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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic infection of woodchucks with woodchuck hepatitis virus (WHV) was associated with the development of hepatitis, foci of altered hepatocytes and hepatocellular adenomas and carcinomas. The cytomorphological and cytochemical analysis permitted the identification of three different types of focal lesions; namely, glycogen-storage foci, mixed-cell foci and intermediate-cell foci, each showing a characteristic pattern. The cells of the glycogen-storage foci had clear to acidophilic cytoplasm, and were overloaded with glycogen. They showed a marked elevation in the activity of glucose-6-phosphate dehydrogenase (G6PDH) and malate dehydrogenase (MDH), increased activity of succinate dehydrogenase (SDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerol-3-phosphate dehydrogenase (G3PDH), reduction in the activity of glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and adenyl cyclase (ADC), and unchanged activity of glycogen synthase (SYN) and gamma-glutamyl transferase (GGT). The mixed-cell foci mainly consisted of basophilic cells poor in glycogen, but were intermingled with cells containing glycogen. These foci were characterized by a marked decrease in activity of PHO, SYN, G6Pase, G6PDH, ATPase and ADC, and increased activity of GGT, SDH, MDH and GAPDH. The intermediate-cell foci consisted of cells with both basophilic and glycogenotic cytoplasmic compartments, and showed a similar enzyme histochemical profile to the mixed-cell foci, with slight differences in the degree of elevation or reduction of some enzymes. The phenotypic similarities and the close spatial relationship between the foci of altered hepatocytes, and the hepatocellular adenomas and carcinomas in WHV-infected woodchucks, suggest that these lesions are preneoplastic. The focal morphological and metabolic aberrations emerging during hepatocarcinogenesis in WHV-infected woodchuck, are in principle similar to those identified in the course of chemical hepatocarcinogenesis in various species. The focal metabolic aberrations apparently represent a general biological response of the liver parenchyma to oncogenic agents and are closely linked to neoplastic transformation of the hepatocytes.
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PMID:Phenotypic patterns of preneoplastic and neoplastic hepatic lesions in woodchucks infected with woodchuck hepatitis virus. 215 41

Hepatocellular carcinoma (HCC), the most frequent malignant tumour of the liver, is the commonest cancer occurring in males in the world. The annual incidence of the disease worldwide is estimated to be one million cases. There are variations in its geographical distribution. It tops the list of malignancies amongst males in sub-saharan Africa; it is the second most common cancer in Southeast Asia, including Hong Kong, and ranks third amongst males in China. It is relatively rare in America, Europe North Africa, and the Middle East. During the last 15 years, epidemiologic and laboratory investigations have established a strong and specific association between chronic hepatitis B virus (HBV) infection and HCC. Hepatic cirrhosis is another major aetiologic factor incriminated. In areas with a low incidence of HCC, cirrhosis due to alcohol may be a relatively more important predisposing factor. Chronic non-A, non-B hepatitis (NANBH) infection has now been incriminated as a cause of HCC, especially in Japan. Other environmental factors, particularly chemical carcinogens such as Aflatoxin, smoking, genetic predisposition and sex hormones may also act to promote hepatocarcinogenesis. The exact mechanisms of neoplastic transformation, however, are still far from understood. The following factors are discussed in detail: 1. HBV infection 2. Cirrhosis 3. NANBH infection 4. Aflatoxin B1 5. Cigarette smoking 6. Alcohol A number of less important associated diseases are also listed in Table I. At the end of this paper, a tentative scheme for hepatocarcinogenesis has been proposed and the methods for prevention is discussed in light of the risk factors considered.
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PMID:Hepatocarcinogenesis. 216 75

