Negative conversion of antimitochondrial antibody in primary biliary cirrhosis: a case of autoimmune cholangitis. (1/380)

Autoimmune cholangitis is a clinical constellation of chronic cholestasis, histological changes of chronic nonsuppurative cholangitis and the presence of autoantibodies other than antimitochondrial antibody (AMA). It is uncertain whether this entity is definitely different from AMA positive primary biliary cirrhosis (PBC), though it shows some differences. We report a case of autoimmune cholangitis in a 59-year-old woman, who had been previously diagnosed as AMA-positive PBC associated with rheumatoid arthritis, has been converted to an AMA-negative and anticentromere antibody-positive PBC during follow-up. The response to ursodeoxycholic acid treatment is poor except within the first few months, but prednisolone was dropping the biochemical laboratory data.  (+info)

Obstructive jaundice and acute cholangitis due to papillary stenosis. (2/380)

Papillary stenosis is characterized by fixed fibrosis leading to structural outflow obstruction and it is usually secondary to inflammation and fibrosis from the chronic passage of gallstones, episodes of acute pancreatitis, chronic pancreatitis, sclerosing cholangitis, peptic ulcer disease, and cholesterolosis. However, obstructive jaundice with or without acute cholangitis which leads the physician to suspect the presence of malignancy as a cause is a rare manifestation of papillary stenosis. We report here a case of papillary stenosis presenting with obstructive jaundice and acute cholangitis. The lesion was so difficult to exclude the presence of malignancy preoperatively and intraoperatively that a pylorus-preserving pancreaticoduodenectomy was performed. Histologic examination of the resected specimen revealed fibrosis, adenomatoid ductal hyperplasia, and mild chronic inflammation of the papilla of Vater and distal common bile duct.  (+info)

Active participation of CCR5(+)CD8(+) T lymphocytes in the pathogenesis of liver injury in graft-versus-host disease. (3/380)

We examined the molecular pathogenesis of graft-versus-host disease-associated (GVHD-associated) liver injury in mice, focusing on the role of chemokines. At the second week after cell transfer in the parent-into-F1 model of GVHD, CD8(+) T cells -- especially donor-derived CD8(+) T cells -- infiltrated the liver, causing both portal hepatitis and nonsuppurative destructive cholangitis (NSDC). These migrating cells expressed CCR5. Moreover, macrophage inflammatory protein-1alpha (MIP-1alpha), one of the ligands for CCR5, was selectively expressed on intralobular bile duct epithelial cells, endothelial cells, and infiltrating macrophages and lymphocytes. Administration of anti-CCR5 antibody dramatically reduced the infiltration of CCR5(+)CD8(+) T lymphocytes into the liver, and consequently protected against liver damage in GVHD. The levels of Fas ligand (FasL) mRNA expression in the liver were also decreased by anti-CCR5 antibody treatment. Anti-MIP-1alpha antibody treatment also reduced liver injury. These results suggest that MIP-1alpha-induced migration of CCR5-expressing CD8(+) T cells into the portal areas of the liver plays a significant role in causing liver injury in GVHD; thus, CCR5 and its ligand may be the novel target molecules of therapeutic intervention of hepatic GVHD.  (+info)

Monolobar Caroli's Disease and cholangiocarcinoma. (4/380)

Caroli's Disease (CD) is a rare congenital disorder characterized by cystic dilatation of the intrahepatic bile ducts. This report describes a patient with cholangiocarcinoma arising in the setting of monolobar CD. In spite of detailed investigations including biliary enteric bypass and endoscopic retrograde cholangiography, the diagnosis of mucinous cholangiocarcinoma (CCA) was not made for almost one year. The presentation, diagnosis and treatment of monolobar CD and the association between monolobar CD and biliary tract cancer are discussed. Hepatic resection is the treatment of choice for monolobar CD.  (+info)

Clinical features and management of biliary ascariasis in a non-endemic area. (5/380)

Biliary ascariasis is common in certain geographical areas of the world. In India, it is common in the Kashmir valley and only stray cases have been reported from other parts of the country. Between January 1995 and May 1997, 14 patients with biliary ascariasis were seen at our centre, which is more than 1000 km from the Kashmir valley. The mean (+/- SD) age of the patients was 31.7 (+/- 6.1) years and all were females. None of them had been to a place known to be endemic for biliary ascariasis. Four patients presented with acute cholangitis, eight with acute abdominal pain and vomiting, and the remaining two were diagnosed incidentally during surgery for gallstone disease. Barring these two patients, ultrasound examination of the abdomen diagnosed the condition accurately. In 10 patients, a part of the worm was visible outside the papilla of Vater. The roundworm was caught in a Dormia basket and could be extracted in nine patients. In one patient the worm migrated inside the bile duct while it was being caught in a Dormia basket. In this and two other patients, in whom the worm had migrated completely inside the bile duct, worms were removed with the help of a Dormia basket after endoscopic sphincterotomy. There were no complications of endoscopic therapy. In the two patients in whom biliary ascariasis was detected during surgery, the worms were removed after choledocholithotomy. On a mean follow-up of 13.8 months, only one patient had a recurrence of biliary ascariasis. It is concluded that biliary ascariasis is not an uncommon disease and must be considered as a possibility in patients presenting with acute cholangitis and biliary pain even in a non-endemic area. Ultrasonography is an excellent diagnostic tool and endoscopic management is very effective and safe in the treatment of these patients.  (+info)

