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  • 1
    ISSN: 1432-0584
    Keywords: Key words Hepatic veno-occlusive disease ; VOD ; Treatment ; Pediatric ; Duplex ultrasound ; Prostaglandin E1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Limited data exist on therapeutic options for established hepatic veno-occlusive disease (VOD) in pediatric patients after stem cell transplantation (SCT). In this report, we present data on the successful treatment of VOD in three children following allogeneic SCT and report the duplex ultrasound criteria for the confirmation of the diagnosis and for the evaluation of the treatment progress. All patients were 〈2 years at the time of transplantation and had received preparative regimens containing busulfan and cyclophosphamide. There were no known pretransplant risk factors for VOD. Allogeneic stem cell transplantation was performed from a sibling donor for CMML and from unrelated donors for Wiskott-Aldrich syndrome and familial hemophagocytic lymphohistiocytosis (FHL). The onset of first clinical symptoms of VOD (as defined by the Seattle and Baltimore criteria) was relatively late in all three patients (days +19, + 20, and +25, respectively). Time from onset of first symptoms until confirmation of diagnosis by serial duplex ultrasound examination was 4–11 days. Duplex ultrasound criteria are as follows: complete change of direction of blood flow in the portal vein, decrease of flow in the hepatic veins, and development of collateral circulation. Treatment was initiated upon confirmation of VOD by continuous infusion of prostaglandin E1 (initial dose 0.075 μg/kg/h) in addition to low-dose heparin (100 units/kg/d). Treatment was continued at the maximum tolerated dose of 0.3–0.5 μg/kg/h of PGE1. After 9, 14, and 25 days of treatment respectively, normal portal vein flow was restored and treatment could be discontinued. All three patients are alive and well without apparent sequelae.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4919
    Keywords: transferrin receptor ; placenta ; trophoblast ; iron
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Placental transferrin receptors, located at the apical side of syncytiotrophoblast, mediate placental iron uptake. Regulation of transferrin receptors on the fetal-maternal exchange area could be a major determinant in the regulation of trans-placental iron transport. Transferrin receptor expression in cultured human term cytotrophoblasts is on a much lower level than in choriocarcinoma cells, with a higher proportion of receptors located on the cell surface. Differentiation of cells, either due to longer culture periods or to 8-bromo-cAMP treatment does not lead to an increase of transferrin receptor expression. In vitro, the level of expression is largely regulated by the cellular density in the culture dishes. Low cellular occupancy of the dish leads to a high level of transferrin receptors. Treatment with iron-sources results in a down regulation of transferrin receptors. Thus, though the level of transferrin receptors in cultured normal trophoblast is at a constant level, unaffected by differentiation, high levels of maternal transferrin-iron availability can lead to a decrease in placental iron uptake. This feed-back mechanism makes placental iron uptake independent of maternal iron stores.
    Type of Medium: Electronic Resource
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