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

Woodchuck hepatitis virus surface antigen (WHsAg) stimulated hepatocytes in culture to produce nitric oxide (NO.), as evidenced by the accumulation of nitrite in the medium. NO. synthesis by hepatocytes was positively correlated with WHsAg concentration. WHsAg-induced NO. synthesis was inhibited by NG-monomethyl-L-arginine and anti-WHsAg antibody. To our knowledge, this is the first demonstration of an increase in NO. formation by a viral antigen. These data, when considered in the light of the known genotoxicity of NO., raise the possibility that viral hepatitis increases the risk of liver cancer by increasing the production of NO.. Long-term elevated production of NO. free radicals due to stimulation by WHsAg in chronic hepatitis may directly cause reactions with cellular DNA leading to mutagenesis, as well as the formation of hepatocarcinogenic N-nitroso compounds. This provides a new mechanism by which hepatitis B virus infection might hypothetically increase the risk of liver cancer.
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PMID:Woodchuck hepatitis virus surface antigen induces nitric oxide synthesis in hepatocytes: possible role in hepatocarcinogenesis. 800 Dec 49

The relationship between family history of selected neoplasms in first-degree relatives and the risk of pancreatic, liver, and gallbladder cancer was investigated using data from a case-control study conducted in northern Italy on 320 histologically confirmed incident cases of liver cancer, 58 of gallbladder cancer, 362 of pancreatic cancer, and 1408 controls admitted to the hospital for acute, nonneoplastic, nondigestive tract disorders. Significant associations were observed between family history of hepatocellular carcinoma and primary liver cancer [relative risk (RR) = 2.4; 95% confidence interval (CI), 1.3 to 4.4], between family history of pancreatic cancer and pancreatic cancer (RR = 3.0; 95% CI, 1.4 to 6.6), and between family history of gallbladder cancer and gallbladder cancer (RR = 13.9; 95% CI, 1.2 to 163.9). The elevated risk of liver cancer associated with family history was not materially modified by adjustment for tobacco, alcohol, and personal history of cirrhosis and hepatitis (RR = 2.9; 95% CI, 1.5 to 5.3). Similarly, the risk for pancreatic cancer did not appreciably change after allowance for tobacco, alcohol, dietary factors, and medical history of diabetes and pancreatitis (RR = 2.8; 95% CI, 1.3 to 6.3). This pattern of risk would support the existence of a genetic component in the familial aggregation of liver and pancreatic cancer. In terms of population attributable risk, approximately 3% of the newly diagnosed liver and pancreatic cancers would be related to this familial component.
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PMID:Family history and the risk of liver, gallbladder, and pancreatic cancer. 801 68

Relationship between blood transfusion and cancer is considered from five points of view: 1) The cancer patient as a blood donor. Cancer must remain a cause of exclusion from blood donation. 2) Autologous blood transfusion for cancer patients. Predeposited autologous blood transfusion is only possible for a small number of patients. Intraoperative blood salvage carries with it the risk of disseminating tumor cells. 3) History of blood transfusion and the risk of having a cancer: a) the persistence of immune alterations following blood transfusion for years might expose the patient to an increased risk of having a cancer; b) blood transfusion might carry immunosuppressive viruses, and hepatitis viruses are related to the risk of liver cancer. 4) Cancer recurrence and blood transfusion. Conclusion of most of the published studies is that blood transfusion is associated with an increased risk of recurrence of colorectal cancer. The only realistic randomized study would compare different transfusion strategies (allogenic, leukocyte poor allogenic and autologous blood transfusion) to determine which is the best for cancer patients. 5) Post-transfusion GVH in cancer patients. Some cases have recently been published. They all can be explained by a particular HLA compatibility between the recipient and one of the blood donors.
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PMID:[Transfusion and cancer]. 804 22

The LEC rat is an inbred mutant strain with spontaneous hepatitis isolated from Long-Evans rats. Since approximately 40% of LEC rats die of fulminant hepatitis, the rat serves an animal model for studying the pathogenesis and treatment of human fulminant hepatitis. The remaining 60% of LEC rats survive and develop chronic (prolonged) hepatitis and subsequently develop liver cancer. Therefore, the LEC rat serves an important animal model for studying the significance of chronic hepatitis in the development of human liver cancer, which often develops in association with chronic hepatitis. The LEC rat can also be used as an animal model of Wilson's disease, since recent studies have disclosed high copper accumulation in the liver and low ceruloplasmin concentration in the serum of this mutant rat.
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PMID:The LEC rat: a model for human hepatitis, liver cancer, and much more. 829 9

