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Biomedical subjects

E de Jonge

Publications and source records attributed to E de Jonge.

45 records · Page 3Linked to original sources
PubMed1998

Sclerosing peritonitis complicated by sepsis: a potential cause of portal hypertension.

A 27-year-old woman with chronic renal failure, who had been treated with chronic ambulatory peritoneal dialysis and had developed sclerosing peritonitis, was admitted to the hospital with intra-abdominal sepsis. In spite of antibiotic therapy, sepsis recurred and was associated with intrahepatic cholestasis. In addition, over a period of about 4.5 weeks she developed hepatomegaly and portal hypertension unassociated with occlusion of the portal vein or one of its main extrahepatic branches. A wedge biopsy of the liver revealed extensive thick fibrosis of the liver capsule, intrahepatic cholestasis, diffuse swelling of hepatocytes, central veins that were difficult to visualize and small portal tracts. It is suggested that the sepsis was responsible for the intrahepatic cholestasis, swelling of hepatocytes and hepatomegaly. It is also suggested that the rigidity of the fibrotic liver capsule provided resistance to the development of hepatomegaly, with the result that intrahepatic pressure increased (compressing intrahepatic branches of the portal vein as well as portal tracts and central veins) and portal hypertension developed.

Acute Disease↗
PubMed1998

Current drug treatment strategies for disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) can be caused by a variety of diseases. Experimental models of DIC have provided substantial insight into the pathogenesis of this disorder, which may ultimately result in improved treatment. Disseminated coagulation is the result of a complex imbalance of coagulation and fibrinolysis. Simultaneously occurring tissue factor-dependent activation of coagulation, depression of natural anticoagulant pathways and shutdown of endogenous fibrinolysis all contribute to the clinical picture of widespread thrombotic deposition in the microvasculature and subsequent multiple organ failure. Cornerstone for the treatment of DIC is the optimal management of the underlying disorder. At present, specific treatment of the coagulation disorders themselves is not based on firm evidence from controlled clinical trials. Plasma and platelet transfusion are used in patients with bleeding or at risk for bleeding and low levels of coagulation factors or thrombocytopenia. The role of heparin and low molecular weight heparin is controversial, but their use may be justified in patients with active DIC and clinical signs of extensive fibrin deposition such as those with meningococcal sepsis. There is some evidence to indicate that low molecular weight heparin is as effective as unfractionated heparin but may be associated with a decreased bleeding risk. Antithrombin III (AT III) replacement appears to be effective in decreasing the signs of DIC if high doses are administered, but effects on survival or other clinically significant parameters are at best uncertain. If AT III supplementation is used, the dosage should be selected to achieve normal or supranormal plasma levels of 100% or higher. Results of studies on protein C concentrate, thrombomodulin or inhibitors of tissue factor are promising, but the efficacy and safety of these novel strategies remains to be established in appropriate clinical trials.

Anticoagulants↗
PubMed1998

Impaired haemostasis by intravenous administration of a gelatin-based plasma expander in human subjects.

The aim of this study was to investigate the effects of a gelatin-based plasma expander on blood coagulation and haemostasis in human subjects. Six healthy men were studied in a randomised, controlled cross-over study to investigate the effects of a 60 min intravenous infusion of either 1 l gelatin-based plasma substitute (Gelofusine) or 0.9% NaCl (control). The infusion of gelatin resulted in a 1.7 fold increase in bleeding time at 60 min and a 1.4 fold increase at 120 min, while saline had no effect (p <0.05). Aggregation studies revealed a significant impairment of ristocetin-induced platelet aggregation (p <0.05), associated with a substantial decrease of vWF:ag (-32% vs. -5%, p <0.05) and ristocetin co-factor (-29% vs. +1%, p <0.05) and without in vitro impairment of the platelet glycoprotein 1b receptor. Gelatin caused a decrease in thrombin-antithrombin complexes (-45% vs. -4%, p <0.05) and F1+2 (-40% vs. +1%, p <0.05). The decrease in circulating levels of vWF:ag, vWF R:Co, thrombin-antithrombin complexes and F1+2 was more than could be expected by the calculated plasma-dilution generated by Gelofusine. Our results demonstrated that the administration of a gelatin-based plasma substitute results in a significant impairment of primary haemostasis and thrombin generation. The defect in primary haemostasis appears to be related to a gelatin-induced reduction in von Willebrand factor, whereas the decreased thrombin generation may be due to the dilution of coagulation factors induced by Gelofusine.

