Cases reported "Placenta Diseases"

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1/5. Coxsackie virus infection of the placenta associated with neurodevelopmental delays in the newborn.

    OBJECTIVE: To determine if viral infection of the placenta was associated with long-term neurodevelopmental delays in the newborn. methods: Placental tissue from seven newborn infants with severe respiratory failure and subsequent neurodevelopmental abnormalities as well as ten normal controls and five cases of known placental infection (cytomegalovirus, herpes simplex virus, and parvovirus) were tested by in situ hybridization or reverse transcriptase in situ polymerase chain reaction (PCR) for adenovirus, coxsackie virus, cytomegalovirus, Epstein Barr virus, herpes simplex virus, influenza a virus, picornavirus, polyoma virus, parvovirus, respiratory syncytial virus, rotavirus, and varicella zoster virus. RESULTS: Coxsackie virus rna was detected in six of the seven cases, and in none of the ten normal controls or five cases with known viral infection. Viral rna localized primarily to the Hofbauer cells and trophoblasts of the terminal villi. Immunohistochemical analysis for the coxsackie virus antigen VP1 yielded equivalent results. CONCLUSIONS: In utero coxsackie virus of the placenta is associated with the development of severe respiratory failure and central nervous system sequelae in the newborn. This underscores the importance of detailed pathologic and viral examination of the placenta in cases of systemic illness in the newborn.
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2/5. Congenital deficiency of alpha-fetoprotein and associated chromosomal abnormality in the placenta.

    In this study we describe two patients with congenital absence of alpha-fetoprotein (AFP). The pathological examination results, including an immunohistochemical stain, which define qualitatively the levels of AFP detected by the biochemical studies and the comparative genomic hybridization (CGH) are enclosed. A description of the suggested functions of AFP and the means of its production are set forth. An explanation is suggested for the lack of symptoms in a newborn with undetectable levels of AFP and the mechanism by which this condition might occur.
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3/5. Granulomatous villitis formed by inflammatory cells with maternal origin: a rare manifestation type of placental toxoplasmosis.

    We present a case of placental toxoplasmosis with granulomatous villitis. The patient was a 26-year-old gravida 1 female with the findings of intrauterine death at 16th week of gestation. The pregnancy was terminated. Pathological examination revealed an autolysed fetus and a placenta with necrotizing granulomas within the villous stroma. Encysted toxoplasma gondii was rarely observed within the granulomas and serologic examination of the mother confirmed acute toxoplasmosis. A fluorocein in situ hybridization examination, using sex chromosome probes, revealed that the villous granulomas were formed by inflammatory cells, originated from the maternal immune system. In conclusion, T. gondii should be taken into consideration as a rare cause of placental granulomatous inflammation. To the best of our knowledge, this is the first case of granulomatous villitis due to toxoplasmosis, in which formation by maternal inflammatory cells has been demonstrated.
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keywords = hybridization
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4/5. The pathogenesis of villitis of unknown etiology: analysis with a new conjoint immunohistochemistry-in situ hybridization procedure to identify specific maternal and fetal cells.

    The conjoint immunohistochemistry-in situ hybridization (IHC-ISH) procedure permits, under routine light microscopic conditions, simultaneous documentation of either a male or female karyotype plus the immunological phenotype of individual cells within paraffin-embedded tissues. We have used this technique to characterize the inflammatory response in placental villitis of unknown etiology (VUE). A male placenta with severe VUE and appropriate control placentas were analyzed. in situ hybridization probes concurrently label both the X and Y chromosomes. On the same tissue section, individual cells were characterized with antibodies to CD3, CD68, or CD20. The amnion and syncytiotrophoblast were delineated by cytokeratin antibody (AE1/AE3). A complete karyotyping was performed on amnion cells to validate the procedure. amnion cell karyotyping confirmed the accuracy of the procedure. The VUE case revealed that 88.8% of intravillous CD3 lymphocytes were female (maternal), while 11.2% were male (fetal). Intervillous CD3 lymphocytes and CD68 macrophages were universally female. Intravillous CD68 cells were only 10.5% female. Perivillous CD68 cells were 94.6% female. Remarkably, multinucleated giant cells were exclusively maternal. This study confirms that lymphocytes in VUE are predominately but not exclusively maternal T cells. Our findings indicate that invasion of fetal villi by maternal T cells is associated with focal destruction of the syncytiotrophoblast, clarifying how placental immuno-defensive mechanisms may be contravened.
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ranking = 6
keywords = hybridization
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5/5. herpes simplex virus infection of the placenta. The role of molecular pathology in the diagnosis of viral infection of placental-associated tissues.

    herpes simplex infections of the placenta and its associated tissues are rarely seen and, consequently, the pathologic features are not well understood. We describe the occurrence of herpes simplex virus infection of the placenta that was limited to maternal-derived cells of the subchorionic tissue. The microscopic findings were remarkable for both the absence of inflammation and characteristic viral inclusions. However, in situ dna hybridization, as well as immunohistochemistry using antibody to herpes simplex virus type 2, revealed herpes virus infection of decidualized cells in the decidua capsularis. The significance of this finding, and the importance of molecular techniques for the diagnosis of herpes virus infection in placental pathology, are discussed.
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ranking = 1
keywords = hybridization
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