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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphometrical analysis of different types of liver cells was performed in cases of chronic active hepatitis (CAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). The area and a form factor (form AR) of nuclei and cytoplasms were determined, and the nucleo-cytoplasmic ratio (N/C) was calculated in normal hepatocytes, HBsAg-positive cells, large dysplastic cells, cancer cells and in a liver cell population identifiable as "small dysplastic cells" (small cells). The nucleo-cytoplasmic ratio of the small cells and of the neoplastic cells was roughly the same and the highest. Large dysplastic cells showed a small nucleo-cytoplasmic ratio, almost comparable with that of normal hepatocytes and similar to that of HBsAg-positive cells. Since cellular precursors of liver cancer are expected to have a nucleo-cytoplasmic ratio similar to that of neoplastic cells, our morphometrical evaluation indicates small cells as the true precancerous cells; liver cell dysplasia (large dysplastic cells), as described by Anthony et al., should not be considered as a true preneoplastic change.
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PMID:Morphological precursors of hepatocellular carcinoma: a morphometrical analysis. 303 18

It seems evident that the development of fully malignant HCC is a multistage process with many variables. One possible mechanism by which many of these variables may interact is as follows. During chronic active hepatitis, viral DNA integration occurs randomly and at a low frequency in hepatocytes. Integration may be stimulated by the increased rate of hepatocyte cell division resulting from liver necrosis and regeneration during chronic disease. The presence of viral integrations in the cellular genome provides focal points for the generation of chromosomal aberrations. One pathway by which these aberrations may be generated involves rearrangement of integrated viral and cellular sequences following viral DNA integration. The rearrangements which occur may include deletion, translocation, transposition or amplification of specific viral and cellular DNA sequences. We and others have directly demonstrated that all of these events are associated with different HBV integrations. The presence of viral integrations in chromosomes may also, by some unknown mechanism, destabilize those chromosomes such that whole chromosomes fail to segregate and are lost from particular cells. Preliminary studies we have conducted using restriction fragment length polymorphisms have revealed the loss of Chromosome 11 alleles in several HCC, indicating that chromosome loss may be a common occurrence in HCC. Our studies with restriction fragment length polymorphisms support such a mechanism involving Chromosome 11 in HCC. Specific chromosomal aberrations associated with all HCCs have not yet been identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular aspects of persistent woodchuck hepatitis virus and hepatitis B virus infection and hepatocellular carcinoma. 380 17

The results from the complex study on 26 patients with primary biliary cirrhosis (PBC), 20 females and 6 males, an average age of 46 years, are reported. The most frequent symptoms of PBC are itching, jaundice, hepatosplenomegaly; from the laboratory tests--most characteristic is the increase of serum 5'-nucleotidase, AP, LAP, gamma GTP, GOT, cholesterol, cholic acid and antimitochondrial antibodies and IgM (AP, 5'-nucleotidase and antimitochondrial antibodies, being most significant in making the early diagnosis). The laboratory results in PBC are compared with those of the chronic active hepatitis, cirrhosis of the liver, liver cancer, extrahepatic cholestasis, with outlining the characteristic differences, depending on the diagnosis. The diagnostic advantages of the various methods are discussed (mainly laparoscopy and liver biopsy) and the histologic and electron microscopic changes of percutaneous transhepatic cholangiography, via echography--81 per cent, laparoscopy--73 per cent, scintigraphy--61.53 per cent and liver biopsy--50 per cent. The results from the treatment with cholestrimine, corticosteroids and azathioprine and surgical treatment, observing a temporary improvement and progressing of PBC, are reported. With the follow-up care of 20 patients, it was established, that 9 had died 5 years, on the average, after making the diagnosis, 11 survived after the 5 years and they are still followed up. The longest survival was reported in two females--11 and 15 years after the onset of PBC.
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PMID:[Primary biliary cirrhosis]. 632 95

