Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum hepatitis B antigen-antibody system was detected by ELISA method in 150 patients suffering from hepatocellular carcinoma (HCC) with positive AFP. The overall infection rate of hepatitis B virus (HBV) was 86.0% (129/150). According to the antigens and antibodies to HBV, two major types of seven models could be demonstrated. In type I (including models 1 to 4) HBV infection was present in 81.9%, 74.6% among whom were considered to be of weak infectivity and 7.3% of strong one. In type II (including models 5 to 7) 18.0% (27/150) had no antigen and antibody to HBV was detected, indicating the absence of HBV infection. This study suggests that chronic infection with HBV is the major etiologic agent for human HCC and the patients with HCC often accompanied by active HBV replication.
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PMID:[Serum hepatitis B antigen-antibody system in patients with hepatocellular carcinoma]. 869 98

The distribution of class I (A, B, C) and class II (DR antigens) histocompatibility antigens (HLA) was examined in 82 patients with hepatocellular carcinoma (HCC) and in 147 patients with chronic liver disease as controls. The diagnosis of HCC was confirmed by histological examination of liver tissue. HLA-B15 antigen was found more frequently in the subgroup of HCC patients who were positive for HBsAG (13/36, 36.1%) compared to the control group (8/147; 5.4%) [p < 0.001, Pc < 0.05, RR = 9.8] and a HBsAg positive control subgroup (1/25, 4%) [p < 0.001, Pc < 0.05, RR = 13.6]. No other statistically significant difference was found for any of the HLA antigens examined either in HCC patients as a whole group or in the subgroups according to sex, course of illness, AFP status, alcohol consumption, liver cirrhosis or blood groups. These data are further evidence that there may be a link between hepatitis B viral (HBV) infection and HLA antigens. The association of HLA-B15 antigen and HbsAg supports the idea of some genetic control of HBV infection in the patients with HCC.
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PMID:Histocompatibility antigens in patients with hepatocellular carcinoma. 877 70

We analyzed the clinical characteristics and survival of 185 patients with hepatitis B virus-related hepatocellular carcinoma (HBV group) and 1033 with hepatitis C virus-related hepatocellular carcinoma (HCV group) by multi center study. The patients in the HBV group (mean age 52.1 yr) were about 10 years younger than those in the HCV group (mean age 62.9 yr). Liver function, as measured by indocyanine green retention at 15 min, was better in the HBV group (17.5%) than in the HCV group (25.4%). A higher proportion of the HBV group (55%) than the HCV group (44%) had clinical stage I, T-factor differed significantly between the groups: 53% of the HBV group were T3-4 compared with 41% of the HCV group. Furthermore, a higher proportion of the HBV group were graded 2-3 for tumor thrombus in the portal vein (20.3%) and had poorly differentiated hepatocellular carcinoma (7%) compared with the HCV group (7.1% and 5% respectively). Univariate analysis identified poor prognostic factors for hepatocellular carcinoma as HBV, age < or = 50 yr, clinical stage II-III, a high AFP level, higher number of tumors, larger tumor size, tumor thrombus in the portal vein 2-3 and in the hepatic vein 2-3. On multivariate analysis, poor prognostic factors were a high AFP level, higher number of tumors, tumor thrombus in the portal vein 2-3 and in the hepatic vein 2-3, but not HBV, age, clinical stage or tumor size. These results suggest that HBV itself is not a stronger prognostic factor than HCV.
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PMID:Comparison of clinical features and survival in patients with hepatitis B and C virus-related hepatocellular carcinoma. 915 92

Chronic hepatitis C and B are the main causes of hepatocellular carcinoma (HCC) worldwide. Little is known about the etiology of HCC in Germany which is regarded as a low-prevalence area for viral hepatitis C (HCV) and B (HBV). To assess the etiologic factors of HCC in Germany we have retrospectively analyzed the records of 100 consecutive patients with hepatocellular carcinoma in our clinic. HCC-patients with documented status on HCV/HBV-infection and daily alcohol intake (n = 55) had HCV antibodies in 53%, HBs-Ag in 20%, isolated chronic alcohol abuse in 11% and genetic hemochromatosis in 2%. In 13% of the HCC-patients no risk factor could be identified. Coinfections with HCV and HBV were not observed. Liver cirrhosis was present in 90% of the HCC-patients. In histologically confirmed HCC (n = 71) serum alpha-fetoprotein level was normal (< 8.5 ng/ml) in 20%, moderately elevated (8.5-300 ng/ml) in 48% and considerably elevated (> 300 ng/ml) in 32% of the patients. Only 31% of all patients presented with small single lesions (< or = 5 cm) without evidence for extrahepatic metastases or portal vein thrombosis. Only 30% of the HCC-patients could be treated with a curative intention (28 hepatic resections, one orthotopic liver transplantation). Patients who underwent resection had cumulative 6-month, 1-year, 2-year and 3-year survival rates of 83.8%, 65.9%, 54.3% and 24.8% respectively. Median survival time after resection was 24.8 months compared with 5.8 months in symptomatically treated patients with unresectable HCC (n = 39). Patients with hepatitis C-associated HCC were significantly older than patients with hepatitis B-associated HCC (mean values: 63.2 vs. 54.2 years). Frequency of cirrhosis, tumor stage, alpha-fetoprotein level and prognosis did not differ between groups. In conclusion hepatocellular carcinoma was predominantly associated with chronic HCV-infection. Most patients presented with normal or moderately elevated serum AFP-levels. Prognosis was poor even after hepatic resection.
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PMID:[Hepatocellular carcinoma in Germany. Epidemiology, etiology, clinical aspects and prognosis in 100 consecutive patients of a university clinic]. 948 38

