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)

The rate of hepatic metabolism of dimethylaminoantipyrine (aminopyrine), which occurs primarily through N-demethylation, was assessed by measurement of the specific activity of 14CO2 excreted in breath samples obtained 2 hours after oral administration of a trace dose of [14C]aminopyrine. The percentage of administered 14C excreted in 14CO2 in 2 hours was 7.0 +/- 1.3 (SD)% in control patients, and significantly less (P less than 0.01) in patients with portal cirrhosis (2.6 +/- 1.2%), fatty liver (4.7 +/- 1.1%), hepatitis (2.6 +/- 1.4%), and hepatic malignancy (3.5 +/- 1.8%). In 16 of 24 subjects with cholestasis not caused by malignant disease the mean 14CO2 excretion was normal. The 14CO2 excretion in patients with portal cirrhosis correlated highly with aminopyrine metabolic clearance rate (r equals 0.92), serum albumin (r equals 0.75), and retention of bromsulphalein (r equals 0.73). Abnormal 14CO2 excretion returned to normal in patients with hepatitis, when the hepatitis resolved. The data suggest that the aminopyrine breath test is a safe, simple, qualitative and quantitative liver function test.
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PMID:Quantitative assessment of hepatic function by breath analysis after oral administration of (14C)aminopyrine. 120 Apr 95

Patients with decompensated liver cirrhosis (n 1441) and those with post-transfusion hepatitis (n 343), whose medical expenses were subsidized by the Aichi Prefectural Government, were followed up for three years by record linkage with the Aichi Cancer Registry. During the follow-up period, 122 incident cases of liver cancer were identified. Compared with the general population, patients with decompensated liver cirrhosis were at a 64.9 times greater risk (50.5 times in males and 100.4 times in females) and those with post-transfusion hepatitis were at a 9.4 times greater risk (8.9 times in males and 13.7 times in females) of developing liver cancer. Information on prognostic factors for 1,068 patients with decompensated liver cirrhosis was also collected in a questionnaire survey by the physicians in charge. Patients positive to hepatitis B surface antigen (HBs Ag) and those positive to HBe Ag had a significantly increased risk of subsequent liver cancer. The risk of developing liver cancer was positively associated with base-line levels of GPT and AFP and age and, inversely associated with total alcohol intake and female sex. In multivariate analyses, the associations with HBe Ag, AFP, sex and age remained statistically significant, whereas the associations with GPT, total alcohol intake and HBs Ag were of borderline significance.
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PMID:The risk and predictive factors for developing liver cancer among patients with decompensated liver cirrhosis. 127 45

Major life-threatening complications following blood transfusion are rare and human error remains an important aetiological factor in many. The infectious risk from blood transfusion is predominantly hepatitis, and non-A, non-B and hepatitis C (HCV) are the most common subtypes noted. The risk of post-transfusion hepatitis (PTH) appears to be decreasing and this is attributed to both deferral of high-risk donors and more aggressive screening of donated blood. Screening for HCV is expected to decrease this risk further. The risk of HIV transmission following blood transfusion is negligibly small. There are data to suggest that perioperative blood transfusion results in suppression of the recipient's immune system. Earlier recurrence of cancer and an increased incidence of postoperative infection have been associated with perioperative blood transfusion although the evidence is not persuasive. Microaggregate blood filters are not recommended for routine blood transfusion but do have a role in the prophylaxis of non-haemolytic febrile reactions caused by platelet and granulocyte debris in the donor blood. Patients should be advised when there is likely to be a requirement for perioperative blood transfusion and informed consent for transfusion should be obtained.
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PMID:Perioperative haemotherapy: II. Risks and complications of blood transfusion. 128 9