In a retrospective study a total of 754 sera from 397 hepatitis patients were assayed for delta antigen and antibody by radioimmunoassay. The study included patients of all age groups (3 months up to 85 years) whose first serum sample, taken from 1978 until January 1984, was positive for HBsAg. Clinically the patients could be subdivided into three major groups: 311 sera were from 181 patients with acute hepatitis, 296 from 135 CPH/CAH patients, including a few cases of liver cirrhosis and 3 cases of HCC, and 147 sera were from 81 asymptomatic carriers. Delta markers were found in 30 patients (7.6%). 20 of these were under the age of 30, and 13 presented with acute, often fulminant hepatitis or (in a minority of cases) exacerbations of preexisting HBV infection. Only two symptomless carriers had anti-delta. It seems of particular interest that all 10 cases where delta antigen could be demonstrated in the first serum sample presented with acute, often fulminant hepatic disease and 9 had anti-HBc-IgM antibodies. Where a second sample could be tested (5 cases), seroconversion to anti-delta was always demonstrated. Delta superinfection could be shown in 2 cases where anti-delta antibodies appeared more than a year after HBsAg positivity was first detected.
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PMID:[Delta hepatitis in Switzerland. Determination of delta antigens and delta antibodies in 397 HBsAg-positive patients (1978-1984)]. 647 32

Chronic delta infection occurs in Greece in about 10 to 15% of HBsAg+ subjects, being largely unrelated to parenteral transmission and/or to drug addiction. The observed cases exhibited histological changes ranging from chronic persistent hepatitis to chronic active hepatitis, cirrhosis, and even hepatocellular carcinoma on cirrhosis. The male/female ratio of patients with delta Ag + CLD was 3.8:1 and their mean age 40 years. They were younger compared to delta Ag-/HBsAg+ CLD and they presented with a wide spectrum of symptoms and signs. About 25% of the patients were oligosymptomatic or asymptomatic and about 40% manifested their disease as an episode of acute hepatitis with protracted or relapsing course followed by chronicity. Biochemical changes appeared to be more severe than in delta Ag-/HBsAg + CLD. The natural history was frequently characterised by a progressive course, terminating, in about 15 years, to death from cirrhosis and liver failure, although remissions occasionally occurred. HCC also developed but probably less frequently than in HBsAg positive, delta Ag negative CLD. Whether the natural course of delta Ag+ CLD can be modified by any form of treatment remains to be proved.
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PMID:Delta antigen positive chronic liver disease in Greece: clinical aspects and natural course. 666 75

Variation of incidence of HBe antigen (HBeAg) and HBe antibody (anti-HBe) was examined by use of RIA in 72 patients with HBsAg positive liver diseases. 1) Percentage of positive HBeAg was highest (71.5%) in chronic active hepatitis with lobular distortion, followed by chronic active hapatitis without lobular distortion (70.0%) and acute hepatitis in asymptomatic HBsAg carriers (66.7%). In contrast, it was low in chronic inactive hepatitis (35.7%) and liver cirrhosis (38.5%). None of liver cancers showed HBeAg positive reaction. 2) Percentage of positive HBe antibody (anti-HBe) was highest in liver cancer (100%), followed by liver cirrhosis (61.5%) and chronic inactive hepatitis (50.0%). In acute hepatitis from asymptomatic HBsAg carriers no anti-HBe was found. In chronic active hepatitis the percentage of positive anti-HBe was low, 21.4 and 30.0% with and without lobular distortion, respectively. 3) In 45 patients with persistently positive HBsAg liver diseases, fluctuations of HBeAg and anti-HBe were followed over a period of one year in relation to serum GPT values, an indicator of clinical conditions. Serum GPT tended to fluctuate or to remain high in patients with persistently positive HBeAg or with sporadically positive HBeAg or anti-HBe, whereas it tended to become low or normal with persistently positive anti-HBe or with seroconversion from HBeAg to anti-HBe. However, there were some exceptions to this tendency. From these results we concluded that it is clinically of significant value to determine HBeAg and anti-HBe levels for the effective assessment of the activity and time course of HBsAg positive liver diseases.
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PMID:[Clinical significance of HBeAg and anti-HBe in HBsAg positive liver diseases]. 684 Jun 66

