Endometrial Neoplasms ; pathology ; Female ; Humans ; Pregnancy ; Trophoblastic Neoplasms ; pathology ; Trophoblasts ; pathology

OBJECTIVE: To investigate the invason of trophoblasts in the placenta bed and the change of spiral arteries and microvessels in pre-eclampsia and normal pregnancy. METHODS: Twenty cases of normal pregnancies, mild pre-eclampsia and severe pre-eclampsia were chosen as Group A, Group B, and Group C. HE staining and immunohistochemistry staining (SP method) were used to observe the depth and the density of trophoblasts invading the placenta bed and the change of spiral arteries and microvessels. RESULTS: The significant difference in the degree of invasion was in the superficial myometrial segment. Group C was the most superficial in the 3 groups (P<0.01). The density of trophoblasts which invaded the placenta bed in the lower half of the basal decidual segment and the myometrial segment showed us Group C was the lowest (P<0.01). There was statistical difference among the 3 groups (P<0.01). The average lumen area of the spiral arteries in the decidual segment and the superficial myometrial segment of the placenta bed was the smallest in Group C among the 3 groups(P<0.01) and there was statistical difference among the 3 groups (P<0.01). The spiral arteries were the thickest in Group C with statistical difference among the 3 groups (P<0.01). The physiological and pathological change of the spiral arteries was mainly in the superficial myometrial segment. The incidence rate of physiological changes in the spiral arteries was the lowest in Group C with statistical difference among the 3 groups (P<0.01). The incidence rate of pathological changes was the highest in Group C (P<0.01) and the normal group was the highest. There was significant difference among the 3 groups(P<0.01). There was positive correlation between the physiological change of the spiral arteries and the invaing degree of the trophoblasts (P<0.05), there was negative correlation between the pathological change of the spiral arteries and the invasion depth as well as the invasion density of the trophoblasts(P<0.05). There was negative correlation between the physiological change and the pathogenetic condition of pre-eclampsia(P<0.05)while there was positive correlation between the pathological change and the pathogenetic condition degree of pre-eclampsia(P<0.05). There was negative correlation between the invasion depth as well as density in uteruso superficial myometrial segment by trophoblast and the pathogenetic condition degree of pre-eclampsia(P<0.05). There was invasion trophoblast in 62.50% lumen wall of spiral arteries in uterus superficial myometrial segment of the placental bed in normal pregnancy while 27.5% was seen in severe pre-eclampsia. Microvascular density in the decidual segment and the superficial myometrial segment of the placenta bed in Group C was the lowest among the 3 groups with statistical difference (P<0.01). CONCLUSION The invasion depth of the trophoblasts in pre-eclampsia was more superficial than normal pregnancy.The changes of the invasion of the trophoblasts and the pathological changes of the spiral arteries in the placenta bed mainly existed in the superficial myometrial segment which was closely related to the severity of the illness. That microvascular density in the placental bed of pre-eclampsia started to decrease from the basal decidual segment shows that the microvessel development in the placenta bed is impaired in pre-eclampsia.
Adult ; Arteries ; pathology ; Capillaries ; pathology ; Female ; Humans ; Placenta ; blood supply ; pathology ; Pre-Eclampsia ; pathology ; Pregnancy ; Trophoblasts ; pathology

Antigens, Neoplasm ; metabolism ; Antigens, Surface ; metabolism ; Colorectal Neoplasms ; immunology ; pathology ; Humans ; Prognosis ; Trophoblasts ; immunology

Pulmonary placental transmogrification (PT) is a rare lung disease that takes on the histologic appearance of placental chorionic villi. We herein report a case of PT in a 66-year-old woman who presented with a single nodule on chest radiography performed during a routine health examination. She had no complaints of any symptoms. Chest radiography showed a focal ill-defined nodular opacity in the right lower lobe; chest computed tomography revealed a 17-mm lobulated, focal irregular mass with fissural retraction in the right lower lobe, suggestive of lung cancer. Pathology of a percutaneous needle aspiration biopsy revealed papillary structures resembling placental villi. These were lined by cytotrophoblast-like cells and syncytiotrophoblasts. This characteristic pathologic finding led to a diagnosis of PT. PT of the lung is found mainly in bullous or cystic lesions. However, this patient presented with a single nodule on chest radiography.
Aged ; Biopsy, Needle ; Chorionic Villi ; Diagnosis ; Female ; Humans ; Lung Diseases ; Lung Neoplasms ; Lung* ; Needles ; Pathology ; Placenta ; Radiography ; Thorax ; Trophoblasts

