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)

An ABC immunohistochemical study of the expression of cytokeratin (CK19 and CK18) was carried out in 315 cases of HBV-caused hepatitis, early-cirrhotic and cirrhotic livers. It was shown that hepatocytes in 73% of chronic active hepatitis (CAH) (80/110) and 81% of early-cirrhotic and cirrhotic livers (117/144) expressed CK19 (the abnormal CK expression), which could be of help in differentiating CAH from chronic persistent hepatitis, subtype CAH (mild, moderate to severe type) and in determining the activity of early-cirrhotic and cirrhotic livers. The abnormal CK expression was shown to be closely related to the activity of liver disorders. The CK19 expression in hepatocytes had the closest relations with the piece-meal necrosis of hepatocytes, isolation of hepatocytes into groups by connective tissue, and fibrosis. It is suggested that CK19 expression may be one of the local reactions to the piece-meal necrosis of hepatocytes.
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PMID:[The abnormal cytokeratin expression in HBV-caused hepatitis, early-cirrhotic and cirrhotic livers, its mechanism and significance]. 128 75

The existence of facultative stem cells in the liver has been advocated based on observations from models of carcinogenesis in rat liver. Observations of human liver material from cases of fulminant hepatitis have shown the presence of ductular hepatocytes expressing markers of both hepatocytes and bile duct cells. We describe the morphologic features and antigenic expression of a population of ductular hepatocytes identified in a patient with end-stage cirrhosis resulting from hepatitis B infection and secondary biliary cirrhosis. By conventional light microscopy and electron microscopy, ductular hepatocytes were seen to form pseudoductules within periportal areas. Using immunohistochemical methods, these ductular hepatocytes were found to be positive for both the hepatitis B surface antigen and bile duct epithelial cytokeratin, phenotypic markers classically restricted to expression on hepatocytes and bile duct epithelium, respectively. These findings show definitively that ductular hepatocytes are intermediate cells bearing morphologic and phenotypic characteristics of both hepatocytes and bile duct epithelium. The presence of these cells indicates the existence of facultative stem cells in the adult mammalian liver.
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PMID:Characterization of ductular hepatocytes in end-stage cirrhosis. 232

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.
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PMID:Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas. 246 75

Cholestatic and hepatitic liver cell rosettes, gland-like formations found respectively in chronic cholestasis and in chronic active hepatitis, represent structural modifications of liver cell plates in response to injury. Differences in cytokeratin expression, ultrastructure and three-dimensional (3-D) configuration have been investigated. Cholestatic rosettes are considered to be a form of biliary metaplasia of hepatocytes, linking with newly-formed bile ductules in adjacent septa and probably providing some protection from injury caused by abnormal bile constituents. Hepatitis rosettes, by contrast, are a form of liver cell regeneration developing in isolated surviving hepatocytes or small groups of hepatocytes within areas of collapse.
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PMID:Liver cell rosettes: structural differences in cholestasis and hepatitis. 246 88

Antibodies against thymus epithelial cells (anti-TEC) and the basal cell layer (BCLA) of squamous epithelia have been described in association with HDV-related chronic liver disease (CLD). Data are lacking on their presence during nAnB virus infection. Sera from 51 patients with nAnB post-transfusion hepatitis, including acute and chronic cases diagnosed during a prospective study on candidates for cardiac surgery, and 167 with various forms of CLD were tested for the presence of anti-TEC and BCLA using indirect immunofluorescence on human thymus and rat forestomach sections. Both antibodies mainly occurred in nAnB, HDV and cryptogenic CLD (anti-TEC: 51%, 47% and 42%; BCLA: 29%, 38% and 31%, respectively). The prevalence of anti-TEC in nAnB CLD turned out to be higher than that recorded in alcoholic, HBV-related, autoimmune, liver and kidney microsomal antibody positive CLD and primary biliary cirrhosis (p ranging from less than 0.03 to less than 0.0004). Two monoclonal antibodies (Mabs) to cytokeratins gave a pattern superimposable on that of spontaneous anti-TEC (both Mabs) and BCLA (only one). Antibodies against epithelial constituents, presumably targeting cytokeratin-associated antigens, occur not only in HDV CLD, as previously reported, but also in nAnB CLD, where they might represent a diagnostic aid, due to the unavailability of reliable serological markers of nAnB infection. The close similarity of anti-TEC and BCLA status between nAnB and cryptogenic CLD suggests a nAnB etiology of at least a proportion of chronic liver patients at present scored as cryptogenic.
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PMID:Serum antibodies to thymus epithelial cells in non-A, non-B and cryptogenic chronic liver disease. 247 4

