Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-cathepsin G antibodies have been detected by using three different methods. i) Binding to azurophilic granules constituents after separation of purified alpha-granules on Matrex gel Orange A chromatography according to Kao. ii) Binding to azurophilic granules freezed and thawed after coating on ELISA plates. iii) Binding to purified cathepsin G in ELISA assay. Anti-cathepsin G antibodies were observed patient's sera with ulcerative colitis, primary sclerosing cholangitis, primary biliary cirrhosis and autoimmune hepatitis but not in controls or patients with chronic viral hepatitis or vasculitis.
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PMID:Methods of detection of anti-cathepsin G autoantibodies in human. 829 15

Here we report an autopsy case with anti-neutrophil antibodies (ANCA) associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma. A 69-year-old woman was admitted to Tokyo Metropolitan Ohtsuka Hospital in October 1995 because of leg edema. She had presented cough in 1990 and diagnosed as interstitial pneumonia, esophageal varices and liver chirosis. On admission, laboratory data showed mild anemia, hypoproteinemia, and marked gammagloblinemia. IgM-HA antibody, HBs antigen, HBs antibody, HCV antibody and HDV antibody were negative. Anti-nuclear antibody, anticentromere antibody, anti-neutrophil cytoplasmic antibody against myeloperoxidase and cathepsin G (MPO-ANCA and cathepsin G), rheumatoid factor and direct coombs test were positive. Serum level of AFP and CEA were elevated. Ultrasonography and computed tomography of abdomen scowed liver chirosis and tumor in left lobe of liver. The diagnosis of liver chirosis based on autoimmune hepatitis and Interstitial pneumonia was made with clinical course, laboratory findings and radiographic findings although liver biopsy was not performed. She complained of bloody stool due to ulcer of the large intestine, and died of liver failure which progressed rapidly. The autopsy findings detected that pulmonary fibrosis, liver fibrosis with multiple hepatocellular carcinoma, necrotizing crescentic glomerulonephritis, and vasculitis of small artery inn colon. This was the first report of MPO-ANCA associated vasuculitis complicated with autoimmune hepatitis and hepatocellular carcinoma. Clinical significance of ANCA and immunogenetic background of these diseases were discussed.
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PMID:[An autopsy case of anti-neutrophil cytoplasmic antibodies associated vasculitis accompanied by autoimmune hepatitis and hepatocellular carcinoma]. 917 69

Administration of alpha-naphthylisothiocyanate (ANIT) to rats causes acute liver injury characterized in part by hepatocellular damage and marked neutrophil infiltration, effects that resemble drug-induced cholangiolitic hepatitis in people. ANIT-induced liver injury is neutrophil dependent. Moreover, ANIT can activate neutrophils in vitro. Since neutrophil-derived proteases can mediate hepatocellular killing, we hypothesized that ANIT stimulates neutrophils to release proteolytic enzymes that are cytotoxic to hepatic parenchymal cells. To test this hypothesis, neutrophils were isolated from Sprague-Dawley rats and incubated with ANIT for 6-24 h. ANIT (6-50 microM) was not toxic to neutrophils as indicated by the lack of lactate dehydrogenase release into the incubation medium. The conditioned medium from ANIT-treated neutrophils (ANCM) was collected, centrifuged, added to isolated hepatocytes, and incubated for 8, 16, or 24 h. Conditioned medium collected from neutrophils exposed to 25 or 50 microM ANIT for 16-24 h caused hepatocellular damage as indicated by the release of alanine aminotransferase into the culture medium. The concentration of ANIT in ANCM was nondetectable (0.5 microM). Analysis of ANCM indicated the presence of both cathepsin G and elastase activities. Inhibitors of these enzymes afforded protection against ANCM-induced hepatocellular injury. These results indicate that ANIT causes neutrophils to release toxic proteases which cause hepatocellular damage in vitro.
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PMID:Alpha-naphthylisothiocyanate causes neutrophils to release factors that are cytotoxic to hepatocytes. 946 76

Primary sclerosing cholangitis is a chronic cholestatic disease that may have an autoimmune basis. Most patients have a circulating antineutrophil cytoplasmic antibody that appears to be targeted against a 50-kD nuclear envelope protein. The clinical applications of this antibody have not yet been defined. Other autoantibodies directed against antigens, such as cathepsin G, elastase, and anticardiolipin, may also be detected in some patients. It is suggested that primary sclerosing cholangitis may have a bacterial cause. Helicobacter gene sequences have been detected in liver tissues in primary sclerosing cholangitis. The role of Helicobacter spp and other bacteria in the etiopathogenesis of primary sclerosing cholangitis remains to be determined. Primary sclerosing cholangitis may overlap with autoimmune hepatitis in some cases, although the real prevalence of this association remains to be determined. Many prognostic models have been created, but they lack cross-validation, and their clinical usefulness remains limited. Endoscopic retrograde cholangiography remains the gold standard for diagnosis, but magnetic resonance imaging may be a viable alternative in many cases. Clinical trials with cladibrine, pentoxifylline, and budesonide have failed to demonstrate benefits. Orthotopic liver transplantation remains the only effective treatment.
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PMID:Sclerosing cholangitis. 1703 Dec 1