Morphological changes of the common bile duct were observed macroscopically and microscopically 20 months after choledochojejunostomy and choledochocolonostomy in rats. The common bile ducts were remarkably dilated in all rats of both experimental models. Choledochal stones consisting of fatty acid calcium and calcium bilirubinate were seen in two of six rats with choledochojejunostomy and two of five rats with choledochocolonostomy. The main pathological change observed in both the groups was remarkable hyperplasia of the choledochal epithelium. Only one rat with choledochojejunostomy revealed normal epithelium with choledochal stone formation. Intestinal metaplasia was seen in two rats with choledochojejunostomy and all with choledochocolonostomy. Squamous pseudostratification of the epithelium indicating atypism was observed in two rats with choledochojejunostomy. Sialomucin producing cells and sulfomucin producing cells were seen in the hyperplastic portion of the epithelium. No malignant alteration of the epithelium was detected. These findings indicate that long-lasting exposure to digestive enzymes and bacteria causes epithelial hyperplasia and further exposure to digestive enzymes plays a major role in appearance of the epithelial atypism. Carcinogenesis of the choledochal epithelium under such an environment will need much more time to be established.
A case of hemophagocytic syndrome (HPS) refractory to corticosteroid therapy was successfully treated by plasma exchange. The patient was a 56‐year‐old woman who had undergone regular hemodialysis for 10 years for complicated myelodysplastic syndrome (MDS) and then had had lung tuberculosis. After the onset of tuberculosis, she suffered from HPS and was treated by antituberculosis agents and high dose corticosteroid administration without any effect on the HPS. After adding a series of plasma exchanges, the HPS improved gradually, and her MDS began to respond to corticosteroid therapy. Plasma hypercytokinemia due to HPS was corrected by plasma exchange, and the correction of a high level of plasma inflammatory cytokine was considered to be one of the contributing factors for the improvement of HPS. These results suggest that therapeutic plasma exchange should be considered as a therapeutic tool for HPS refractory to conventional therapy.
The direct effects of recombinant human erythropoietin(rHuEPO) on coagulation and fibrinolysis factors were evaluated in a cultured endothelial cell (EC) system. Confluent quiescent ECs were incubated with or without 5.0 U/ml rHuEPO for 1, 6, and 18 hours, and supernatant concentrations of plasminogen activator inhibitor-1 (PAI-1): antigen (Ag), tissue plasminogen activator and thrombomodulin, and supernatant activities of tissue factor pathway inhibitor and von Willebrand factor were measured. The results showed that only PAI-1 levels were increased by the presence of rHuEPO. In order to assess the effect of rHuEPO on PAI-1 production by EC more precisely, confluent ECs were incubated with various doses of rHuEPO (0, 1.0, 2.5, 5.0, 10.0 U/ml) for 1, 6, 12, and 18 hours, and PAI-1:Ag concentrations in the supernatants of media were measured. PAI-1:Ag in the supernatants were increased by the presence of rHuEPO at all incubation times (P < 0.01) and the increase in PAI-1:Ag was dependent on rHuEPO concentration. The increases in PAI-1:Ag by 5.0 U/ml rHuEPO were comparable to those by 0.1 U/ml tumor necrosis factor-alpha, 1.0 microgram/ml lipopolysaccharide, and 0.5 U/ml thrombin. The increase in PAI-1:Ag by rHuEPO was suppressed by pre-incubation with 10 micrograms/ml cycloheximide (P < 0.01) or 0.2 microgram/ml actinomycin D (P < 0.01). These results indicate that rHuEPO directly stimulates PAI-1 production in cultured EC via de novo protein and RNA syntheses.
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