Interaction between woodchuck hepatitis virus surface antigen and proteins of hepatocyte plasma membranes were examined in the course of woodchuck hepatitis virus infection. Membranes purified from animals with histologically confirmed acute hepatitis, active or persistent chronic hepatitis and the virus-related hepatocellular carcinoma were evaluated for the virus surface antigen contents, treated with agents eluting plasma membrane-bound antigen to test the extent of the antigen-membrane associations and incubated with purified, particulate woodchuck hepatitis virus surface antigen to determine membrane potential for the antigen adsorption. Hepatocyte plasma membranes originating from woodchucks chronically infected with the virus showed the highest quantities of the incorporated virus surface antigen among membranes studied, the behavior of bound antigen as an integral and a peripheral membrane protein and the resistance to bind an exogenous antigen. Similar properties were expressed by plasma membranes prepared from hepatocytes of nontumor parenchyma displaying chronic active hepatitis of a woodchuck hepatitis virus carrier with hepatoma. Furthermore, plasma membranes originating from animals with active or persistent chronic hepatitis demonstrated identical properties, implicating that histologic activity of the chronic liver inflammatory process is not dependent on the quantity of the virus surface antigen insertion into the membrane. In contrast, hepatocyte plasma membranes from animals with acute hepatitis showed significantly lower antigen quantities, presence of the antigen specificity exclusively behaving as an integral membrane protein and noticeable ability to bind an exogenous surface antigen of the virus. Comparable, but not identical, features were observed for hepatocyte membranes purified from nodules of hepatocellular carcinoma, suggesting that neoplastic transformation of infected hepatocytes is associated with loss of the membrane-bound antigen and with simultaneous, partial recovery of the membrane potential for the antigen binding. Comparative analysis of the properties on the woodchuck hepatitis virus surface antigen incorporation into hepatocyte plasma membranes in studied cases indicated that sustained infection with woodchuck hepatitis virus leads to an increase in the quantity of the membrane-incorporated antigen and to the appearance of the virus surface antigen specificity behaving as a peripheral membrane protein. In conclusion, this study demonstrated that the extent and the character of the antigen interaction with hepatocyte plasma membranes undergoes significant variations in the natural course of hepadna viral infect
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PMID:Characterization of the incorporation of woodchuck hepatitis virus surface antigen into hepatocyte plasma membrane in woodchuck hepatitis and in the virus-induced hepatocellular carcinoma. 253 20

IgM antibody to hepatitis B core antigen (IgM anti-HBc) was determined in 348 subjects with hepatitis B virus infection, in order to evaluate, in an area of high hepatitis D virus (HDV) endemicity, its usefulness in discriminating acute HBV hepatitis from HDV superinfection of HBsAg carriers, and to see whether in chronic HBV infection IgM anti-HBc can be related to viral replication, disease activity, or risk of neoplastic transformation. The positive predictive value (PV) of IgM anti-HBc for acute hepatitis was low at the standard 2.1 cut-off (35.2%), but a cut-off of 7 raised the positive PV, retaining a negative PV of above 90% and a sensitivity of 59.5%. No significant relationship was found in chronic infection between IgM anti-HBc, the level of HBV replication or the type of liver disease. Patients with HDV infection were mostly IgM anti-HBc negative. Hepatocellular carcinoma was not associated with a raised prevalence of IgM anti-HBc.
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PMID:IgM anti-HBc in acute and chronic hepatitis B virus (HBV) infection: diagnostic value and correlation with viral replication and disease activity. 307 40

We analyzed the DNA ploidy and the nuclear size of hepatocytes within hepatocellular carcinoma, putative preneoplastic (clear cell and basophilic foci) and adjacent non-neoplastic liver in 30 woodchucks neonatally infected with the woodchuck hepatitis virus. In livers from control woodchucks, in clear cell foci and in most chronic portal hepatitis, the hepatocytes were diploid, with less than 10% tetraploid cells. Aneuploid peaks were found in 50% of the livers with chronic active hepatitis, in 63% of basophilic foci and in 90% of hepatocellular carcinoma. Within the same tumor, aneuploid peaks with different DNA indices were observed frequently, indicating heterogeneity of tumor. S-phase was always elevated, indicating an increased rate of proliferation. Aneuploid cells had nuclei that were larger than those of control liver cells. In some basophilic foci and in some livers with chronic active hepatitis, abnormal DNA was demonstrated before the development of hepatocellular carcinoma, suggesting that these may be populations of hepatocytes at risk of neoplastic transformation.
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PMID:DNA ploidy analysis of hepatic preneoplastic and neoplastic lesions in woodchucks experimentally infected with woodchuck hepatitis virus. 802 Aug 90

