Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ultrasonographic screening and follow-up of patients with chronic liver disease lead to the detection of a large number of small asymptomatic hepatocellular carcinomas, so that the changing appearance of this neoplasm during its natural history has now been recognized. Ultrasonography provides information on shape, echogenicity, growth pattern and vascular involvement of the neoplasm. Three different shapes may be identified, depending upon the size and the invasiveness of the neoplasm: nodular, massive and diffuse. The echogenicity is variable and the tumour mass may appear hypo, hyper or isoechoic in comparison with the surrounding liver tissue. A mixed pattern and/or a hypoechoic ring may also be visualized. A tendency to change from a low echo pattern to a low periphery and finally to a massive pattern with increasing echogenicity has been shown in Japanese patients. The infiltrative growth pattern may be grossly distinguished from the expansive one on the basis of the aspect of the tumour boundary. Vascular invasion is easily recognizable as a mass within a major portal branch or even in the portal trunk. Duplex and color Doppler ultrasonography enable further insights on the vascular alterations related to this neoplasm. Abnormal signals, typical of HCC, are characterized by high-peak with broadening of spectrum. Low impedance continuous signals are less characteristic. Finally, ultra-sound guidance allows puncture of intrahepatic nodules as small as 1cm. The sensitivity of this procedure in the diagnosis of focal liver lesions is very high, varying between 91% and 95% with a specificity of 92%-100%.
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PMID:Ultrasonography and guided biopsy in the diagnosis of hepatocellular carcinoma. 131 77

The prevalence of antibodies to hepatitis C virus (HCV) was investigated in 129 patients with chronic liver disease (85 with chronic active hepatitis and 44 with cirrhosis) and 53 patients with hepatocellular carcinoma. The commercially available second generation anti-HCV enzyme immunoassay kit was used. Antibodies to hepatitis C virus were detected in 16.2% of the patients with chronic liver disease and in 15.1% with hepatocellular carcinoma. Of the HCV positive patients in all groups 51.7% were positive for hepatitis B virus (HBV) markers indicating present or past infection. Prevalence of HBV markers in all the three groups (CAH, cirrhosis and HCC) was higher as compared with anti-HCV prevalence. These results suggest that HCV infection may not be a major cause of chronic liver disease and hepatocellular carcinoma in India and indicate the presence of other aetiological agents.
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PMID:Prevalence of hepatitis C virus antibodies in chronic liver disease and hepatocellular carcinoma patients in India. 132 97

The aim of our study was to confirm by Recombinant Immunoblot Assay (RIBA) and by neutralization assay the repeat positive reactions found by two commercially available EIAs (Ortho and Abbott) when testing samples from volunteer blood donors, patients with chronic liver disease and with hepatocellular carcinoma. Our data show a high confirmatory rate among patients with chronic viral NANBH and HCC, while among donors and patients with CLD other than NANBH the percentage of presumptive EIA positive reactions confirmed by RIBA and/or neutralization assay is much lower. In our experience, the neutralization assay appears to be somewhat more sensitive than RIBA, especially when samples show low EIA optical densities.
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PMID:Confirmation of anti-HCV EIA reactivities by RIBA and neutralization assay among blood donors and patients with chronic liver disease and hepatocellular carcinoma. 133 25

Hepatitis viruses, particularly HBV and HCV, are major causes of hepatocellular carcinoma worldwide, due to the induction of chronic liver disease and of cirrhotic transformation of the liver. Cirrhosis certainly represents the most important link between chronic viral hepatitis and HCC. Under these circumstances, risk of HCC development in chronic HBV and HCV infection is strictly dependent on the propensity to cirrhotic transformation. Intervention of other, more direct, molecular events induced by the virus itself are suspected, particularly for HBV which is able to integrate into the host genome, but not yet incontrovertibly proved.
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PMID:Hepatitis viruses as aetiological agents of hepatocellular carcinoma. 166 Mar 32

This article presents 14 patients of single-nodular minute hepatocellular carcinoma (HCC less than or equal to 2 cm) with coexisting cirrhosis. Of these nine patients were discovered by alpha-fetoprotein (AFP) mass screening or health check-up; and five by follow-up observations of chronic liver disease. All the 14 patients received radical resection with no operative mortality. The 1-5 year survival rates after resection were 100% (14/14), 100% (12/12), 100% (11/11), 100% (9/9), and 100% (7/7), respectively. This study demonstrates that the key point of further improvement in the detection of minute HCC lies in the establishment of diagnosis at a relatively low AFP level (less than 200 ng/ml). Realtime ultrasonography is the diagnostic modality of first choice in screening and monitoring. Surgery is strongly indicated for minute HCC with compensated liver function; Limited resection is the main type of resection for minute HCC with liver cirrhosis. The present data also indicate that HCC is not always multicentric in origin, even in patients with liver cirrhosis Intrahepatic spreading rather than multicentric origin may play a more important role in the multinodular pattern of HCC.
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PMID:[Diagnosis, treatment and prognosis of single-nodular minute hepatocellular carcinoma]. 169 22

