The origin of "X cells" of the human placenta and their possible relationship to intrauterine growth retardation: an enigma.
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Biomedical subjects
Publications and source records attributed to G Altshuler.
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Anatomic study of placental dysfunction may benefit from the applications of new routine techniques. Immunohistochemical staining for human placental lactogen (HPL) was used in 3 cases illustrating different perinatal disorders. The amount of HPL labeling ranged from high in an acute anoxic death due to abruptio placentae, through decreased in a case of maternal hypertension, to low in severe intrauterine growth retardation. Such information complements standard clinical and pathologic studies. Ten percent buffered Formalin was superior to Bouin's fixative and alcoholic Formalin for the demonstration of HPL. Even after 4 days of refrigeration at 4 degrees C, all of the syncytiotrophoblastic tissue was labeled in sections of paraffin-embedded, Formalin-fixed normal placentas.
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This article on the placenta includes considerations of chorioamnionitis, villitis, preeclampsia, and other low placental blood flow states and aspects of the circulating lupus anticoagulant syndrome. The author explains that, although gross and microscopic placental findings document placental features at one point in time, they also reflect ongoing pathophysiologic changes. Pathogenetic relationships between placental pathology, fetal hypoxia, intrauterine growth retardation, and cerebral palsy are discussed. The reader will learn that low placental blood flow states and chorioamnionitis are important means by which endothelins may eventually participate in the production of placental and fetal vasoconstriction and critical hypoperfusion. The author explains means by which reduced umbilical, placental, and fetal blood flow can result from chronic fetal exposure to meconium, meconium-induced vasoactivity, and ultimate vascular necrosis. Clinically important complications therein may include anoxic-ischemic neuronal necrosis in the brain, necrotizing enterocolitis, and ischemic lesions in the fetal heart, lungs, kidneys, and liver. The article includes a review of nucleated red blood cells that most often signify chronic fetal hypoxia rather than infrequent acute intrapartum asphyxia. The reader will also find information on chorangiosis (placental villous capillary hypervascularity), an important sign of placental malperfusion and very long-standing fetal hypoxia.