In Japanese blood donors, positivity for antibodies to hepatitis C virus (HCV) ranges from 0.2% in subjects under 20 to 3.9% in those over 50 years. It is estimated that at least 2.3 million Japanese have contracted HCV infection through contaminated blood. HCV carrier state was confirmed by polymerase chain reaction for HCV-RNA in subjects positive for antibodies to more than one viral protein (70% of cases). Subjects positive for core antibody alone, however, were found to be HCV-RNA negative with normal liver function, and are considered to have only a past history of HCV infection (30% of cases). Acute hepatitis C progresses to chronic infection in about 90% of cases. In comparison with hepatitis B, chronic hepatitis C leads more frequently to cirrhosis and liver cancer, and rarely remits spontaneously. In typical HCV infection, aminotransferase activities fluctuate markedly in the early stages, then become relatively stable for 10 years or more, with chronic persistent hepatitis shown by histological examination. Thereafter, aminotransferase activities may change dramatically, with progression to chronic active hepatitis and rapid development of cirrhosis and hepatocellular carcinoma. On average, it takes about 30 years for chronic hepatitis C to progress from initial infection to cirrhosis and cancer, but the disease progresses much more rapidly in elderly patients.
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PMID:Epidemiology and long term prognosis of hepatitis C virus infection in Japan. 768 12

Chronic infections by hepatitis B and C viruses are major risk factors for primary liver cancer. In both infections, induction of chronic active hepatitis followed by cirrhosis precedes development of the tumor and is a major mechanism of liver carcinogenesis. For hepatitis B virus, several elements indicate that the virus might also exert direct effects through cis and transactivation of cellular genes. For hepatitis C virus, such a direct effect has not yet been demonstrated.
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PMID:[Hepatitis B and C viruses and primary liver cancer]. 772 21

During the period 1982-1990, 544 patients with clinical evidence of liver disease were admitted to King Fahd University Hospital, Al-Khobar, Saudi Arabia. Besides routine laboratory and sonographic investigations, all were subjected to either a needle liver biopsy, laparoscopy or a laparotomy. The tissue diagnoses were as follows: liver cirrhosis 17.3%, periportal fibrosis 14.3%, metastatic cancer 12.9%, primary hepatoma (hepatocellular carcinoma: HCC) 12.1%, hepatic granuloma 11.2%, chronic active hepatitis 7.7%, chronic persistent hepatitis 2.2%, fatty liver 7.2%, hydatid liver disease 4.6% and others 2.8%. In 7.7% the histology was normal. These results will be discussed and compared with results reported in local and international literature.
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PMID:Pattern of chronic liver disease in the eastern province of Saudi Arabia. A hospital-based clinicopathological study. 789 3

A synthetic HDAg 27 peptide which was selected and designed by the authors and synthesised by Shanghai Institute of Biochemistry, Chinese Academy of Science was used with ELISA method to detect serum anti HD in HBV infected subjects in Chongqing. Anti HD was positive in one of 300 blood donors and was negative in all of 113 cases of hepatitis A and 58 cases of hepatitis non-B. Anti HD was positive in 106 out of 882 cases with positive HBV marker (12.02%), among which anti HD was positive in 3.17% (13/410) of HBsAg carrier, 14.4% (11/76) of acute hepatitis, 7.6% (1/13) of chronic persistent hepatitis, 17.68% (22/121) of chronic active hepatitis, 19.77% (17/86) of severe hepatitis, 29.49% (23/78) of liver cancer and 19.39% (19/98) of primary hepatic cancer. These results coincided with those of previous reports. The coincidence rate was 94.9% (74/78) when compared with Abbott EIA kit. When the natural HDAg was used to compete anti HD in four anti HD positive and two anti HD negative serum specimens, anti HD was negative in all specimens. It is shown that the HDAg 27 peptide has natural HDAg activity capable of being recognized by natural anti HD and is a new diagnostic agent being more simple, save, stable and reliable.
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PMID:[Application of synthetic 27 oligopeptide of HDV antigen for detecting serum anti-HD in HBV infected subjects in Chongqing]. 795 61


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