To investigate the epidemiology of HCV in Taiwan, anti-HCV was studied by radioimmunoassay or enzyme immunoassay in patients with chronic liver disease, healthy adults, and subjects at risk. The anti-HCV prevalence was 0.95% in 420 volunteer blood donors, 90% in 100 hemophiliacs and 81% in 58 parenteral drug abusers. Anti-HCV was present in 6 (7.7%) of 78 HBsAg-positive and 28 (65%) of 43 HBsAg-negative patients with chronic hepatitis, 3 (10%) of 31 HBsAg-positive and 13 (43%) of 30 HBsAg-negative cirrhotics, and 7 (17%) of 42 HBsAg-positive and 15 (63%) of 24 HBsAg-negative patients with HCC. An outbreak of non-A, non-B hepatitis revealed 18% of 57 patients to be positive for anti-HCV. In a prospective study of PTH, 37 or 13% patients contracted hepatitis and 22 (60%) were due to HCV, and at least 17 (77%) of them became chronic. Cloning of HCV genome in a Taiwanese patient with acute posttransfusion non-A, non-B hepatitis by using reverse transcription polymerase chain reaction was performed, and partial characterization of the nucleotide sequences showed 80% and 92% homology as compared to HCV sequences from Chiron and one of the published Japanese isolates, respectively. It is concluded that HCV infection plays a relatively minor role in HBsAg-positive liver decrease in Taiwan, but is strongly associated with HBsAg-negative chronic liver disease and HCC. It is also important in PTH, and the infection is extremely common in hemophiliacs and parenteral drug abusers. The Taiwanese strain of HCV seems more similar to that from Japan, as revealed by nucleotide sequences.
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PMID:Hepatitis C virus infection in Taiwan. 190 59

To evaluate the diagnostic value of Lipiodol-CT for small hypovascular HCC, we injected 3 ml or less Lipiodol into the hepatic artery of patients with chronic liver disease and small SOL in the liver detected on echogram but not on angiogram. About seven days after injection CT was used to check for accumulation of Lipiodol in the liver SOL. We found that the sensitivity of this method for detection of hypovascular HCC is only 25%. We assume that Lipiodol does not accumulate in small hypovascular HCC lesions because they have little vascular stroma. Lipiodol-CT has high diagnostic value for the detection of small hypervascular daughter HCC lesions, but this method should not be relied on for the detection of small hypovascular HCC.
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PMID:[Lipiodol-CT for the detection of small hypovascular HCC]. 217

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

The prevalence of serum hepatitis B virus markers was studied in three groups of age- and sex-matched patients: a. 31 patients with liver cirrhosis and hepatocellular carcinoma (c-HCC); b. 31 patients with chronic liver disease (CLD) and c. 62 hospitalized control subjects. The overall exposure rate to the hepatitis B virus was 90% in c-HCC, 80% in CLD and 58% in control subjects. The prevalence of hepatitis B surface antigen (HBsAg) was 29%, 13% and 1.6% in the three groups, respectively. The prevalence of hepatitis B surface antibody was significantly lower in c-HCC (9.6%) than CLD (42%) and control subjects (40%). The serological evidence of continuous viral replication (HBsAg positivity or isolated high titre hepatitis B core antibody positivity) was more common in c-HCC (39%) than CLD (12%) and control subjects (1.6%). The prevalence and patterns of aggregation of serum hepatitis B virus markers were similar in the 31 patients with c-HCC and in 11 patients with HCC without concomitant liver cirrhosis (n-HCC). In conclusion, the overall exposure rate to the hepatitis B virus is similar in c-HCC and CLD. However, serological evidence of continuous viral replication is more common in the former group. A defective clearance of the hepatitis B virus in hepatocellular carcinoma is a possible explanation of the phenomenon. The strength of the association between hepatitis B virus infection and hepatocellular carcinoma appears to be similar in c-HCC and n-HCC.
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PMID:Case-control study of hepatitis B virus infection in chronic liver disease and hepatocellular carcinoma. 632 29

Forty patients with chronic liver disease and HCC were analyzed for infection with hepatitis C (HCV) and hepatitis B (HBV) viruses. All patients were negative for HBsAg, 16 were alcoholics, 6 had previous blood transfusions and 18 had sporadic chronic hepatitis. Antibodies to HCV were determined by EIA 2nd generation. HBV-DNA was detected by PCR using primers of the precore region. Analysis of HCV-RNA was done with nested PCR amplifying the 5' non-coding region of the HCV genome, using primers complementary to nucleotides 1-20 and 305-320 and nested primers complementary to nucleotides 21-31 and 271-286 of the HCV-J1. Anti-HCV were positive in 35/40 patients (87.5%). HCV-RNA was detected by PCR in 34 patients (85%) all of them positive for the anti-HCV. HCV-RNA was detected in 70.5% of the alcohol abusers, in 100% of patients with history of transfusion(s) and 94.1% of patients with cryptogenic chronic liver disease. HBV-DNA was detected in only 2 patients. In conclusion, there is a high rate of HCV and a low rate of HBV viremia detected by PCR in Spanish patients with HCC HBsAg negative. No patient without anti-HCV presents HCV-RNA. Our results suggest that persistent HCV replication may play a role in hepatic carcinogenesis, as HBV-DNA could be found in only 5% of our HCC patients.
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PMID:Demonstration of HCV-RNA and HBV-DNA in the serum of HBsAg negative patients with hepatocellular carcinoma. 781 97


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