The placenta is an important functional unit for gas transfer between mother and fetus. The placental membrane, consisting of trophoblast layer interposed between maternal and fetal blood, plays an active role for intensity of respiration, but no morphological evidence has been documented. Until now, it has been reported that fetal growth retardation and increased fetal mortality rate usually could be seen at high altitude. In an attempt to find the cause of high perinatal mortality rate in Nepal, this study was undertaken to examine pathologically about 1000 Himalayan placentas obtained in Nepal and Tibet since 1977, and the results were compared with those of 5500 Japanese placentas at Saitama Medical School since 1990. In this study, characteristics of ultrastructural features of the Nepalese placental villi investigated in recent years are reported. (1) The gross characteristics of placental pathology in the Himalayan group were represented by marked subchorionic fibrin deposits and increased chorionic cysts in contrast to low incidence of intervillous thrombosis compared with those of the Japanese group. (2) As characteristics of histological findings of the placental villi between Himalayan and Japanese groups, the incidence of chorangiosis and chorangioma in the Himalayan group was significantly higher than that in the Japanese group. (3) Accompanying an increase of vasculosyncytial membrane (VSM) in the villi, thickness and separation of basement membrane of the syncytium in addition to increased apoptosis of syncytial cell nuclei were recognized. (4) As characteristic ultrastructural features of chorionic villi of Nepalese placentas, an increase of mitochondria and cystic formation of rough endoplasmic reticulum (rER), in addition to appearance of lamellar bodies similar to alveolar epithelial type II cell in organellae of the syncytium, were observed. These ultrastructural changes of the placental villous capillaries may be ascribed to hypervascularization caused by the chronic hypoxic state. It is, therefore, presumed that trophoblast cells may play an important role for gas transfer mechanism under such a hypoxic state at high altitude.
Serial ultrasound examinations have demonstrated that one of two gestational sacs in a twin pregnancy may often disappear. When it disappears at an early stage of gestation, the pregnancy may advance without any disturbance and the cotwin can be delivered well developed and lively. When the intrauterine death occurs in the second trimester, the dead fetus usually results in a fetus papyraceus and the cotwin continues to be alive near term. However, when death occurs in the last trimester, the viable twin may be spontaneously delivered soon and be premature. In some cases of late fetal death, the dead fetus may induce intravascular thromboses in many organs of the surviving cotwin, so that the living infant may develop cerebral palsy later after birth.
A 37-year-old G1-P1 was diagnosed by ultrasonography at 26 weeks of gestation as having an abnormally large placenta with hemangiomas and a fetus associated with exomphalos. Placental protein 5 levels were relatively high in placental protein levels in maternal serum. The infant, delivered by cesarean section at 34 weeks, had the typical clinical features associated with Beckwith-Wiedemann syndrome. The abnormally large placenta weighed 1,492 g, measured 25 × 25 × 5.1 cm, and featured multiple hemangiomas. Microscopic placental features included edematous villi, increased fibrin deposition, intervillous thrombi, and multiple angiomatous and cellular chorangiomas.
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