Inflammatory cytokines induce DNA damage and inhibit DNA repair in cholangiocarcinoma cells by a nitric oxide-dependent mechanism. (6/380)

Chronic infection and inflammation are risk factors for the development of cholangiocarcinoma, a highly malignant, generally fatal adenocarcinoma originating from biliary epithelia. However, the link between inflammation and carcinogenesis in these disorders is obscure. Because nitric oxide (NO) is generated in inflamed tissues by inducible nitric oxide synthase (iNOS) and because DNA repair proteins are potentially susceptible to NO-mediated nitrosylation, we formulated the hypothesis that inflammatory cytokines induce iNOS and sufficient NO to inhibit DNA repair enzymes leading to the development and progression of cholangiocarcinoma. iNOS and nitrotyrosine were demonstrated in 18/18 cholangiocarcinoma specimens. Furthermore, iNOS and NO generation could be induced in vitro by inflammatory cytokines (mixture of interleukin-1beta, IFN-gamma, and tumor necrosis factor alpha) in three human cholangiocarcinoma cell lines. NO-dependent DNA damage as assessed by the comet assay was demonstrated during exposure of the three cholangiocarcinoma cell lines to cytokines. Moreover, global DNA repair activity was inhibited by 70% by a NO-dependent process after exposure of cells to cytokines. Our data indicate that activation of iNOS and excess production of NO in response to inflammatory cytokines cause DNA damage and inhibit DNA repair proteins. NO inactivation of DNA repair enzymes may provide a link between inflammation and the initiation, promotion, and/or progression of cholangiocarcinoma.  (+info)

Tissue plasminogen activator and plasminogen activator inhibitor-1 in human choledochal bile. (7/380)

Fibrinolytic properties have been detected in animal and human gallbladder (GB) bile. Plasminogen activator inhibitor-1 (PAI-1) has been reported in greater concentration in GB stone bile and may be a nucleating factor in the pathogenesis of GB stone formation. It is unknown whether or not human choledochal bile has similar properties, which could have a role in choledocholithiasis. The aims of this study were to determine the presence of fibrinolytic properties of human choledochal bile and to compare those properties among normal, acalculous, and calculous-infected choledochal bile. Tissue plasminogen activator (t-PA) and PAI-1 of choledochal bile were measured by enzyme linked immunosorbent assay in patients with cholangitis due to acalculous bile duct obstructions (n = 9), choledocholithiasis with cholangitis (n = 20), and normal bile (n = 7). The t-PA concentration of choledochal bile was no different among the three groups (acalculous-infected bile, median 4.61 ng/ml, and calculous-infected bile, 4.61 ng/ml, versus normal bile, 7.33 ng/ml). PAI-1 was detected in choledochal bile in significantly greater concentrations in patients with acalculous cholangitis due to bile duct obstructions and choledocholithiasis with cholangitis (acalculous-infected bile, median 0.36 ng/ml, and calculous-infected bile, 0.1 ng/ml, versus normal bile, 0.02 ng/ml, p < 0.05), but the bile concentration of PAI-1 was no different between the acalculous and calculous-infected choledochal bile. Human choledochal bile possesses t-PA and PAI-1. PAI-1 was present in greater concentrations in both acalculous and calculous-infected choledochal bile. Increased levels of PAI-1 may be an epiphenomenon of cholangitis rather than a factor in the pathogenesis of choledocholithiasis.  (+info)

Enterococcus hirae enteropathy with ascending cholangitis and pancreatitis in a kitten. (8/380)

A 2-month-old female Persian cat that had been showing episodes of anorexia and diarrhea for the previous 4 weeks was presented in shock and died 2 days later. Numerous Gram-positive cocci were located along the brush border of small intestinal villi, without significant inflammatory infiltration. Similar bacteria were present within hepatic bile ducts and pancreatic ducts and were associated with suppurative inflammation and exfoliation of epithelial cells. Culture of the liver and lung yielded bacteria identified as Enterococcus hirae. Fecal culture from an asymptomatic adult female from the same cattery also yielded large numbers of E. hirae. To our knowledge, this is the first report of E. hirae enteropathy in a cat and the first report of ascending cholangitis and ductal pancreatitis caused by an Enterococcus spp.  (+info)

• 1
• 2
• 3
• 4
• 5
• 6
• 7
• 8
• 9
• 10