Factors that affected the HRQOL of UC patients varied according to the patients' disease duration. Our findings should assist in the development of a long-term strategy for the treatment of UC patients.
A 64-year-old woman with CREST syndrome developed prominent telangiectases mimicking hereditary hemorrhagic telangiectasia (HHT) of Osler-Rendu-Weber. We have been following her since she first came to us with discrete telangiectatic mats and Raynaud's phenomenon 11 years ago. Telangiectatic lesions have been seen on her larynx and esophagus in addition to commonly affected sites. She has experienced spontaneous epistaxis and marked bleeding from the lesions on her lips, oral mucous membrane, and soles. This case illuminates new aspects of telangiectasia in CREST syndrome.
A 47-year-old male was admitted because of severe chest pain after repeated vomiting. A little amount of coffeegrounds was seen in the vomitus, and emergency endoscopic examination was performed 1 hour after the onset of symptoms. Endoscopy demonstrated a lacerated wound about 3 cm long on each side of the terminal esophagus. With a diagnosis of spontaneous rupture of the esophagus, a primary closure of the rupture was performed 4 hours after the onset, and a pedicled omental graft was applied over the suture site. The patient was discharged in improved condition on the 99th day. In Japan, more than 250 cases of spontaneous rupture of the esophagus have been reported, and 59 cases (including ours) have been observed endoscopically. Many authors have said that emergency endoscopy is useful for definitive diagnosis and for selection of the appropriate surgical procedure. The diagnostic accuracy with emergency endoscopy is 58 percent, so it has been suggested that emergency endoscopy is a valuable initial examination, but systematic diagnosis is necessary for early establishment of correct diagnosis.
Lectin histochemistry revealed that Kupffer cells in the normal liver bound lectins such as Concanavalin A (Con A), Ricinus communis agglutinin (RCA) and Wheat germ agglutinin (WGA), but did not bind Peanut agglutinin (PNA), Dolichos biflorus agglutinin (DBA), Ulex europaeus agglutinin I (UEA‐I) or Soybean agglutinin (SBA). Kupffer cells in viral liver diseases, however, bound the PNA lectin and the binding was specific to Kupffer cells in liver parenchyma. Computer image analysis was performed using light micrographs of sections stained with immuno‐peroxidase and diaminobenzidine (DAB). The dark brown area of reaction products was detected by analyzing each color component (red, green and blue) in the picture and was expressed as the percent area in the parenchyma. Quantitative analysis revealed the percent area occupied by Kupffer cells positive for the PNA lectin was as follows: acute hepatitis, 2.83 ± 0.74; chronic persistent hepatitis, 2.51 ±0.88; chronic aggressive hepatitis, activity moderate and severe, 4.71 ± 2.23 and 3.45 ± 1.84; and liver cirrhosis, 1.96 ± 0.99. The percent area of Kupffer cells was significantly higher in CAH2A than that in chronic persistent hepatitis or in liver cirrhosis. These results suggest that the PNA lectin could be used as a marker for activated Kupffer cells and that activated Kupffer cells were increased in volume in chronic aggressive hepatitis.
Neonatally thymectomized mice are unique in that they are prone to organ-specific autoimmune diseases. We investigated whether autoimmune cholangitis could be induced in these mice when they were immunized with biliary antigens. Neonatally thymectomized A/J mice were immunized with porcine intrahepatic bile duct epithelial cells (group 1), porcine gallbladder epithelial cells (group 2), porcine splenocytes (group 3) or Freund's adjuvant (group 4). Nonthymectomized mice were immunized with bile duct epithelial cells (group 5) or Freund's adjuvant (group 6). The cell suspensions were injected intraperitoneally with Freund's adjuvant once a week for 8 wk. In group 1 varying amounts of mononuclear cells infiltrated around the bile duct in 14 of 22 mice, whereas little or no accumulation was noted in other groups. Ultrastructural observations revealed that the inflammatory cells consisted of lymphocytes, plasma cells and macrophages. The bile duct showed degenerative changes and some lymphocytes infiltrated between bile duct epithelial cells. An immunohistochemical study showed that the accumulated lymphocytes consisted of CD4+ and CD8+ T cells, as well as B cells. Both major histocompatibility complex class I and class II antigens were expressed on bile duct epithelial cells. Antimitochondrial antibody was demonstrated in some mice in groups 1 (9 of 17), 2 (2 of 3) and 5 (4 of 5) by immunofluorescence; the antibody reacted with the 68, 52 and 47 kD polypeptides of the pyruvate dehydrogenase complex on Western blotting. These findings suggest that autoimmune cholangitis can be induced in neonatally thymectomized mice stimulated with biliary antigens and that these mice could be a suitable animal model for primary biliary cirrhosis.
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