We investigated the affinity and special combination of anti-human AFP variant monoclonal antibody (AFP-R-LCA McAb) for cells of AFP positive hepatocellular carcinoma (HCC). AFP-R-LCA McAb was labeled by 131I radioisotope (131I-AFP-R-LCA McAb injected into the peripheral veins of patients with HCC or liver cirrhosis after hepatitis B. 131I-AFP-R-LCA McAb was gathered in tumor of HCC in 6 AFP positive patients, but there was no positive gathering in HCC in 6 AFP negative or 4 liver cirrhosis patients. AFP-R-LCA McAb has strong affinity and special combination to AFP positive cells of HCC and can be recognized as a carrier for radioimmunodetection and radiommunotherapy.
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PMID:[Anti-human AFP variant McAb in radioimmunodetection for primary hepatocellular carcinoma]. 959 55

Combined hepatocellular (HCC) and cholangiocellular carcinoma (CCC) (mixed carcinoma) is a rare subtype of primary hepatic carcinoma. We report a case of mixed carcinoma that developed in a non-cirrhotic liver, in a patient who was serologically negative for both hepatitis B and C viruses. A 65-year-old Japanese woman with a 25-year history of chronic rheumatoid arthritis had been treated with steroids and anti-inflammatory drugs, and was diagnosed by ultrasonography with an asymptomatic solitary tumor in the right lobe of the liver. On computed tomography scan and hepatic arteriography, the tumor was well enhanced by contrast medium in the early phase. Based on the findings of elevated serum alpha-feto protein (AFP, 245 ng/ml) and normal carcino-embryonic antigen (CEA, 2.6 ng/ml) levels, a preoperative diagnosis of hepatocellular carcinoma was made. Right lobectomy of the liver was performed on January 7, 1997. Histological examination showed that the resected tumor consisted of combined CCC cells and HCC cells in an intermingled form, with CCC being far more dominant than HCC. The tumor was therefore determined to be a combined carcinoma, subclassified as intermingled type. This case appears to indicate that mixed type carcinoma developed in a non-cirrhotic liver, with CCC being dominant; such a finding is extremely unusual, based on previously published reports.
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PMID:Combined hepatocellular and cholangiocellular carcinoma in a non-cirrhotic liver. 971 50

Hepatocellular carcinoma (HCC) is increasing in many countries as a result of an increase in hepatitis C virus (HCV) infection since World War II. The epidemiology of HCC varies with the global region. There have been conflicting observations from different parts of the world concerning the frequency of HCC in patients who in the distant past had post-transfusion non-A, non-B hepatitis. The genetic basis of hepatocarcinogenesis is still poorly understood. In hepatitis B virus (HVB) associated HCC, codon 249 mutation in the p 53 gene seems more related to exposure to aflatoxin B1 than to hepatocarcinogenesis itself. HCC that occurs in children in high HBV endemic regions could be associated with germ-line mutations, but little information is available; not much is known about chemical hepatocarcinogens in the environment other than aflatoxins. The X gene of HBV seems to play an important role in HBV-associated hepatocarcinogenesis. There are preliminary observations on the molecular mechanism of HCV-associated HCC, such as HCV core protein inducing HCC in transgenic mice and the NS3 genome transforming NIH 3T3 cells. Pathological distinction between preneoplastic and very early transformed lesions still depends on classical morphology, and a more genetically oriented differential diagnosis is required. Clinical diagnosis based on modern imaging has improved greatly, but is still unsatisfactory in the differential diagnosis of preneoplastic and early transformed nodules, because the vasculature changes that occur within the nodule are not accurately discerned with the current imaging. Use of sensitive des-gamma-carboxy prothrombin (PIVKA II) assay, and lectin affinity chromatography separating HCC specific subspecies of AFP molecules with a more practical biochemical technique will further improve diagnosis. Early diagnosis and transplantation are the best treatment at the moment, but transplantation is not widely available because of the donor shortage. Despite successful resection, the remnant cirrhotic liver frequently develops new HCC lesions, seriously curtailing long-term survival. All-out efforts should be directed to the prevention of HCC, through prevention of viral hepatitis, prevention of acute hepatitis from becoming chronic, prevention of chronic hepatitis from progressing to cirrhosis, and prevention of the cirrhotic liver from developing HCC (chemoprevention). At the moment, very few such studies exist.
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PMID:Hepatocellular carcinoma. 1072 7