The hypothesis that adult infection with the hepatitis B virus in the United States leads to a carrier state with a high risk of primary liver cancer was tested in two ways: (a) a cohort mortality study of U.S. Army veterans given yellow fever vaccine contaminated with hepatitis B virus in 1942 and controls and (b) a case-control study comparing veterans with hepatocellular carcinoma in Veterans Affairs hospitals with matched controls with respect to receipt of contaminated vaccine in 1942. Three groups totaling 69,988 men were the subjects of the cohort study: group 1 comprised men hospitalized with hepatitis in 1942, group 2 comprised men subclinically infected in 1942 and group 3 comprised controls who entered service after the contaminated vaccine was discontinued. Hepatocellular carcinoma cases (n = 24) and control subjects (n = 63) derived from Veterans Affairs hospital discharge files were the subjects of the case-control study. Group comparisons of death rates from liver cancer were refined by expert review of records to select hepatocellular carcinoma from among all causes of death so diagnosed in the cohort study. Slightly excess mortality was found for hepatocellular carcinoma in group 2 (subclinical hepatitis B) but not for group 1 (overt hepatitis B) compared with group 3 (controls) (p = 0.08). Mortality from nonalcoholic chronic liver disease was less in group 2 than in group 3. In the case-control study, the relative risk for hepatocellular carcinoma conferred by receipt of contaminated vaccine was estimated as 3.3 (p = 0.06). We conclude from the cohort study that immunocompetent adult males rarely become carriers after hepatitis B virus infection, probably far less often than the frequently assumed rate of 5% to 10%. The small excess liver cancer mortality seen in the cohort study and the results of the case-control study are consistent, nevertheless, with the now well-established etiological role of hepatitis B virus infection in liver cancer.
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PMID:Mortality follow-up of the 1942 epidemic of hepatitis B in the U.S. Army. 840 52

The expression of 14 forms of cytochrome P450 in the liver as well as changes in the testosterone hydroxylation activities of hepatic microsomes were investigated during the development of hepatitis in Long-Evans Cinnamon (LEC) rats. P4501A1 and -1A2 (3-methylcholanthrene-inducible forms) and P4502B1 and -2B2 (phenobarbital-inducible forms) were barely detected in the hepatic microsomes of male and female LEC rats. In immature male rats, the levels of male-specific forms (P4502C11 and -2C13) were higher in LEC rats than in control Long-Evans Agouti (LEA) rats. P4502C11 appeared in female LEC rats from 4 to 16 weeks of age, reflecting that testosterone 2 alpha- and 16 alpha-hydroxylation activities were detected at significant levels in female LEC rats. In immature female rats, the level of P4502C12 (a major female-specific form) was higher in LEC rats than in LEA rats. The level of P4502C13 in male LEC rats and that of P4502C12 in female LEC rats decreased markedly with ageing or during the development of hepatitis. The level of P4503A2 (a male-predominant form) was especially high in immature male and female LEC rats, reflecting that both rats had high 2 beta- and 6 beta-hydroxylation activities toward testosterone. These sex-specific forms are regulated by androgens and by pituitary growth hormone. Thus, there may be abnormalities of the hypothalamo-pituitary-gonadal axis in LEC rats. Furthermore, P4503A2 efficiently activates aflatoxin B1, a potent hepatocarcinogen, and the increased levels of this form in LEC rats may be related to the onset of hepatitis or liver cancer.
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PMID:Expression of cytochrome P450 in LEC rats during the development of hereditary hepatitis and hepatoma. 842 59

To investigate the clinicopathologic characteristics of primary liver cancer (PLC) in young adults, 77 patients aged 35 or younger were compared with 603 patients older than 35 years during the same period. In the young patients, PLC showed: (1) a low incidence detected at mass survey (young 15.6% vs older 28.7%, P < 0.05); (2) a low level of history of hepatitis (young 36.8% vs older 66.3%, P < 0.01); (3) a high incidence of positivity for hepatitis B surface antigen (HBsAg) (young 79.2% vs older 67.6%, P < 0.05); (4) a relatively low incidence of associated cirrhosis (young 64.9% vs older 90.7%, P < 0.01); (5) larger tumor size (PLC > 5 cm; young 87.0% vs older 73.0%, P < 0.01); and (6) a more advanced stage of the disease according to the TNM classification (stage III; young 29.9% vs older 18.2%, P < 0.05). It is suggested that hepatitis B virus (HBV) may play an important role in the development of PLC without associated liver cirrhosis in young patients. Close periodic surveillance of young adults who are positive for HBsAg is important to detect PLC at an early stage.
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PMID:Characteristics and prognosis of primary liver cancer in young patients in China. 857 36

