chorioamnionitis and its clinical significance

1
Placenta (lYY8), Vol. 19 A.26 CHORIOAMNIONITIS AND ITS CLINICAL SIGNIFICANCE. M.Nakavama, H. Arai, M. Take”&, T. Takeshima. A. Mivano, Department of Pathology and Laboratory Medicine, &aka Medical Center and Resarch Institute for Maternal and Child Health. The chorioamnionitis(CAM) of the placenta is not rare condition. Nevertherless it is frequently detected especially in the cases with premature infants. We examined 30,000 placents from 1981 to 1998 in our center. A close relationship between placental findings and clinical course, laboratory deta was detected. Diagnosis of CAM was correctly done by histological sections but most of CAM was tentatively diagnosed by macroscopic findings. Turbid amniotic membrane and/or yellow edematous umbilical cord led quick diagnosis suggestive of CAM. CAM was not detected until 16 weeks of gestation. However, frequency of CAM revealed gradual increase from 17 weeks and about half of placentas showed CAM between 20 weeks and 30 weeks. Over 30 weeks, CAM ratio gradually decreased and increased again over 40 weeks. The level of complement system was most influenced by the severity ov CAM in the placenta. IgM in cord blood and LecithinJsphingomyelin(L/S) ratio in the amniotic fluid were significantly higher in the cases with CAM. Some of interleukins are elevated by CAM. IL6 and IL8 are highly elevated in the cases with CAM. In cases with Wilson-Mikitv syndrome, placenta showed unique calcified lesion in thb umbilical cord associated with CAM, which was called subacute necrotizing funisitis(SNF’). Wilson-Mikity syndrome was related to the fetal pneumonia and/or bronchiolitis. On the contrary, CAM was not detected in the cases with respiratory distress syndrome(RDS). Cytomegalovims infection(CMV) is usually transmitted by hematogenous route. They were detected clearly at the trophoblasts in the villi by in situ hybridization methodUSH). But, sometimes CMV was transmitted by ascending infection. In those cases, CMV was detected in the chorionic membrane. THE HUMAN PLACENTA IN DIABETES MELLITUS. G. Desoye, Department of Obstetrics and Gynaecology, University of Graz, A-8036 Graz, Austria. Owing to its position the human placenta is exposedto metabolic and hormonal diabetes-associated derangements of both mother and fetus, and one can expect someimpact of diabeteson the placenta. Severalstudiesare available, but most have produced divergent results. This may be due to the variety of confounding factors, which which may affect the outcome of such studiesand thus need to be controlled for in studieson diabetes.The most important factor appears to be the time point of the metabolic or endocrineinsult. Poor control in the first trimester may result in impaired invasion and inadequate or delayed vascularremodelling with the potential of ensuing IUGR or microsomia.This opposes to poor control later in gestation, which may lead to placental oversupplyof the fetus with maternal nutrients, foremost of amino acidsand fatty acids and subsequent stimulation of the fetal pancreas with resulting fetal hyperinsulinemia and placentomegaly. Recent data suggestsome capacityto reduce transplacental glucose flux by downregulation of the GLUT1 system in the wake of longstanding hyperglycemia.(grant PI 0900) THE PATHOPHYSIOLOGY OF THE UMBILICAL CORD IN PREECLAMPSIA CASES. K. Kobayashi, T. Kubota and T. Aso, Department of Obstetrics & Gynecology, Tokyo Medical & Dental University, Tokyo, Japan To confirm the function of the umbilical cord in severe preeclampsia,we investigated the morpholigical changes of the umbilical cord of severe preeclampsia compared with those of normal pregnancy. The structural changes of the umbilical cord obtained from five patients with severe preeclanpsia and five uncomlpicated pregnant women were investigated by means of electron microscopy. It was revealed that structural changes of the stromal cells of Wharton’s jelly (WJSCs) in the umbilical cord were conspicuous. At normal full-term pregnancy, WJSCs exhibited the ultrastructural characteristicsof mvofibroblasts with microfilamentous bundles positive fo; a, -smooth muscle actin (ASMA), which were found only in cells having contractile functions. As the result Gf smooth muscle cells (SMCs) differentiation, more numerous microfilaments in cytoplasm were observed in the umbilical cord of severe preeclampsia than those of normal pregnancy. In addition, WJSCsexhibited aging process such as a large amount of lipid droplets and a decreased amount of cellular organelle. WJSCs in severe preeclampsia were observedto resemble the phenotype of SMC, recognized as further full-matured differentiation of myofibloblasts than those fo normal pregnancy. These finding suggest that these cells try to adapt the situation of placental dysfunction to maintain the umbilical blood flow through their contractile functions. WlJOLVEMENtOF EAT, A ECL-2 RELATEDGENE, IN THE APOPTOTlC MECHANISMS UNDERL’IING HUMAN PLACENTAL FORMATION AND MAINTENANCE. W&i !&&if, Akihiro Umezawa’,Jun-ichi Hata2,Shiro Nozawa’: Department of Obstetricsand Gynecology’, Departmentof Pathology2; School of Medicine, KeioUniversity. [ OBJECTIVE I : The EAT gene was isolated during differentiation of a human embryonic carcinomaline to the trophoectodefm lineage. The purposeof this study was to eluckfate the role of this genein the regulation of apo@osis as we4 as its involvement in human placentalformation and maintenance. [ METHODS]: Expression andlocalization of the EAT mRNA and proteinwere studiedin placental specimens. [RESULTS] : EAT was found to be strongly expressed in placental specimens and its expressionlocalized to the syncytiotmphoblast. [CONCLUSIONS] : EATis believed to Wgger differentiation to the trophcectcderm lineage. its involvementin apoptotic mechanisms suggests a role in placental fom3ation and maintenance. The strong correlation of EAT expression with syncytiotm~astic cells points to an important role for EATin the differentiation to the trophoectoderm lineageand in the regulation of apoptosis in syncytiotrophoblasts.

