Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients undergoing treatment at a community-based renal dialysis clinic were monitored monthly for hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs). Of 160 patients who began treatment HBsAg(-)/anti-HBs(-), 77 subsequently became HBsAg(+). Once HBsAg(+), males were more likely to remain HBsAg(+) indefinitely, whereas females were more likely to convert to HBsAg(-) and develop anti-HBs. This was not due to a sex difference in exposure to hepatitis B virus because only patients who became infected while undergoing treatment were included in the analysis. These data are clear evidence of a sex difference in response to hepatitis B virus, which may partially explain the greater incidence of several chronic liver diseases, including primary hepatocellular carcinoma, in males.
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PMID:Sex differences in response to hepatitis B infection among patients receiving chronic dialysis treatment. 26 50

Response to hepatitis B virus (HBV) infection [HBV surface antigen (HBsAg) and antibody to HBsAg (anti-HBs)], serum iron, total iron-binding capacity, hematological status (erythrocytes, Hb, and hematocrit), and evidence of liver damage (serum glutamic pyruvic transaminase; aspartate aminotransferase, L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1) were determined for 201 patients on chronic renal dialysis. Four factors-serum iron level, transminase level, sex, and HBV response [i.e., infected-HBsAg(+) (HBsAg positive), anti-HBs(+) (anti-HBs positive), or no response]-were analyzed simultaneously to test the hypothesis that serum iron is higher in those with HBsAg in their serum than in those without HBsAg, independent of the transaminase level. Four independent, statistically significant two-factor interactions were identified. (i) Serum iron is higher in those HBsAg(+). (ii) Serum iron is higher in those with increased transaminase. (iii) Transaminase is higher in those HBsAg(+). (iv) Males are more likely to be HbsAg(+) and females are more likely to be anti-HBs(+). Also, those who are HBsAg(+) have significantly higher percent iron saturation (serum iron/total iron-binding capacity). That is, the hypothesis was supported by the findings. Several additional biological hypotheses are suggested, including a possible role of increased iron levels in susceptibility and response to HBV infection and the possible relationship between higher iron levels and the likelihood of HBV infection progressing to primary hepatocellular carcinoma. In addition, further tests of the initial hypothesis in nonhospitalized populations with endemic HBV infection are proposed.
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PMID:Serum iron levels and response to hepatitis B virus. 28 82

Immune complexes (IC) were investigated in sera from 208 individuals with various clinical types of viral hepatitis diagnosed by clinical and laboratory criteria, including liver biopsy. Immune complexes were assessed by platelet aggregation (PI A) and by radioimmunoassay (RIA). The data were related to autoimmune phenomena (especially rheumatoid factors) and to the role that the IgM class of hepatitis B (HB) antibody might have in IC formation. Although the highest frequency of P1 A was in the few sera from patients with cirrhosis or hepatoma, the next highest was in sera from acute hepatitis patients (71%), and the lowest in sera from chronic active (57%) and chronic persistent (46%) hepatitis patients. A proportional number of patients with IC's were positive for hepatitis B surface antigen (HBs). A parallel prevalence was noted between P1 A and autoantibodies, with anti-Ig's being found more frequently in sera from acute hepatitis and chronic active hepatitis patients. The relationship between RIA results for complexes and RIA results for anti-IgG was inverse, as though anti-IgG interfered with IC reactivity by RIA. Anti-IgM pre-incubated with sera increased the amount of P1 A in sera from patients with acute hepatitis as well as in those from patients with chronic persistent hepatitis, suggesting a more frequent IgM involvement in IC's in these diseases than in chronic active hepatitis. Whereas liver cell damage in acute and active hepatitis may reflect elevated autoantibodies, the IgM class of HBs antibody may be involved in acute as well as chronic persistent hepatitis.
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PMID:Autoimmune implications of immune complexes in clinical variants of hepatitis B. 49 83

