Cases reported "Placenta Diseases"

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1/95. Mesenchymal dysplasia of the placenta.

    A severe case of placental mesenchymal dysplasia occurred in association with intrauterine fetal death (IUFD). The gravida-1, para-1 mother was a 26-year-old Japanese. The first pregnancy was unremarkable and a healthy female infant was delivered. The present pregnancy had been uneventful until 34 weeks of gestation when IUFD was detected. The 1516-g (mean /- SD, 2050 /- 387 g) stillborn infant had no external abnormalities and the karyotype was 46,XX. The placenta was markedly enlarged (1050 g; mean /- SD, 452 /- 202 g), and approximately 80% was occupied by extraordinary enlarged villous structures with a myxoid appearance. Histologically, the dysplastic villi had myxoid stroma and a decreased number of, occasionally obliterated, fetal vessels. There was no abnormal trophoblastic proliferation. Large-sized fetal vessels in the chorionic plate frequently contained organized thrombi. This is the first case of placental mesenchymal dysplasia, which possibly lead to the IUFD.
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2/95. placenta percreta.

    A patient with an unsuspected placenta percreta presented with intraperitoneal bleeding at 33 weeks' gestation. Because of the clinical picture and a lecithin/sphingomyelin ratio of 1:1, this patient was treated conservatively until 38 weeks' gestation when an L/S ratio test indicated fetal maturity. The pregnancy was successfully terminated by cesarean hysterectomy.
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3/95. Placental floor infarction complicating the pregnancy of a fetus with long-chain 3-hydroxyacyl-coa dehydrogenase (LCHAD) deficiency.

    By postmortem biochemical and molecular genetic analyses, an 8-month-old infant was diagnosed with long-chain 3-hydroxyacyl-coenzyme a dehydrogenase deficiency, an inborn error of mitochondrial fatty acid beta-oxidation. He was born following a pregnancy complicated by a maternal floor infarction of the placenta, a disorder of unknown etiology. We speculate that the child's autosomal recessive fatty acid beta-oxidation disorder and the pregnancy complication are causally related.
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keywords = pregnancy complication, pregnancy
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4/95. Hyperplacentosis: a novel cause of hyperthyroidism.

    Human chorionic gonadotropin (hCG), which is capable of thyrotropic activity, is believed responsible for the hyperthyroidism of gestational trophoblastic disease and hyperemesis gravidarum. Hyperplacentosis is a condition of heightened trophoblastic activity characterized by increased placental weight and circulating hCG levels higher than those associated with normal pregnancy. We report the first case of hyperthyroidism associated with hyperplacentosis. Correction of the hyperthyroidism occurred after hysterotomy and correlated with declining hCG levels. Hyperplacentosis should be included among the causes of hCG-mediated hyperthyroidism.
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5/95. Severe intrauterine herpes simplex disease with placentitis in a newborn of a mother with recurrent genital infection at delivery.

    We present a case of fatal herpes simplex type 2 (HSV-2) in a premature infant born to a mother diagnosed with recurrent HSV-2, based on history and HSV serology results. It was clinically evident at delivery, and subsequently confirmed by laboratory studies that the infant was infected before delivery. There was histopathologic evidence of placentitis and chorioamnionitis upon examination of the placenta and fetal membranes. This case illustrates a relatively uncommon complication of recurrent genital herpes at delivery--intrauterine transmission to the fetus from a primary episode during pregnancy.
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6/95. Placental pathology in fetal bartter syndrome.

    bartter syndrome, which presents clinically with polyuria, urinary potassium loss, hypokalemia, hypercalciuria, and alkalosis, is an autosomal recessive disorder with mutations in genes encoding the Na-K-2Cl cotransporter, the chloride channel CLC-NKB, and the potassium channel ROMK. prenatal diagnosis of bartter syndrome is now possible; however, there are no reports of the placental pathology associated with fetal bartter syndrome. We present the placental pathologic findings in two siblings with fetal bartter syndrome. Both pregnancies were complicated by polyhydramnios and preterm delivery. The first pregnancy delivered at 30 weeks, and bartter syndrome was diagnosed in the perinatal period. The subsequent pregnancy required periodic therapeutic amniocentesis secondary to massive polyhydramnios and delivered at 32 weeks gestation. The suspicion of fetal bartter syndrome was very high in this second pregnancy, and the infant was confirmed to have bartter syndrome subsequently. Both placentas were large for gestational age, weighing greater than the 95th percentile. Microscopic examination showed extensive subtrophoblastic basement membrane mineralization (special stains positive for iron and calcium) in the chorionic villi. This striking finding was present in both placentas. Subtrophoblastic mineralization has been described in the literature in placentas of fetuses with abnormalities including anencephaly, trisomy 21, and other congenital abnormalities; however, it has also been described in normal pregnancies. Mechanisms of calcification in the placenta are not well understood, but these striking cases suggest that defects in fetal renal excretion of ions can lead to dystrophic calcification within the placenta, particularly in a subtrophoblastic pattern.
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7/95. placenta percreta in week 10 of pregnancy with consecutive hysterectomy: case report.