Adult↗
PubMed1990

Large-scale purification of factor VIII by affinity chromatography: optimization of process parameters.

The optimization of a new process for the extraction of human coagulation factor VIII (FVIII) from plasma with the tailor-made affinity matrix dimethylamino-propylcarbamylpentyl-Sepharose CL-4B (C3-C5 matrix) is described. First, plasma is applied to DEAE-Sephadex A-50 anion exchanger in order to separate a number of proteins, including coagulation factors II, IX and X (prothrombin complex), from FVIII. Subsequently, the unbound fraction of the ion exchanger, containing FVIII, is contacted with the C3-C5 affinity matrix. Optimization of the FVIII affinity chromatographic procedure is accomplished in terms of the ligand density of the matrix, adsorption mode (batch-wise versus column-wise adsorption and matrix to plasma ratio), and conditions of pH and conductivity to be applied on washing and desorption. In scale-up experiments, by processing 20 l of plasma, the recovery (340 U VIII:C/kg plasma) and the specific activity (s.a.) (1.2 U VIII:C/mg protein) are better than those obtained by cryoprecipitation (recovery 300 U VIII:C/kg plasma, s.a. 0.3 U VIII:C/mg protein). The newly developed process using the specially designed C3-C5 affinity matrix has potential application in the process-scale purification of FVIII.

Buffers↗
PubMed1986

Thermal inactivation of human immunodeficiency virus in lyophilised blood products evaluated by ID50 titrations.

Inactivation of human immunodeficiency virus (HIV) in lyophilised small pool cryoprecipitate, factor VIII concentrate, prothrombin complex and C1-esterase inhibitor concentrate by prolonged heat treatment (72 h, 60 degrees C) was studied. Plasma products, inoculated prior to lyophilisation, had infectious titres ranging from 10(7) to 10(10.5). Residual infectivity (TCID50) was assessed by multiple titrations on H9 cells in a macro system and subsequent detection of virus replication by determining reverse transcriptase activity. Kinetics of inactivation showed a biphasic pattern: during the first 8 h a variable TCID50 reduction up to 10(4.3) was observed, followed by an additional loss of 10(1)-10(2.7) during the next 64 h. Heat treatment for 72 h resulted in a mean TCID50 reduction of 10(5). It is concluded that prolonged heat treatment may lead to the adequate prevention of HIV transmission by lyophilised plasma products.

Acquired Immunodeficiency Syndrome↗
PubMed1978

Non-electrolyte permeability as a tool for studying membrane fluidity.

1. The reflection coefficient for the permeation of thiourea through bilayers of phosphatidylcholine is a function of the fatty-acid composition of the lipid molecules. By means of these reflection coefficients an index for membrane fluidity has been given to each of those lipids, relative to that of egg phosphatidylcholine. 2. The maximum number of water molecules that can copermeate with each molecule of solute by means of solute-solvent interaction is a function of the packing of the lipid molecules in the bilayer. This parameter has been used in this paper for characterizing the fluidity of cholesterol-containing membranes and for membranes with their lipids in the gel state.

Chemical Phenomena↗
PubMedDate not supplied

Immunohistochemical expression of CD10 antigen in uterine adenosarcoma.

Uterine adenosarcoma (UAS) is microscopically characterized by a biphasic growth pattern. By definition, the epithelial component is benign, whereas the stromal component typically has the appearance of a low-grade sarcoma, usually an endometrial stromal sarcoma. CD10 acts by reducing cellular response to peptide hormones and is currently regarded as a specific marker for endometrial stromal tumors. In this international multicenter study, we further explored CD10 immunoreactivity in 30 UASs. We encountered CD10 positivity of the sarcomatous component in 18/20 (90%) of UASs, in five of eight (63%) of UASs with sarcomatous overgrowth as well as in both cases of recurrent UAS. The epithelial component stained negative in all cases. These findings suggest that CD10 can be used to differentiate UAS from cellular leiomyoma, or in case endometrial stromal cells exhibit muscle differentiation. Furthermore, CD10 positivity in recurrent UAS might guide the pathologist toward an endometrial stromal origin.

Adenosarcoma↗