Cases reported "Edema"

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1/7. Chronic active Epstein-Barr virus infection in an adult.

    We report a rare adult case of chronic active Epstein-Barr virus (EBV) infection. A 54-year-old woman was admitted to our hospital with intermittent fever, weight loss, hepatosplenomegaly, pancytopenia and liver disturbance. In serological tests for EBV, anti-virus capsid antigen (VCA)-IgG antibody and anti-early antigen (EA)-IgG antibody were markedly elevated and anti-EBV nuclear antigen (EBNA) antibody was negative. EBV genome was detected in the bone marrow nucleated cells and peripheral lymphocytes by Southern blot hybridization. The patient developed left facial edema, bilateral breast tumor and pneumonia. She died one year after admission in spite of the administration of prednisolone, interferon and acyclovir.
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2/7. Congenital idiopathic corneal endotheliopathy.

    Two unrelated boys had a history of bilateral corneal clouding at birth following uncomplicated full-term gestations and spontaneous vaginal deliveries (without forceps). Clinical examinations disclosed bilateral corneal edema, no inflammation, and normal intraocular pressures. There was no history of similarly affected family members. The patients underwent penetrating keratoplasty at ages 4 months (patient 1) and 12 years (patient 2). light and electron microscopic studies of the corneal buttons from both patients revealed areas of degeneration of the endothelium and separation of rounded endothelial cells. The morphologic features were strikingly similar to those in two acquired forms of corneal disorders--autoimmune endotheliopathy and "acute endotheliitis." Immunocytologic and in situ hybridization studies for herpes simplex virus were not consistent with either productive or latent corneal infection. Ultrastructural changes in Descemet's membrane reflect delayed or abnormal development of the postnatal nonbanded layer in patients 1 and 2, respectively. These suggest an intrauterine insult that resulted in endothelial dysfunction. The histologic and ultrastructural features of these two congenital cases are not typical of those seen in any of the recognized causes of congenital corneal clouding. We propose that these cases represent a unique congenital corneal endotheliopathy of undetermined origin.
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3/7. Fetal infection with human parvovirus B19.

    The case of premature infant with nonimmune hydrops secondary to human parvovirus B19 infection is presented. The infection was not suspected clinically. The fetal autopsy showed intranuclear inclusions in erythroid cells that stained positively with a DNA hybridization probe for B19 parvovirus.
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4/7. Nonimmunologic hydrops fetalis resulting from intrauterine human parvovirus B-19 infection: report of two cases.

    Two cases of nonimmunologic hydrops fetalis associated with intrauterine human parvovirus B-19 infection are reported. In these cases, hydrops fetalis was diagnosed with ultrasound at 21 and 22 weeks' gestation after 10 or more days of maternal flu-like symptoms. The outcome was stillbirth in one case and neonatal death in the other. In both cases, intrauterine infection by human parvovirus B-19 was confirmed based on two findings: maternal serum positive for human parvovirus B-19 immunoglobulin m (IgM) antibody, and human parvovirus B-19 DNA detected in the fetal organs using Southern blotting and hybridization with a 32P-labeled probe. Laboratory tests on cord blood demonstrated a red blood cell count of 163 x 10(4)/microL, and nucleated red cells numbering 1267 per 50 white cells in the live-birth case. Histologic examinations of fetal tissues demonstrated leukoerythroblastic reaction in the liver and spleen, granular hemosiderin deposition in hepatocytes and kupffer cells, and bilirubin deposition in the intercellular space in the liver. This evidence indicates that, in some fetuses with intrauterine human parvovirus B-19 infection, hydropic changes may be induced by the sudden decrease in oxygen-carrying capacity of the blood due to severe anemia caused by the infection.
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5/7. Human parvovirus infection in pregnancy and hydrops fetalis.

    Human parvovirus is the causative agent of erythema infectiosum, a mild epidemic illness. In a recent outbreak in northeast scotland, six women had serologic evidence of having contracted human parvovirus infection during pregnancy. Two of the women had midtrimester abortions, and both abortuses were grossly hydropic with anemia. They had similar microscopical histopathological features--a pronounced leukoerythroblastic reaction, hepatitis, excessive iron pigment in the liver, and eosinophilic changes in the hematopoietic cell nuclei. Dot hybridization with radiolabeled human parvovirus dna probes revealed viral DNA in several tissues from both fetuses, indicating that they had been infected by the virus in utero. The remaining four women had uncomplicated pregnancies and delivered apparently healthy babies, none of whom had human parvovirus-specific IgM antibody at delivery. We conclude that this common virus may pose a serious risk to the fetus after maternal infection.
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6/7. Fetal-maternal hydrops syndrome in human parvovirus infection.

    A case of maternal generalized edema with hyponatremia, hypoosmolality and secondary hyperaldosteronism was associated with pseudomolar plasma human chorionic gonadotropin (hCG) concentrations in a case of fetal and placental hydrops due to parvovirus B19 infection. digoxigenin in situ hybridization techniques were effective in demonstrating parvovirus B19 infection on fixed tissues. Hydropic changes in the placenta may have massively increased the maternal plasma hCG concentration with subsequent fluid imbalance leading to maternal hydrops mimicking molar pregnancy.
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7/7. De novo duplication of 7pter-->p21.2 and deletion of 9pter-->p23.5: clinical and cytogenetic diagnosis.

    We report on a male patient with a de novo derivative chromosome 9. From clinical and conventional cytogenetic data, it was assumed that the derivative chromosome might be caused by a translocation between the short arms of chromosomes 7 and 9: der(9)t(7;9)(p21.2;p23.5). fluorescence in situ hybridization with a chromosome 7-specific and a chromosome 9-specific paint confirmed this supposition. The phenotype of the patient described is compared to cases in the literature.
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