PLC/PRF/5 hepatoma cells continue to produce hepatitis B surface antigen (HBsAg) after greater than 80 passages in vitro, but they do not express other markers of heaptitis B virus (HBV) replication. In this respect, they resemble most liver cells that are persistently infected with HBV. PLC/PRF/5 cells were cultured in the presence of adenine arabinoside, human fibroblast interferon, and ribavirin to determine whether production of HBsAg was sensitive to these antiviral agents. HBsAg released into culture media was detected by radioimmunoassay, and cellular protein synthesis was assessed by [3H]amino acid incorporation studies. A dose-related inhibition of HBsAg occurred with each antiviral agent that was tested, but in each case, this inhibition was matched by a reduction of cellular protein synthesis to a similar degree. Thus, no specific effect on the production of HBsAg was found with any of the antiviral agents tested.
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PMID:Lack of specific effect of adenine arabinoside, human interferon, and ribavirin on in vitro production of hepatitis B surface antigen. 52 92

Six patients with hepatitis B surface antigen-positive (HBsAg-pos) chronic liver disease have been treated with transfer factor (TF) prepared from leucocytes of normal blood donors with no history of hepatitis, and with TF from subjects recently recovered from type B hepatitis. In three patients there were transient elevations of aspartate transaminase (AsT) after 'specific' TF, representing damage or destruction of hepatocytes, and in two of these patients there was coincidental complement consumption, suggesting that TF had stimulated production of antibody. In one other patient there was an increase in E-rosetting lymphocyte (ERL) concentration representing a change in T-lymphocyte reactivity. One of the two patients who had no measured response to TF had a primary liver cell carcinoma and was receiving prednisolone therapy. TF prepared from subjects who have recently recovered from type B hepatitis may have temporarily altered the immunological status of patients with HBsAg-pos chronic liver disease, but it did not have a beneficial therapeutic effect.
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PMID:Transfer factor in the attempted treatment of patients with HBsAg-positive chronic liver disease. 60 32

The sensitivities of three technqiues used to detect serum hepatitis B surface antigen (HBsAg) were compared in 411 patients with various types of chronic liver disease. Counterimmunoelectrophoresis proved an unreliable test. Two haemagglutination technqiues were slightly less sensitive than radioimmunoassay but were more rapidly performed. Less sensitive techniques were particularly unreliable in active liver disease where HBsAg titres were low. HBsAg was detected in patients with chronic persistent hepatitis, alcoholic liver disease, chronic active liver disease with or without cirrhosis, and primary liver cell carcinoma. Forty-six of the 68 (68%) HBsAg positive subjects were males coming from outside the United Kingdom. The HBsAg titres in 13 subjects with chronic persistent hepatitis were significantly higher (P less than 0-001) than those in 43 subjects with chronic active liver disease. Corticosteroid therapy did not alter the HBsAg titre significantly. None of the 28 HBsAg positive subjects studied serially for up to two years cleared HBsAg from the serum. Anti-HBs was examined by passive haemagglutination and found in 35 subjects, 26 of whom had no evidence of liver disease, 80% came from abroad. Anti-HBs was believed to be of epidemiological rather than of pathological importance.
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PMID:Detection, by three techniques, of hepatitis B surface antigen (HBsAg) and determination of HBsAg and anti-HBs titres in patients with chronic liver disease. 83 98

Fifty Kenyan patients with chronic liver disease or hepatocellular carcinoma were tested for hepatitis B surface antigenaemia by radioimmunoassay. The hepatitis B surface antigen was detected in 77% of the patients with chronic persistent or chronic aggressive hepatitis, or cirrhosis confirmed by liver biopsy, compared with 15% in a control group. All six patients with hepatocellular carcinoma had detectable hepatitis B surface antigen or antibody. 50% of the controls had hepatitis B surface antibody in their plasma detectable by haemagglutination. Auto-immune associated liver disease appeared infrequent. The possibility that the hepatitis B virus is an important cause of cirrhosis in Kenya is discussed.
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PMID:Hepatitis B surface antigenaemia in Kenyans with chronic liver disease. 84 49

