Disease relevance of Cholangitis, Sclerosing

• Endoscopic retrograde cholangiograms from 23 patients with primary biliary cirrhosis (PBC), 10 controls with either normal livers or hepatocellular disease, and 4 patients with sclerosing cholangitis, were compared [1].
• Ursodeoxycholic acid as a chemopreventive agent in patients with ulcerative colitis and primary sclerosing cholangitis [2].
• RESULTS: Notch-1, but not other Notch receptors, were up-regulated by cholangiocytes in primary sclerosing cholangitis and cholangiocarcinoma [3].
• In this study, to accumulate further evidence for the importance of genetic factors in pathogenesis of inflammatory bowel disease, sera of patients with inflammatory bowel disease and primary sclerosing cholangitis and their unaffected family members were tested for pANCA [4].
• METHODS: Three hundred twenty-seven sera from 11 families of patients with primary sclerosing cholangitis, 43 families of patients with ulcerative colitis, 11 families of patients with Crohn's disease, and 11 healthy families were tested for pANCA in immunofluorescence on cytospin slides with isolated neutrophils [4].

High impact information on Cholangitis, Sclerosing

• CONCLUSIONS: In a group of patients with well-defined primary sclerosing cholangitis, ursodiol provided no clinical benefit [5].
• Ursodiol for primary sclerosing cholangitis. Mayo Primary Sclerosing Cholangitis-Ursodeoxycholic Acid Study Group [5].
• Hepatic endothelial CCL25 mediates the recruitment of CCR9+ gut-homing lymphocytes to the liver in primary sclerosing cholangitis [6].
• CONCLUSIONS: 24-norUrsodeoxycholic acid ameliorates sclerosing cholangitis in Mdr2(-/-) mice [7].
• The colocalization of Notch-1 and iNOS also was observed in large bile ducts from the hilar region of primary sclerosing cholangitis patients [3].

Chemical compound and disease context of Cholangitis, Sclerosing

• High-dose ursodeoxycholic acid in primary sclerosing cholangitis: a 5-year multicenter, randomized, controlled study [8].
• A patient with primary sclerosing cholangitis ponders pulse: methotrexate paper [9].
• Prospective trial of penicillamine in primary sclerosing cholangitis [10].
• Diagnosis of sclerosing cholangitis with technetium 99m-labeled iminodiacetic acid planar and single photon emission computed tomographic scintigraphy [11].
• METHODS: We examined sera from patients with PBC (n = 105), primary sclerosing cholangitis (n = 70), and rheumatoid arthritis (n = 28) as well as healthy volunteers (n = 43) for reactivity against lipoic acid [12].

Biological context of Cholangitis, Sclerosing

• BACKGROUND AND AIMS: We have investigated the influence of a biallelic polymorphism of the promoter region of stromelysin (matrix metalloproteinase 3) on susceptibility to primary sclerosing cholangitis (PSC) [13].
• Primary sclerosing cholangitis is associated to an extended B8-DR3 haplotype including particular MICA and MICB alleles [14].
• The interleukin-1 and interleukin-10 gene polymorphisms in primary sclerosing cholangitis: no associations with disease susceptibility/resistance [15].
• In this study, sera from 22 adults with idiopathic cholestatic liver disease (16 primary biliary cirrhosis (PBC) and six primary sclerosing cholangitis (PSC] were tested for antibody to Reo-3 virus by a standard hemagglutination inhibition assay [16].
• Tissue distribution of autoantigen specific for primary sclerosing cholangitis [17].

Anatomical context of Cholangitis, Sclerosing

• A case of primary sclerosing cholangitis with extensive intrahepatic biliary as well as pancreatic duct strictures that resolved to near normal on ursodeoxycholic acid therapy is reported [18].
• BACKGROUND/AIMS: Primary sclerosing cholangitis (PSC) is an inflammatory disease of the biliary tree associated with an increase in the HLA alleles DR3, DR52a, DR2, Dw2, and a decrease in DR4 [19].
• Moreover, bile duct epithelial cells in primary sclerosing cholangitis (PSC) showed very strong expression of COX-2 protein, that was comparable with carcinoma cells [20].
• To investigate the etiology of FUDR-associated sclerosing cholangitis, portal vein catheters were placed in mixed-breed hounds (N = 4) and connected to an implanted infusion pump system [21].
• Natural killer cells were twice as common in patients with primary sclerosing cholangitis (P < 0.05) as in those with PBC [22].

Gene context of Cholangitis, Sclerosing

• ERBB-2, MET, and COX-2 immunoreactivities were also assessed in both large and small hyperplastic biliary ducts (HBDs) in 27 archival cases of hepatolithiasis and 20 archival cases of primary sclerosing cholangitis (PSC), both of which are risk conditions for human cholangiocarcinogenesis [23].
• However, the role of AIRE mutations in AIH, primary sclerosing cholangitis (PSC), and primary biliary cirrhosis (PBC) is not known [24].
• BSEP and MDR3 haplotype structure in healthy Caucasians, primary biliary cirrhosis and primary sclerosing cholangitis [25].
• In human liver diseases, DMBT1 was expressed in ductular reactions after infection with hepatitis B and acetaminophen intoxication, but not in primary biliary cirrhosis, primary sclerosing cholangitis, and obstruction of the large bile duct [26].
• Cystic fibrosis transmembrane conductance regulator (CFTR) gene defects in patients with primary sclerosing cholangitis [27].

Analytical, diagnostic and therapeutic context of Cholangitis, Sclerosing

• Mdr2(-/-) mice developed liver lesions resembling sclerosing cholangitis characterized by biliary strictures and dilatations [28].
• In an enzyme-linked immunosorbent assay for immunoglobulin G neutrophil antibodies, neutrophil binding by primary sclerosing cholangitis sera was significantly greater than that for primary biliary cirrhosis, chronic hepatitis B, and chronic non-A, non-B hepatitis [29].
• Liver transplantation (LT) is an established therapy for patients with end-stage primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC) [30].
• Frozen sections of griseofulvin-fed mouse liver and human liver of primary biliary cirrhosis and primary sclerosing cholangitis were extracted by Triton X-100 and nuclease [31].
• The etiology of cirrhosis in the control group was alcohol in 16.3%, chronic viral hepatitis in 30.6%, autoimmune hepatitis in 8.2%, and primary biliary cirrhosis (PBC) or primary sclerosing cholangitis in 35.7% [32].

References