Pregnancy-induced hypertension (PIH) is a multi-system disorder unique to human pregnancy. Although the etiology of PIH is still unknown, there is a large evidence suggesting that abnormal trophoblast invasion is occurring in early pregnancy and that this may contribute to relative placental hypoxia and oxidative stress that may further exacerbate placental pathology. This study was undertaken to determine placental Cu/Zn superoxide dismutase (SOD) and Mn SOD activities and evaluate the use of M30 CytoDeath antibody to assess trophoblasts apoptotic activity in normal and PIH pregnancies. We also compared apoptotic rates as detected by M30 and TdT-mediated dUTP nickend labelling (TUNEL). Placental expression of Cu/Zn SOD and Mn SOD were reduced in PIH as compared to normal pregnancies. M30 immunoreactivity occurred predominantly in the syncytiotrophoblasts, and a significantly higher number of M30 positive cells in the preeclamptic placentas were found when compared with normal placentas. The number of M30 positive cells correlated with another apoptotic index previously detected by TUNEL method.
Anoxia ; Apoptosis ; Female ; Humans* ; Hypertension, Pregnancy-Induced* ; In Situ Nick-End Labeling ; Oxidative Stress ; Pathology ; Placenta ; Pregnancy ; Superoxide Dismutase ; Trophoblasts*

Intracranial teratomas are rare entities that can present as a pure type or as mixed germ cell tumor. Cases of mixed germ cell tumor composed of immature teratoma and choriocarcinoma have been reported. Also, immature teratoma can be mixed with only syncytiotrophoblasts. We report a case of immature teratoma with syncytiotrophoblasts of the brain discovered in a 3-year-old male baby. Serum human chorionic gonadotrophin (hCG) was normal and serum alpha-fetoprotein (AFP) was elevated. The tumor was mainly composed of intestinal glands, and neither endodermal sinus tumor nor embryonal carcinomatous elements were found. The cells lining the intestinal glands were positive for hCG and AFP. These findings suggest that the syncytiotrophoblasts are differentiated from the endoderm and AFP is not necessarily a marker exclusive to endodermal sinus tumor or embryonal carcinoma.
Brain Neoplasms/metabolism/*pathology ; Case Report ; Child, Preschool ; Chorionic Gonadotropin/metabolism ; Giant Cells/*pathology ; Human ; Intestines/*metabolism/pathology ; Male ; Teratoma/metabolism/*pathology ; Trophoblasts/*pathology ; Tumor Markers, Biological/*metabolism ; alpha-Fetoproteins/metabolism

Invasive mole is a benign gestational trophoblastic disease that arises from the myometrial invasion of any gestational event via direct extension through tissue or vascular structures. Invasive mole (and other gestational trophoblastic diseases) may present with life-threatening complications including uterine perforation, excessive bleeding, acute hemoperitoneum, and abdominal pain. We report a case of invasive mole presenting as abdominal distention in a 51-year-old perimenopausal woman (gravida 12, para 12, abortion 0). The patient was admitted to the gynecology clinic with a giant uterine mass filling the pelvic and abdominal cavity. To our knowledge, this is the first case in the literature of a gestational trophoblastic neoplasia presenting with uterine mass of 28 weeks' gestational size in this age group. Interestingly, complications such as uterine rupture or invasion of the adjacent structures (such as parametrial tissues or blood vessels) had not developed in our patient despite the considerable enlargement of the uterus.
Abdominal Cavity ; Abdominal Pain ; Female ; Gestational Trophoblastic Disease ; Gynecology ; Hemoperitoneum ; Hemorrhage ; Humans ; Hydatidiform Mole, Invasive* ; Hysterectomy ; Middle Aged ; Pathology* ; Pregnancy ; Trophoblasts ; Uterine Perforation ; Uterine Rupture ; Uterus

BACKGROUND: Histologic examination of the placentas from intrauterine growth retardation (IUGR) fetuses can supplement clinical knowledge of the cause of IUGR. The present study was undertaken to observe the pathologic findings regarding the placentas in IUGR fetuses. METHODS: Clinicopathologic findings in 45 cases with IUGR at the third-trimester were reviewed, and they were compared with those of 24 normal control cases. An IUGR fetus was defined as one with a birth weight less than those in the 10th percentile. Of the IUGR cases, 15 were hypertensive IUGR with or without preeclampsia, and 30 were normotensive IUGR. RESULTS: The IUGR groups had significantly shorter mean gestational ages, lower mean placental weights, and higher incidences of oligohydramnios, compared to the normal controls (p<0.05). Histologically, IUGR was characterized by increased incidence of decidual vasculopathy (31.1%, p<0.05), multiple and severe infarct (p<0.05), villous fibrosis (31.1%, p<0.05), syncytiotrophoblastic knots (86.7%, p<0.05), and higher degree of increased perivillous fibrin deposition (p<0.05). However, there were no statistically significant differences in the placental lesions between hypertensive and normotensive IUGR cases, except for the presence of decidual vasculopathy. CONCLUSIONS: Abnormal uteroplacental vasculature and chronic uteroplacental insufficiency, coagulation-related pathology in the uteroplacental, intervillous and/or fetoplacental vasculature, and chronic inflammatory lesions may be the primary disease processes related to the placental pathology of IUGR. Although the cause of IUGR pregnancies is heterogeneous, careful cilinicopathologic correlations in individual cases are necessary in the interpretation of placental lesions of IUGR, and the total burden of several placental lesions may be more important than a single histologic feature.
Birth Weight ; Female ; Fetal Growth Retardation* ; Fetus ; Fibrin ; Fibrosis ; Gestational Age ; Incidence ; Oligohydramnios ; Pathology* ; Placenta ; Pre-Eclampsia ; Pregnancy ; Trophoblasts ; Weights and Measures

