microM and 25 microM). The dose effect of glucocorticoids on cytokines (TNF-alpha, IL-6 and IL-10) production was examined using ELISA. There was a stepwise reduction of TNF-alpha (23.6-97.5% reduction) and IL-6 (13.7-71% reduction) with increasing doses of betamethasone and methyl-prednisolone from placentas of women with preeclampsia and normal pregnancy. However, IL-10 was not altered in conditioned medium by increasing doses of glucocorticoids. Our data suggest that the ratio of pro-inflammatory to anti-inflammatory cytokine (Th1/Th2) is potentially altered by exogenous glucocorticoids. These changes have a favourable effect on the ratio in preeclampsia with a reduction in the potentially vascular active pro-inflammatory cytokines but without altering or decreasing the necessary anti-inflammatory cytokine IL-10 production in placental tissue.     

Relationship of maternal placental blood flow to the placental clearance of maternal plasma dehydroisoandrosterone sulfate through placental estradiol formation

We have suggested that the placental clearance of maternal plasma dehydroisoandrosterone sulfate (DS) through estradiol (E2) formation (PC-DSE2) is reflective of uteroplacental blood flow (F). Clewell and Meschia13 suggested that PC-DSE2 is related to F as follows: Cobs = F(1-e-C/F), where Cobs = PC-DSE2 and C = total placental clearance of maternal plasma DS. This equation contains two unknown quantities, F and C. To solve the equation, Clewell and Meschia assumed that C was constant. Using 19.7 ml/min for C, they allowed PC-DSE2 to vary widely and computed F. Upon finding that F was unrealistically low for some values of PC-DSE2, they concluded that reductions in PC-DSE2 do not reflect alterations in uteroplacental blood flow. In the analysis of the relationship of F to PC-DSE2, it is important to know the value of C. Since the direct measurement of C is not possible at this time, we have evaluated C by measuring the difference between the metabolic clearance rate of DS (MCR-DS) prior to and immediately following delivery. Any change in MCR-DS before and after delivery should be a reflection of the amount of maternal plasma DS cleared by the placenta through all metabolic routes including PC-DSE2, providing nonplacental clearances of maternal plasma DS before and immediately after delivery are the same. We measured MCR-DS and PC-DSE2 in 15 pregnant women within 5 days before delivery and repeated the MCR-DS measurement in these women beginning 90 minutes after delivery. Among these 15 women, C ranged from a low of 4.7 ml/min in a woman with severe pre-eclampsia to a high of 28.5 ml/min in a woman with twins. In addition to the finding that C varied widely, it was also ascertained that PC-DSE2 was positively correlated with C (r = 0.908; p less than 0.001). The finding that low or high values for PC-DSE2, observed in complicated pregnancies, were associated with similar changes in C is suggestive that a change in PC-DSE2 is reflective of a change in uteroplacental blood flow.     

Pregnancy following placental abruption

The aim of the present study by a retrospective chart review was to examine the recurrence rate after placental abruption. Between 1985 and 1998, 81 patients had a placental abruption. We had 2-year follow-up information about 31 patients and 27 of them had a total of 34 subsequent pregnancies. Recurrent placental abruption was observed in 6 pregnancies in 6 patients (6/27, 22.2%). Of the 6 recurrent placental abruptions, the gestational age was 1–3 weeks earlier than that of previous abruption in 4 patients. One patient delivered a healthy baby after her first abruption and then experienced a second abruption. We conclude that careful management is needed after 30 weeks in pregnant women with a previous history of placental abruption. Received: 24 April 2001 / Accepted: 2 July 2001 Acknowledgments We thank medical staff of the Department of Obstetrics and Gynecology in Handa City Hospital, Nagoya Daini Red Cross Hospital, and Toyohashi Municipal Hospital for their support.