The availability of the anti-HCV assay has confirmed most of the suspicions and predictions regarding the epidemiology of NANB hepatitis virus made before the discovery of HCV. It is now clear that HCV is responsible for the majority of cases of post-transfusion and sporadic NANB hepatitis, as well as of most cases of unidentified chronic liver disease. It seems plausible that HCV may act as a negative co-factor in other chronic liver diseases, especially those caused by alcohol, other hepatitis viruses, and so-called 'autoimmune hepatitis'. The issue of perinatal and sexual transmission of HCV has not yet been clarified, and further studies are urgently needed. Finally, the high prevalence of anti-HCV detected in HCC suggests that HCV is a major co-factor in the development of HCC and again raises the issue of viral persistence and neoplastic transformation, an issue that for HBV has not yet been elucidated.
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PMID:Epidemiology of hepatitis C virus infection. 850 43

Hepatitis B virus (HBV) plays a major role in liver carcinogenesis. HBV-DNA integration into cellular DNA provides some molecular basis for understanding the mechanisms of neoplastic transformation of the liver cell. Persistence of HBV-DNA episomic forms, necro-inflammation in the liver, and cirrhosis appear to be additional promoting factors. We studied the possible association between hepatocellular carcinoma (HCC) and the defective hepatitis D virus (HDV), a virus that requires the helper function of HBV. Patients infected with HDV and HBV develop HCC about 10 years earlier than those infected with HBV alone. Persistence of active HDV disease and low levels of "wild-type" HBV (i.e., secreting the hepatitis B surface antigen [HBsAg]) are associated with progressive liver disease and HCC. Therefore, HBV replication, in spite of being inhibited by HDV, appears to play a major role sustaining HDV pathogenicity. Detection of antibody to the hepatitis C virus (HCV) in many HCC patients raises the important question whether HCV has oncogenic potential. Clinico-epidemiological data show that the most severe forms of liver disease in patients with multifactorial liver damage occur in those infected with HCV. The prevalence of HBV markers in patients with cirrhosis, HCC, and HCV infection is higher than in individuals with comparable age and other diseases. HBV-DNA integration occurring early during HBV infection can persist in those with and without detectable HBsAg in their serum. Therefore, one can speculate that in patients with integrated HBV-DNA and concurrent HCV infection, cirrhosis and HCC may develop more easily than in patients without HBV-DNA integration. HCV hampering the immune system also might play a role in the genesis of HCC. The evidence that multiple hepatitis viruses are more frequently associated with HCC than infections of one virus alone has important practical consequences. It warrants the identification of high risk patients so that they can be monitored frequently for early diagnosis and treatment.
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PMID:Hepatocellular carcinoma and infections with multiple hepatitis viruses. 887 10