The relative sensitivities of counterimmunoelectrophoresis (CIE) and haemagglutination assays for the detection of hepatitis B surface antigen (HB(s)Ag) and antibodies (anti-HB(s)) were compared. Twelve scientists from ten countries in Asia, Africa and the Pacific region participated in the study. The participants provided serum samples from 15 953 subjects comprising patients with acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC), as well as blood donors and other normal individuals. For the detection of HB(s)Ag in a reference panel serum, immune adherence haemagglutination (IAHA) was slightly more sensitive than passive haemagglutination inhibition (PHI); CIE was the least sensitive. Mean HB(s)Ag frequencies in patients with acute hepatitis, chronic hepatitis, cirrhosis, and HCC were significantly higher than in healthy controls. Passive haemagglutination (PHA) was more sensitive than CIE for the detection of anti-HB(s). The frequency of anti-HB(s) in patients with HCC was significantly lower than that in the other groups. Mean anti-HB(s) frequencies in patients with acute hepatitis, chronic hepatitis, and cirrhosis were not significantly different from that in normal subjects. Subtyping of HB(s)Ag was performed by PHI. Among asymptomatic carriers the predominant HB(s)Ag subtype in northeast Asia was adr.In India, ayw predominated in carriers, with the demarcation between adr and ayw occurring west of Burma. In West Africa the only subtype detected was ayw, but in East Africa the majority subtype was adw. The r subtype was found only in Asian populations east of India and in Western Pacific populations. In Papua New Guinea all four subtypes were identified. With one possible exception, the subtypes of HB(s)Ag-positive patients with liver disease reflected the predominant type in each geographic location.
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PMID:Hepatitis B antigen, antigen subtypes, and hepatitis B antibody in normal subjects and patients with liver disease. 108 99

Structural and nonstructural regions of the HCV-encoded polyprotein have been expressed in recombinant yeast, bacteria, or insect cells and used to capture and measure reactive antibodies circulating in different individuals. The putative nucleocapsid protein (C) and nonstructural proteins 3-5 (NS3-NS5) were found to contain the most immunodominant epitopes. The NS3, NS4, and C regions were expressed in yeast in the form of a fused, chimeric polyprotein (C25) and a capture assay for reactive antibody was developed. This anti-C25 assay detects all previously identified HCV-seropositive cases and provides a substantially more sensitive diagnostic for both acute and chronic HCV infections than the current anti-C100-3 (NS4) assay. Anti-C25 was detected more frequently than anti-C100-3 in chronic, transfusion-associated non-A, non-B hepatitis patients from the United States (95% vs. 71%) and Japan (98% vs. 82%), in cryptogenic cirrhosis patients from the United States (62% vs. 28%), and in hepatitis B surface antigen-negative cases of hepatocellular carcinoma from Japan (83% vs. 63%). These data indicate that HCV has a greater role in these liver diseases than was previously thought. In volunteer United States blood donors sampled following the introduction of anti-C100-3 screening, the prevalence of anti-C25 and anti-C100-3 was 0.5% and 0.08%, respectively.
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PMID:Diagnosis of hepatitis C virus (HCV) infection using an immunodominant chimeric polyprotein to capture circulating antibodies: reevaluation of the role of HCV in liver disease. 127 66

The effects of agents which are known to be differentiation inducers on a human hepatoma cell line PLC/PRF/5 were investigated. Dexamethasone (DEX), sodium butyrate (SB) or dimethylsulfoxide (DMSO) were examined. They all reduced cell proliferation but differ from each other in effect on the secretion of alphafetoprotein (AFP) and hepatitis B surface antigen (HBsAg), changes in morphology and RNA transcription. SB changed the cell from polygonal into a fibroblast-like type and decreased AFP secretion. DMSO decreased the cell size and changed AFP secretion in the same manner as SB. DEX changed the cell into a larger size, as well as increased AFP secretion. HBsAg secretion and also HB virus DNA transcription was enhanced by 3 agents. AFP and myc gene transcriptions were reduced by SB but DMSO reduced only AFP. Albumin gene transcription was enhanced by SB and DEX. These results indicate that the decrease of PLC/PRF/5 proliferation is induced through different mechanisms by these 3 agents.
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PMID:Effect of dexamethasone, dimethylsulfoxide and sodium butyrate on a human hepatoma cell line PLC/PRF/5. 128 20


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