Dimethyl diphenyl bicarboxylate (dimethyl-4,4'-dimethyloxy-5,6,5',6'-dimethylene-dioxy-di phe nyl-2,2'- bicarboxylate, DDB), a synthetic mimic of the natural product schizandrin C, is used in China as a hepatoprotective agent to improve the liver functions of patients with hepatitis or under cancer chemotherapy. In this study, we investigated the effects of DDB on liver microsomal drug-metabolizing enzymes. When male Sprague-Dawley rats were treated with a daily intragastric dose of DDB (200 mg.kg-1) for 3 d, the microsomal pentoxyresorufin dealkylase activity and P-450 2B1 protein levels were markedly increased. The fold increase was lower than that by phenobarbital (75 mg.kg-1, ip once daily x 3 d). The level of P-450 2B1 mRNA was elevated by DDB but the magnitude of the elevation was much less than that caused by phenobarbital. DDB also increased the rates of testosterone hydroxylation at positions 16 beta, 16 alpha, 6 beta, and 2 beta as well as the rate of ethoxyresorufin dealkylation, suggesting moderate increases in the levels of P-450 3A and P-450 1A1 in addition to the huge increase in P-450 2B1. The level of glutathione S-transferase was also slightly increased, but the levels of P-450 2E1 and NAD(P)H: quinone oxidoreductase were not changed. The results indicate that DDB is an inducer of P-450 2B1.
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PMID:Induction of liver microsomal cytochrome P-450 2B1 by dimethyl diphenyl bicarboxylate in rats. 130 34

Based on our 7 and one-half-year experience with liver transplantation at the University of Nebraska Medical Center: 1. Success and growth of the program has been, in part, the result of close interaction and support of the various specialists involved. 2. We have demonstrated that outstanding patient and graft survival rates can be obtained with cyclosporine/prednisone immunosuppression. 3. Few, if any, technical contraindications exist to liver transplantation. 4. Surgical advances have allowed allografts to be salvaged which would otherwise require replacement. 5. Routine donor-liver biopsy prior to implantation has reduced the rate of primary nonfunction. 6. New strategies to improve survival for patients with hepatitis-B-related liver disease and hepatic malignancies undergoing liver transplantation need to be developed. 7. The management of patients with fulminant hepatic failure is evolving and now includes innovative approaches such as the use of ECLS and auxiliary transplants.
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PMID:Liver transplantation at the University of Nebraska Medical Center from 1985 to 1992. 130 94

To evaluate the role of hepatitis C virus (HCV) in Chinese patients with hepatocellular carcinoma (HCC), the antibodies to HCV (anti-HCV) were detected by enzyme immunoassay in 41 (12.6%) of the 326 patients with HCC. However, none of 35 patients with metastatic carcinoma of the liver had detectable anti-HCV. The prevalence of anti-HCV was significantly higher in patients with hepatitis B surface antigen (HBsAg)-negative HCC than those with HBsAg-positive HCC (37.3% versus 4.1%, P less than 0.0001). However, the prevalence of anti-HCV was much higher in patients with HCC with negative results for HBsAg and antibody to hepatitis B core antigen (54.5%). The mean age of patients with HCC with positive results for anti-HCV was significantly greater than that of patients with HBsAg-positive HCC (65.1 versus 55.5 years, P less than 0.0001). Alpha-fetoprotein levels greater than 20 ng/ml were found in 70.7% of patients with HCC with positive results for anti-HCV and in 73.3% of patients with HBsAg-positive HCC. Of the Chinese patients with HCC, 74.5% had HBsAg-positive results and 96.6% had positive results for antibody to hepatitis core antigen. These data indicate that, although HCV may play an etiologic role in HCC, hepatitis B virus is still the most important causal agent among most Chinese patients with HCC.
Cancer 1992 Jan 15
PMID:The prevalence of anti-hepatitis C virus among Chinese patients with hepatocellular carcinoma. 130 28

Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China. To test this hypothesis, nine tumors induced by aflatoxin B1 in nonhuman primates were analyzed for mutations in the p53 gene. These included four hepatocellular carcinomas, two cholangiocarcinomas, a spindle cell carcinoma of the bile duct, a hemangioendothelial sarcoma of the liver, and an osteogenic sarcoma of the tibia. None of the tumors showed changes at the third position of codon 249 by cleavage analysis of the HaeIII enzyme site at codon 249. A point mutation was identified in one hepatocellular carcinoma at the second position of codon 175 (G to T transversion) by sequencing analysis of the four conserved domains (II to V) in the p53 gene. These data suggest that mutations in the p53 gene are not necessary in aflatoxin B1 induced hepatocarcinogenesis in nonhuman primates. The occurrence of mutation in codon 249 of the p53 gene in selective samples of human hepatocellular cancers may indicate involvement of environmental carcinogens other than aflatoxin B1 or that hepatitis B virus-related hepatitis is a prerequisite for aflatoxin B1 induction of G to T transversion in codon 249.
Cancer Res 1992 Feb 15
PMID:Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates. 131 Jun 37