Helicobacter hepaticus causes hepatitis in selected strains of mice and in A/JCr mice is linked to liver cancer. To analyze whether H. hepaticus persists in specified ecological niches, to determine whether biomarkers of infection exist, and to analyze the influence of H. hepaticus on hepatocyte proliferation, a longitudinal study of H. hepaticus-infected A/JCr mice was undertaken. A/JCr mice were serially euthanatized from 3 through 18 months and surveyed by enzyme-linked immunosorbent assay; bacterial culture of liver, colon, and cecum; histology; electron microscopy; hepatocyte proliferation indices determined by using 5-bromo-2'-deoxyuridine; and measurement of the liver enzyme alanine aminotransferase. In infected animals throughout the 18-month study, H. hepaticus was consistently isolated from the lower bowel but only sporadically from the liver. By electron microscopy, H. hepaticus was noted infrequently and only in bile canaliculi. Infected mice, particularly males, showed chronic inflammation; oval cell, Kupffer cell, and Ito cell hyperplasia; hepatocytomegaly; and bile duct proliferation. The inflammatory and necrotizing lesion was progressive and involved the hepatic parenchyma, portal triads, and intralobular venules. Hepatic adenomas were noted only in male mice, whereas 5-bromo-2'-deoxyuridine proliferation indices were markedly increased in both sexes, but especially in males, compared to control A/J mice. Infected mice also developed sustained anti-H. hepaticus serum immunoglobulin G antibody responses and elevated alanine aminotransferase levels. H. hepaticus, which persists in the lower bowels and livers of A/JCr mice, is associated with a chronic proliferative hepatitis, and hepatomas in selected male mice indicate that this novel bacterium may cause an increased risk of hepatic cancer induction in susceptible strains of mice. This murine model should prove useful in dissecting the molecular events operable in the development of neoplasms induced by bacteria belonging to this expanding genera of pathogenic Helicobacter species.
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PMID:Chronic proliferative hepatitis in A/JCr mice associated with persistent Helicobacter hepaticus infection: a model of helicobacter-induced carcinogenesis. 861 59

The Long-Evans Cinnamon (LEC) rat is a mutant strain established from Long-Evans rats that displays spontaneous hepatitis and liver cancer. We previously demonstrated that LEC rats died of acute ethanol intoxication after being fed a liquid diet containing 5% ethanol. Furthermore, we found that both alcohol dehydrogenase (ADH) and aldehyde dehydrogenase activities were remarkably suppressed in the liver of LEC rat, compared with Wistar rats. In the present study, we further investigated ethanol metabolism in the non-ADH pathway and what caused the decrease of liver ADH activity in LEC rats. Blood ethanol concentration 5 hr after intraperitoneal administration of ethanol in LEC rats was higher than in the Wistar rats, indicating that ethanol oxidation was impaired in LEC rats. The expression of liver cytochrome P-450IIE1 in the LEC rat was as much as that in Wistar rats. Regarding decreased ADH activity in the liver of LEC rats, we examined an alternating purine-pyrimidine (CA) repeat-length polymorphism in the first intron of a class I ADH gene that would play a role in altering ADH activity. A polymerase chain reaction method was used to amplify the CA repeat in the first intron of this class I ADH gene, a nine CA repeat insertion and a point mutation were detected in LEC rats. These results suggest that this alternating sequence would modify transcription of the class I ADH gene in LEC rats. Thus, LEC rats have abnormal ethanol metabolism in the ADH pathway.
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PMID:Analysis of CA repeats in first intron of class I ADH gene in Long-Evans Cinnamon rats developing fatal intoxication after ethanol intake. 865 85

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. The majority of patients who develop HCC have underlying cirrhosis, which suggests that cirrhosis itself represents a preneoplastic condition. Nevertheless, whereas patients with cirrhosis of any origin are at increased risk of developing HCC, those with chronic hepatitis B or C infection seem to be at greatest risk. Patients with cirrhosis resulting from chronic alcohol use, hemochromatosis, autoimmune hepatitis, or alpha-1 antitrypsin deficiency have less risk of developing this cancer, and some hepatic diseases, such as primary biliary cirrhosis and Wilson's disease, do not predispose affected persons to an appreciable risk of developing HCC. Certain histological features, such as liver cell dysplasia and macroregenerative nodules, may represent preneoplastic alterations of hepatocytes, but these changes do not seem to be a necessary step in the evolution of liver cancer. The pathogenesis of HCC is unclear, but seems to involve several steps. Hepatitis B virus infection may result in the malignant transformation of hepatocytes by some directly oncogenic mechanism, whereas other necroinflammatory conditions probably predispose to the development of HCC through the introduction of genetic alterations coupled with a reduction of genetic repair functions. Screening patients at risk for the development of HCC using alpha fetoprotein measurements and ultrasonography is widely practiced despite inconclusive evidence of efficacy. If screening is performed, the program used should be tailored to the perceived risk for a particular patient.
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PMID:Preneoplastic conditions of the liver. 870 61


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