We present a case of fibrolamellar hepatocellular carcinoma (FLHCC) in a 22 year old Thai man whose presenting symptom was hypoglycemic coma with right hemiparesis. The serum marker for hepatitis B virus (HBsAg) was positive and serum AFP was very high (over 100,000 IU/ml). The abdominal ultrasonography revealed a solitary heterogenic mass, size 5.5 x 6.5 cm in the right lobe. Chest X-ray showed multiple lung metastases. Ultrasound-guided needle liver biopsy was performed and typical histologic features of FLHCC in non-cirrhotic liver were diagnosed. The patient's comatose state and neurological deficits recovered rapidly after glucose administration. Unfortunately, the tumor mass could not be resected on account of far-advanced stage with metastases. Here, we also review of the literature concerning FLHCC in many aspects.
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PMID:Fibrolamellar hepatocellular carcinoma in a Thai man who presented with hypoglycemia: case report and review of literature. 1093 18

Patients with hepatocellular carcinoma (HCC) frequently experience intrahepatic HCC recurrence even after complete ablation of primary lesions. Because the oncogenic process may be different for hepatitis B viral (B-viral) and hepatitis C viral (C-viral) HCC, the present study was conducted to elucidate the factors contributing to HCC recurrence with respect to the infected hepatitis virus. Two hundred thirty-six patients with a single HCC lesion who underwent complete ablation of the tumor by PEIT and/or PMCT or surgical resection at Tokyo University and its affiliated hospitals from 1993 to 1997 were enrolled. The patients were classified into 3 groups: the B-viral group, C-viral group, and NBNC group. After complete removal of tumors, the patients were followed for a mean period of 39 months. The factors contributing to HCC recurrence were analyzed by univariate and multivariate analysis using the Cox proportional hazard model. The rate of intrahepatic recurrence in enrolled patients at 1, 3, and 5 years was 19%, 50%, and 64%, respectively. The intrahepatic recurrence rate in C-viral and B-viral HCC was higher than that in the NBNC-related HCC. Fibrosis staging, pathological grading of HCC, and serum AFP levels were significantly linked to intrahepatic recurrence by univariate analysis, and fibrosis staging was strongest in the multivariate analysis for C-viral HCC (P = .004). In contrast, fibrosis staging did not affect the recurrence in B-viral (P = .51) and NBNC-related (P = .77) HCC. Risk factors for HCC recurrence differed according to the infected viral state.
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PMID:Risk factors for recurring hepatocellular carcinoma differ according to infected hepatitis virus-an analysis of 236 consecutive patients with a single lesion. 1109 27

Hepatocellular carcinoma (HCC) often develops in patients with chronic liver diseases associated with hepatitis B (HBV) and hepatitis C (HCV) virus infections with high incidences. Particularly, post-therapeutic recurrence encountered after the curative treatment of the preceding HCC may limit the prognosis. Thus, prevention of HCC is of great significance. In the present review, immunopreventions with alpha-interferon and glycyrrhizin, as well as chemoprevention with acyclic retinoid, are discussed. alpha-Interferon prevents the development of HCC not only in patients with a long-term elimination of HCV (sustained virological responders), but in ones with normalized serum aminotransferases (sustained biochemical responders). Glycyrrhizin also suppresses serum aminotransferases and thereby prevents the tumor development, even though the compound does not have antiviral activity for HBV or HCV by itself. Therefore, suppression of hepatic necroinflammation by these drugs may serve to prevent hepatocarcinogenesis. In contrast, acyclic retinoid suppresses the post-therapeutic recurrence in cirrhotic patients who underwent curative treatment of preceding tumors. The retinoid induces the disappearance of serum lectin-reactive alpha-fetoprotein (AFP-L3), a tumor marker indicating the presence of unrecognizable tumors in the remnant liver, suggesting a deletion of such minute (pre)malignant clones (clonal deletion). As a molecular mechanism of the clonal deletion, a novel mechanism of apoptosis induction by the retinoid via tissue transglutaminase is implicated. In future, a combination of immunopreventive and chemopreventive therapies may give a clue to the further advances of cancer prevention, and thereby to the improvement of the prognosis of cirrhotic patients.
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PMID:Chemoprevention of hepatocellular carcinoma: concept, progress and perspectives. 1185 28


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