The development of ductular structures in acute hepatitis with panacinar necrosis was studied in 15 cases of fulminant hepatitis with variable clinical duration, using immunohistochemical markers. The immunophenotype of ductular structures was assessed by the expression of two bile duct epithelium determinants, wide spectrum cytokeratin and epithelial membrane antigen (EMA), and by their glycoconjugate expression using the specific binding lectins Dolichos biflorus agglutinin (DBA) and soybean agglutinin (SBA). Ductular structures showed a predilective, but not a strictly selective location in acinar zone 1 and at the periphery of newly formed parenchymal nodules. All were positive for keratin, while EMA and the lectins were identified less frequently. Cytokeratin expression was additionally observed in hepatic cells with no other phenotypic alteration: this occurred along isolated hepatic cords, within parenchymal remnants, in the spared parenchyma in acinar zone 1 and occasionally at the periphery of parenchymal nodules. The presence of cytokeratin expression in liver cell plates in association with intermediate morphological stages of tubular remodelling speaks in favour of biliary metaplasia of hepatocytes. This process may represent a phenotypic-functional accommodation of hepatocytes to an altered microenvironment, due to loss of parenchymal integrity. During the phenotypic shift, altered cytokeratin expression appears as one of the earliest biliary features, while EMA and the expression of glycoconjugates represent maturation markers.
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PMID:Ductular structures in acute hepatitis with panacinar necrosis. 753 48

Oval cell proliferation occurs during spontaneous hepatitis in Long-Evans cinnamon (LEC) rats. It has been reported that oval cells undergo differentiation into mature hepatocytes via small hepatocytes during carcinogenesis. This study was designed to demonstrate in vivo differentiation of oval cells into typical bile ductular cells in the liver lobule and the characteristic feature of intralobular bile ductule formation in LEC rats. We have examined kinetics, intralobular distribution, and morphology of oval cells, small hepatocytes, and bile ductular cells in LEC rat livers at prehepatitic, acute hepatitic, chronic hepatitic, and precancerous stages by conventional light and electron microscopy, immunostaining for cytokeratin, and 3-dimensional reconstruction analysis. Our results indicate that oval cells proliferated and extended into the periportal zone of the liver lobule during acute hepatitis at 20 to 23 weeks after birth. They exhibited tubular structures with a poorly defined lumen and incomplete basement membrane. After remission of the jaundice, small hepatocytes proliferated in association with oval cells and predominated in the periportal zone at 26 weeks. In a chronic hepatitic stage at 28 to 30 weeks, tubular structures were transformed into typical bile ductules, which had a well defined lumen and complete basement membrane, and small hepatocytes became a normal size. Intralobular bile ductules originated from the interlobular bile ducts, ran in the space of Disse, giving rise to several branches in the course, and were terminated at the hepatocytes. The present results indicate that oval cells that proliferate in the liver lobule of LEC rats after spontaneous hepatitis not only differentiate into small hepatocytes but also into typical bile ductular cells. This study suggests that intralobular bile ductules may play roles in maintaining the bile excretion during and after the disorganized proliferation of oval cells and small hepatocytes.
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PMID:Development of intralobular bile ductules after spontaneous hepatitis in Long-Evans mutant rats. 868 39