Between 1986 and 1996, 263 patients, 156 females and 107 males, affected by oral lichen planus (OLP), were followed at the Division of Oral Medicine and Pathology, University of Naples 'Federico II', Italy, and at the Institute of Dentistry and Maxillofacial Surgery, University of Bari, Italy. During this follow-up, the possible association of OLP with oral squamous cell carcinoma (SCC), together with the possible association of OLP, oral SCC and chronic HCV-hepatitis, were investigated. 14 cases (5.32%) were known to have developed oral SCC: 10 (3.8%) in an area of pre-existing OLP, 3 (1.14%) in other sites, in 1 case the diagnosis of OLP and SCC was synchronous (0.38%). 3 patients were positive for anti-HCV antibody. Many carcinomas were in areas of reticular/plaque OLP. 3 patients had multiple simultaneous sites of oral involvement (21.42%); 5 patients developed oral SCC in different sites during the follow-up period (35.71%). These data, together with a clear histological evidence of progression to carcinoma within OLP lesions, suggest the probability of some cases of at least OLP having an intrinsic property predisposing to neoplastic transformation, confirming previous studies. For these reasons, the authors think that it is necessary to follow-up the patients regularly at least annually and possibly for life for the early diagnosis of a possible neoplastic degeneration. These consideration are particularly important in the case of atrophic or erosive OLP, and plaque OLP, especially when involving the dorsum of tongue.
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PMID:The possible association between oral lichen planus and oral squamous cell carcinoma: a clinical evaluation on 14 cases and a review of the literature. 981 16

Drugs may cause acute or chronic liver damage depending on their mode of action. Hepatotoxic drugs include anaesthetics, psychotropic and anticonvulsant drugs, antiinflammatory agents, steroids, antimicrobial agents and cardiovascular drugs as well as antineoplastic agents. Hepatotoxic agents, including drugs, fall into two categories: (i) intrinsic and obligatory liver toxins with dose-dependent and predictable adverse effects, and (ii) facultative (idiosyncratic) hepatotoxins with non-predictable and non-dose-dependent liver toxicity affecting only few exposed individuals. Intrinsic hepatotoxins may either injure hepatocytes directly, e.g. by direct physicochemical effects, or indirectly by interfering with specific metabolic processes. In the idiosyncratic type of liver injury immunologic hypersensitivity reactions or toxic metabolites may be involved. Clinical and morphologic consequences of adverse drug reactions are acute or chronic liver diseases, including parenchymal damage (finally leading to necrosis or apoptosis), steatosis, cholestasis, various types of vascular alterations, granuloma formation and also neoplastic transformation. Thus, drugs are important causes of liver diseases and may account for up to 40% of cases of hepatitis and up to 25% of fulminant hepatic failure. Moreover, drug-induced injury also plays a leading role as cause of acute cholestasis.
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PMID:[Drug-induced liver injury]. 1264 60

The diseases of the intrahepatic biliary tree are a large group of potentially evolutive congenital and acquired liver disorders affecting both the adult and pediatric populations. They represent a relevant cause of liver-related morbidity and mortality and an important indication for liver transplantation, particularly in children. While the practical approach to patients affected by biliary tree diseases has not significantly changed yet, the conceptual approach to the pathophysiology of cholangiopathies has witnessed important advances that will be discussed. The primary cell target of the pathogenetic sequence of these disorders is the biliary epithelium. Cholangiocytes have multifaceted functions, not limited to bile production. Their capability to secrete a range of different pro-inflammatory mediators, cytokines, and chemokines indicates a major role of cholangiocytes in the inflammatory reaction. Furthermore, paracrine secretion of growth factors and peptides mediates an extensive cross-talk with other liver cell types, including hepatocytes, stellate, and endothelial and inflammatory cells. Cholangiopathies share a number of pathogenetic mechanisms, including inflammation, cholestasis, fibrosis, apoptosis, altered development, and neoplastic transformation. These basic disease mechanisms will be discussed in detail, along with the distinct features of a number of cholangiopathies. Furthermore, an increase in the biliary cell compartment is a common response to many forms of liver injury, from cholangiopathies to viral and fulminant hepatitis. Elucidation of these pathophysiologic mechanisms will likely provide clues for future therapeutic strategies. Furthermore, understanding the role of cholangiocytes in liver regeneration/repair and the mechanisms of cholangiocyte activation and their relationship with liver progenitor cell will be of further interest.
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PMID:Pathophysiology of cholangiopathies. 1575 66


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