The mechanism of apoptosis was first discovered at the end of the 19th century, but it was only recently that its importance was recognized. Not only in a pathologic environment but also in a normal environment, apoptosis has an important role in homeostasis. The number of cells is restricted by apoptosis which is controlled by several SlgBS lll VlVO. In pregnancy, the placenta regulates the maternal-fetal exchange of molecules and functions as a barrier for the protection of the fetus. As the pregnancy proceeds, changes occur in the number and components of placental cells. Observing the placental tissues, apoptosis was found in the syncytiotrophoblasts of early and late pregnancy. In particular, the fact that apoptosis observed in the placenta of late pregnancy supports the hypothesis that pmgrammed cell death is a normal sequence. Pregnancy-induced hypertension is usually accompanied by abnormal placenta and intrauterine growth restriction. In this study, using the TdT-FragEL DNA fragmentation detection kit, the changes in the nucleus by apoptosis in the placental tissues of 23 to 40 gestational weeks in preeclampsia and eclampsia were compared with normal placenta. Apoptosis was observed in the normal term placenta and in pregnancy-induced hypertension patients, regardless of whether vasculopathy was observed in Doppler ultrasound or confirmed by pathology, more apoptoses were observed aside from the number of gestational weeks.
Apoptosis ; Cell Death ; DNA Fragmentation ; Eclampsia ; Female ; Fetus ; Homeostasis ; Humans ; Hypertension, Pregnancy-Induced* ; Maternal-Fetal Exchange ; Pathology ; Placenta* ; Pre-Eclampsia ; Pregnancy ; Trophoblasts ; Ultrasonography

BACKGROUNDPreeclampsia is a multifactorial disease during pregnancy. Dysregulated lipid metabolism may be related to some preeclampsia. We investigated the relationship between triglycerides (TGs) and liver injury in different preeclampsia-like mouse models and their potential common pathways.

METHODSPreeclampsia-like models (Nw-nitro-L-arginine-methyl ester [L-NAME], lipopolysaccharide [LPS], apolipoprotein C-III [Apo] transgnic mice + L-NAME, β2 glycoprotein I [βGPI]) were used in four experimental groups: L-NAME (LN), LPS, Apo-LN and βGPI, respectively, and controls received saline (LN-C, LPS-C, Apo-C, βGPI-C). The first three models were established in preimplantation (PI), early-, mid- and late-gestation (EG, MG and LG). βGPI and controls were injected before implantation. Mean arterial pressure (MAP), 24-hour urine protein, placental and fetal weight, serum TGs, total cholesterol (TC) and pathologic liver and trophocyte changes were assessed.

RESULTSMAP and proteinuria were significantly increased in the experimental groups. Placenta and fetal weight in PI, EP and MP subgroups were significantly lower than LP. Serum TGs significantly increased in most groups but controls. TC was not different between experimental and control groups. Spotty hepatic cell necrosis was observed in PI, EG, MG in LN, Apo-LN and βGPI, but no morphologic changes were observed in the LPS group. Similar trophoblastic mitochondrial damage was observed in every experimental group.

CONCLUSIONSEarlier preeclampsia onset causes a higher MAP and urine protein level, and more severe placental and fetal damage. Preeclampsia-like models generated by varied means lead to different changes in lipid metabolism and associated with liver injury. Trophoblastic mitochondrial damage may be the common terminal pathway in different preeclampsia-like models.

Animals ; Cholesterol ; blood ; Disease Models, Animal ; Female ; Fetal Weight ; physiology ; Liver ; injuries ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondrial Diseases ; blood ; pathology ; Placenta ; metabolism ; Pre-Eclampsia ; blood ; pathology ; Pregnancy ; Triglycerides ; blood ; Trophoblasts ; pathology