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Page 1: Chorioamnionitis and its clinical significance

Placenta (lYY8), Vol. 19 A.26

CHORIOAMNIONITIS AND ITS CLINICAL SIGNIFICANCE. M.Nakavama, H. Arai, M. Take”&, T. Takeshima. A. Mivano, Department of Pathology and Laboratory Medicine, &aka Medical Center and Resarch Institute for Maternal and Child Health.

The chorioamnionitis(CAM) of the placenta is not rare condition. Nevertherless it is frequently detected especially in the cases with premature infants. We examined 30,000 placents from 1981 to 1998 in our center. A close relationship between placental findings and clinical course, laboratory deta was detected. Diagnosis of CAM was correctly done by histological sections but most of CAM was tentatively diagnosed by macroscopic findings. Turbid amniotic membrane and/or yellow edematous umbilical cord led quick diagnosis suggestive of CAM. CAM was not detected until 16 weeks of gestation. However, frequency of CAM revealed gradual increase from 17 weeks and about half of placentas showed CAM between 20 weeks and 30 weeks. Over 30 weeks, CAM ratio gradually decreased and increased again over 40 weeks. The level of complement system was most influenced by the severity ov CAM in the placenta. IgM in cord blood and LecithinJsphingomyelin(L/S) ratio in the amniotic fluid were significantly higher in the cases with CAM. Some of interleukins are elevated by CAM. IL6 and IL8 are highly elevated in the cases with CAM. In cases with Wilson-Mikitv syndrome, placenta showed unique calcified lesion in thb umbilical cord associated with CAM, which was called subacute necrotizing funisitis(SNF’). Wilson-Mikity syndrome was related to the fetal pneumonia and/or bronchiolitis. On the contrary, CAM was not detected in the cases with respiratory distress syndrome(RDS). Cytomegalovims infection(CMV) is usually transmitted by hematogenous route. They were detected clearly at the trophoblasts in the villi by in situ hybridization methodUSH). But, sometimes CMV was transmitted by ascending infection. In those cases, CMV was detected in the chorionic membrane.