    placenta percreta in early pregnancy is rare and has been documented in only a few cases. We report on a patient with abdominal pain in week 10 of pregnancy. Sonography revealed a defective embryonic development and the absence of a border line between trophoblast and myometrium, as well as invasive growth in the region of isthmocervical transition, so curettage was performed. Heavy bleeding at this stage made a hysterectomy necessary. Histological examination revealed a placenta percreta. Because of possible complications, the therapy of choice for a placenta percreta is a hysterectomy, as was performed in this case.
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keywords = pregnancy
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8/95. Congenital nephrosis of the Finnish type: overview of placental pathology and literature review.

    Congenital nephrosis of the Finnish type (CNF) is a rare, autosomal recessive disorder of glomerular filtration that results in massive proteinuria, edema, and ascites. Although previous studies describe the classic renal lesions characterizing this disorder, there are few documenting in detail the associated placental alterations. In this context, we present a case of CNF with emphasis on the placental pathology and compare our findings to what has been previously reported in the literature. A 36-year-old G2P1 with no significant medical history developed persistently elevated amniotic fluid alpha-fetoprotein in the absence of neural tube defects. Because of a clinical suspicion of CNF, she electively terminated the pregnancy at 19 weeks. Postmortem examination revealed characteristic renal changes, confirmed by electron microscopy, as well as significant placental villous edema. Although the placenta was not enlarged, the villi appeared profoundly hydropic. Extensive cystic vacuolar change was documented in both stem villi and tertiary villi, affecting 95% of the villi present. Since the fetus was not grossly edematous, the placental findings may represent the first sign of systemic hypoproteinemia.
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9/95. Twelve cases of placental chorioangioma. pregnancy outcome and clinical significance.

    INTRODUCTION: To determine perinatal complications and pregnancy outcome in 12 women with chorioangioma of placenta. STUDY DESIGN: During the period between January 1986 and December 1997, 12 women with histologic diagnosis of chorioangioma of placenta who delivered in our institution were studied. Case-control study was designed. Sixty women with histologic examination of the placenta without chorioangioma were randomly identified as control group matched for maternal age and parity. Statistical analyses included t-test, Chi-square test and Fisher's exact test when appropriate. RESULTS: Nine cases (75%) were diagnosed postnatal. The mean gestational age was significantly lower and preterm delivery rate was significantly higher among the chorioangioma group (34 vs. 38.8 weeks P<0.0001; 66% vs. 10%; P<0.001 respectively). CONCLUSIONS: Chorioangioma of the placenta, in a high risk population, although small, is associated with significantly higher risk for preterm delivery. This emphasizes the need for pathologic examination of all placentas of patients with preterm delivery
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10/95. Alcoholization: the choice of intrauterine treatment for chorioangioma.

    Chorioangioma is a vascular tumor of the placenta. Most are small and asymptomatic, whereas the large tumors are clinically significant and often associated with polyhydramnios and fetal heart failure. To prevent fetal loss from these complications, many interventions have been proposed, including intrauterine transfusion in anemic cases and fetoscopic surgery to ablate the feeding vessels. The case presented herein had large chorioangiomas, 8 and 4cm in diameter, associated with polyhydramnios and early signs of hydrops fetalis, diagnosed at 27 weeks gestation. After extensive counseling, we performed alcohol ablation of the feeding vessel of the larger tumor. Signs of fetal heart failure and hydrops fetalis disappeared dramatically. The pregnancy was extended for 2 weeks, followed by premature rupture of the membranes and spontaneous labor at 32 weeks gestation and a surviving female baby, weighing 1360g, was delivered uneventfully. This preliminary experience suggests that alcoholization may be one of the best choices for this condition due to its high efficacy, simplicity, safety and very low cost. To our knowledge, this is the first report using alcoholization for the treatment of hydrops fetalis secondary to chorioangioma.
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