Clinical, animal, and epidemiologic evidence indicates that exogenous steroids influence the risk of hepatocellular carcinoma (HCC) and a recent study suggested that parity also may increase the risk of this tumor in women. The latter hypothesis was evaluated in the data from a case-control study which was carried out in Athens and covered 166 male and 19 female cases of HCC, and 381 male and 51 female hospital controls. Among males, there was no association between the number of liveborn children and risk of HCC, whereas among women, there was a suggestive positive association. Compared with women with one or two children, the relative risk for HCC was 0.6 among nulliparous women, 1.3 among those with three or four children and 1.7 among those with five or more children. The association of parity with risk of HCC was limited to women who were positive for hepatitis-B surface antigen (HBsAg) and was not confounded by hepatitis-C virus infection or tobacco smoking. The small number of HCC cases does not permit firm conclusions. If confirmed, however, these results would provide the foundation for a practical preventive advice that could be given to women who are positive for HBsAg.
Cancer Causes Control 1992 Mar
PMID:Liveborn children and risk of hepatocellular carcinoma. 131 8

Estimates have been made of the cancer potency of aflatoxin exposure among the U.S. population. Risk modeling is used to assess the dose-response relationship between aflatoxin exposure and primary liver cancer, controlling for hepatitis B virus (HBV), based on data provided by the Yeh et al. study in China. A relative risk model is proposed as a more appropriate alternative to the additive ("absolute" risk) model for transportation of risk coefficients between populations with different baseline rates. Several general relative risk models were examined; the exponential model provided the best fit. The Poisson regression method was used to fit the relative risk model to the grouped data. The effects of exposure to aflatoxin (AFB1) and hepatitis B infection were both found to be statistically significant. The risk of death from liver cancer for those exposed to AFB1 relative to the unexposed population, increases by 0.05% per ng/kg/day exposure of AFB1 (p less than 0.001). The results also indicated a 25-fold increase in the risk of death from liver cancer among those infected with hepatitis B virus, relative to noncarriers (p less than 0.0001). With a hepatitis prevalence rate of 1%, the aflatoxin intake level associated with liver cancer lifetime excess risk of 1 x 10(-5) for the U.S. population was estimated as 253 ng/day, based on a liver cancer baseline rate of 3.4/100,000/yr.
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PMID:Risk assessment for aflatoxin: III. Modeling the relative risk of hepatocellular carcinoma. 845 64

Our purpose was to ascertain whether alcohol abuse is a risk factor for the development of hepatocellular carcinoma in urban southern Africa blacks and, if so, to relate alcohol consumption to other possible risk factors such as persistent hepatitis-B-virus infection, smoking, male sex, in this subpopulation. A prospective, hospital-based, case-control format involving 101 patients with hepatocellular carcinoma and 101 controls was used. The mean age of the patients was 53.7 +/- 1.85 years and the male:female ratio 3.2:1. An increased risk was found, but only in urban men over the age of 40 years who habitually drank more than 80 g of ethanol daily. The risk remained after adjusting for chronic hepatitis-B infection, smoking, and sex (odds ratio 4.4, 95% confidence interval 1.3 to 16.6; p = 0.003). Smoking proved not to be a risk factor, either alone or in concert with alcohol consumption. Hepatitis-B infection was confirmed as a major risk in younger men and in women, but in urban men over the age of 40 years alcohol abuse was a greater risk. Current hepatitis-B infection and alcohol abuse were additive risks.
Int J Cancer 1992 Jun 19
PMID:Alcohol consumption as a risk factor for hepatocellular carcinoma in urban southern African blacks. 131 67


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