We clinicopathologically studied 23 surgically resected cases of combined hepatocellular and cholangiocarcinoma (HCC-CC). The frequency of this cancer in our subjects, who had primary liver cancer and who underwent hepatectomy, was 6.3%. The mean age of patients was 64.0 years old and the male: female ratio was 1.9:1. Serum alpha-fetoprotein was positive in 70% of cases and its levels were relatively low (< or = 1000 ng/mL) in most cases. The positive rate of serum carcinoembryonic antigen was 18% and its levels were also low. In regard to hepatitis virus markers, 17% of the 20 combined HCC-CC cases were positive to HBs antigen and 70% were positive to the HCV antibody. Of the 23 combined HCC-CC cases, 9 cases (39%) were associated with liver cirrhosis. Tumours were classified macroscopically into a separated type (HCC and CC are clearly separated 17%), a HCC-predominant type (resembles HCC 49%), and a CC-predominant type (resembles CC 34%). The separated and HCC-predominant types were associated with liver cirrhosis in 50 and 55% of cases, respectively. These cases with liver cirrhosis presented the features of HCC more apparently, while those without liver cirrhosis presented the features of CC. Histologically, all cases were classified into either Type I (HCC and CC were clearly distinguished; 17%), Type II (HCC and CC were contiguous and shared transitional features; 66%), and Type III (cancer cells were able to be evaluated as either HCC or CC and were considered to be an intermediate type; 17%). Immunohistological stains for cytokeratin were useful to distinguish HCC and CC. Specifically, CC was positive to cytokeratin 7 and 19. The tumour, in which HCC and CC were almost indistinguishable, such as Type III), indicates the presence of intermediate tumour cells that can differentiate either to HCC or CC.
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PMID:A clinicopathological study on combined hepatocellular and cholangiocarcinoma. 887 74

Didanosine (ddI) that inhibits the reverse transcriptase of human immunodeficiency virus (HIV) causes steatosis and fulminant hepatitis in some patients with HIV. We studied hepatic histopathologic changes with particular attention to ddI-induced Mallory body formation. Three liver biopsies were performed on three patients with HIV who were treated with ddI; an autopsy was performed on a patient with HIV who was also treated with ddI. All hepatic specimens were studied with a routine liver immunohistochemical panel including antibodies to ubiquitin and cytokeratin (CAM 5.2). Morphologically, all hepatic specimens showed focal to diffuse steatosis with a predominance of macrovesicular fatty change. Fibrosis was minimal in three cases. No secondary bacterial and fungal infections were noted. Single or clusters of "empty cells" were present, and some contained Mallory bodies validated by ubiquitin stain. Empty cells are hepatocytes that fail to stain positive for cytokeratin. The Mallory bodies were different from the others because they were randomly distributed and occurred in noncirrhotic hepatic tissue. In the autopsy specimen, the Mallory bodies had a centrilobular location with central fibrosis (central sclerosing hyaline necrosis).
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PMID:2',3'-Dideoxyinosine-induced Mallory bodies in patients with HIV. 929 55

Double primary liver carcinomas, i.e. hepatocellular carcinoma (HCC) and cholangiocellular carcinoma (CCC) are rare. Two patients in whom double primary liver carcinomas were surgically resected are described herein. Case 1: A 51-year-old Japanese man with chronic type B hepatitis underwent hepatectomy for primary HCC with intrahepatic metastasis. Case 2: A 67-year-old Japanese man with a history of rectal cancer and CCC underwent lateral hepatic segmentectomy for a suspected recurrence of intrahepatic CCC. Lack of direct contact between tumors, no evidence of histological transition and clearly different immunohistochemical staining for cytokeratin support a distinct histogenesis of the tumors in these two patients. The findings indicate that combined HCC and CCC can arise synchronously or metachronously as an intrahepatic double cancer.
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PMID:Separate histogenesis of combined hepatocellular and cholangiocellular carcinoma in two patients. 963 42


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