THE HUMAN PLACENTA IN DIABETES MELLITUS. G. Desoye, Department of Obstetrics and Gynaecology, University of Graz, A-8036 Graz, Austria.

Owing to its position the human placenta is exposed to metabolic and hormonal diabetes-associated derangements of both mother and fetus, and one can expect some impact of diabetes on the placenta. Several studies are available, but most have produced divergent results. This may be due to the variety of confounding factors, which which may affect the outcome of such studies and thus need to be controlled for in studies on diabetes. The most important factor appears to be the time point of the metabolic or endocrine insult. Poor control in the first trimester may result in impaired invasion and inadequate or delayed vascular remodelling with the potential of ensuing IUGR or microsomia. This opposes to poor control later in gestation, which may lead to placental oversupply of the fetus with maternal nutrients, foremost of amino acids and fatty acids and subsequent stimulation of the fetal pancreas with resulting fetal hyperinsulinemia and placentomegaly. Recent data suggest some capacity to reduce transplacental glucose flux by downregulation of the GLUT1 system in the wake of longstanding hyperglycemia. (grant PI 0900)

THE PATHOPHYSIOLOGY OF THE UMBILICAL CORD IN PREECLAMPSIA CASES. K. Kobayashi, T. Kubota and T. Aso, Department of Obstetrics & Gynecology, Tokyo Medical & Dental University, Tokyo, Japan

To confirm the function of the umbilical cord in severe preeclampsia, we investigated the morpholigical changes of the umbilical cord of severe preeclampsia compared with those of normal pregnancy. The structural changes of the umbilical cord obtained from five patients with severe preeclanpsia and five uncomlpicated pregnant women were investigated by means of electron microscopy. It was revealed that structural changes of the stromal cells of Wharton’s jelly (WJSCs) in the umbilical cord were conspicuous. At normal full-term pregnancy, WJSCs exhibited the ultrastructural characteristics of mvofibroblasts with microfilamentous bundles positive fo; a, -smooth muscle actin (ASMA), which were found only in cells having contractile functions. As the result Gf smooth muscle cells (SMCs) differentiation, more numerous microfilaments in cytoplasm were observed in the umbilical cord of severe preeclampsia than those of normal pregnancy. In addition, WJSCs exhibited aging process such as a large amount of lipid droplets and a decreased amount of cellular organelle. WJSCs in severe preeclampsia were observed to resemble the phenotype of SMC, recognized as further full-matured differentiation of myofibloblasts than those fo normal pregnancy. These finding suggest that these cells try to adapt the situation of placental dysfunction to maintain the umbilical blood flow through their contractile functions.

WlJOLVEMENt OF EAT, A ECL-2 RELATED GENE, IN THE APOPTOTlC MECHANISMS UNDERL’IING HUMAN PLACENTAL FORMATION AND MAINTENANCE. W&i !&&if, Akihiro Umezawa’, Jun-ichi Hata2, Shiro Nozawa’: Department of Obstetrics and Gynecology’, Department of Pathology2; School of Medicine, Keio University.

[ OBJECTIVE I : The EAT gene was isolated during differentiation of a human embryonic carcinoma line to the trophoectodefm lineage. The purpose of this study was to eluckfate the role of this gene in the regulation of apo@osis as we4 as its involvement in human placental formation and maintenance. [ METHODS] : Expression and localization of the EAT mRNA and protein were studied in placental specimens.

[RESULTS] : EAT was found to be strongly expressed in placental specimens and its expression localized to the syncytiotmphoblast. [CONCLUSIONS] : EAT is believed to Wgger differentiation to the trophcectcderm lineage. its involvement in apoptotic mechanisms suggests a role in placental fom3ation and maintenance. The strong correlation of EAT expression with syncytiotm~astic cells points to an important role for EAT in the differentiation to the trophoectoderm lineageand in the regulation of apoptosis in syncytiotrophoblasts.