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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well known that primary hepatocellular carcinoma could be derived from chronic hepatitis and liver cirrhosis in epidemiologic studies. However, it is still not clear what kinds of hepatocyte are premalignant cells. Recently we have focused on liver cell dysplasia as a possible premalignant cell, and showed localization of alpha-fetoprotein in the cytoplasma of these cells. Although the dysplastic cells were often seen in the liver of chronic active hepatitis, hepatitis B virus associated DNA polymerase activity was also significantly high in the sera from the patients with chronic active hepatitis. In this paper, we discuss the possible role of hepatitis B virus through hepatocarcinogenesis in human.
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PMID:Early lesions and development of primary hepatocellular carcinoma in man--association with hepatitis B viral infection. 7 Mar 87

Liver failure and hepatic coma present with various clinical and morphological counterparts. While fulminant viral hepatitis is the most common cause of acute liver failure, liver cirrhosis with vascular bypass most often is responsible for the hepatic coma in chronic diseases. Prognosis is mainly determined by the extent of liver cell necrosis and regeneration, provided extrahepatic complications do not cause death. Prognosis can best be judged by stereology of liver biopsies and determination of the alpha-fetoprotein.
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PMID:[Pathology of liver failure and hepatic coma (author's transl)]. 7 Jul 32

In 31 patients with an initial diagnosis of cirrhosis or chronic hepatitis hepatocellular carcinoma (HCC) was detected after a clinical follow-up of 8 months to 14 years with an average of 59 months. They had had no scintigraphic and biochemical abnormalities suggestive of HCC at the beginning. The follow-up period before the detection of carcinoma was shorter in patients positive for hepatitis B surface antigen compared with those negative for hepatitis B surface antigen. Analyses of clinical data during the follow-up and liver scans made shortly before tumor detection suggested that in most of these patients HCC became discernible relatively early in the course of cirrhosis or long before cirrhosis reached an advanced stage. A sharp rise in serum alpha-fetoprotein level proved highly diagnostic in 11, it remained low throughout in 7, and tumor was already unresectable in the majority. Although continuous and regular check for alpha-fetoprotein is imperative in patients with chronic liver disease, particularly in those with hepatitis B surface antigenemia, additional diagnostic tools are necessary for the detection of small HCC in its resectable stage.
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PMID:Detection of hepatocellular carcinoma during a clinical follow-up of chronic liver disease: observations in 31 patients. 7 17

The serum alpha-fetoprotein level was measured by radioimmunoassay in 200 patients when admitted to hospital, 63 with idiopathic hemochromatosis and 137 with liver cirrhosis. In addition, repeated controls were performed in 19 subjects of each group for a mean period of 11 months (range 3--18 months). Elevated alpha-fetoprotein levels were observed initially or during the study period in 15 patients, a malignant liver tumor being demonstrated in 12 of them. In 4 of these patients, the abnormal alpha-fetoprotein concentration was the clue to the diagnosis of an unsuspected malignant hepatoma, but in none of these cases could the tumor be resected. The present results indicate that screening the serum alpha-fetoprotein level may contribute to the detection of malignant hepatoma in high-risk clinical groups, but the practical interest of such screenings may keep limited until more efficient therapeutic methods are developed.
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PMID:alpha-Fetoprotein screening in patients with idiopathic hemochromatosis and liver cirrhosis. 7 12

Serum alpha-fetoprotein (AFP) concentrations were estimated by sensitive radioimmunoassay in 30 patients with cirrhosis complicated by hepatocellular carcinoma and in 100 patients with cirrhosis in whom malignancy was excluded. Twenty-nine of the 30 patients with hepatocellular carcinoma had concentrations above 10 IU/ml (10.5 ng/ml) (median 3500 IU/ml (3675 ng/ml)), whereas only one of the 100 patients with cirrhosis and no tumour development had a raised concentration. Eleven out of 20 patients in whom hepatocellular carcinoma had developed in an apparently normal liver had raised AFP concentrations. In this group the differential diagnosis is usually secondary carcinoma, and three of 50 such patients had AFP concentrations above 10 IU/ml. Noting raised AFP concentrations is thus of considerable value both in detecting and in excluding hepatocellular carcinoma in cirrhosis, for in this case such concentrations gave only 1% false-positive and 3% false-negative results. They are less useful, however, in distinguishing between primary tumours arising in patients without cirrhosis and secondary hepatic deposits, giving 6% false-positive and 45% false-negative results.
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PMID:Alpha-fetoprotein concentrations measured by radioimmunoassay in diagnosing and excluding hepatocellular carcinoma. 8 Oct 86

The association between hepatitis B virus (HBV) infection and hepatocellular cancer (HCC) in southern African blacks was investigated by examination of patients' sera for all the currently known markers of HBV. Hepatitis B surface antigen (HBsAg) was present in the sera of 61.6% (178/289) of the patients compared with only 11.3% (24/213) of age-matched, sex-matched, and ethnically matched controls (P less than 0.001). Antibody against HBsAg was found in 17% of the patients and 41.7% of the controls (P less than 0.001). In 74 patients studied in more detail, antibody against the hepatitis B core antigen (anti-HBc) was detected in 89%, almost always in high or moderately high titer. Anti-HBc was found in 37.5% of the controls. Active HBV infection, as indicated by positive tests for HBsAg or anti-HBc, was present in 91% of the patients compared with 39.4% of the controls (P less than 0.001). Hepatitis B e-antigen was detected in 2.3% and its specific antibody in 20.5% of the patients. The corresponding figures in the controls were 0 and 55%. HBs antigenemia was more common in younger patients with HCC. No relationship was demonstrated between alpha-fetoprotein and HBs antigenemia. HBV infection was equally common in patients with and without cirrhosis in the nontumorous liver.
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PMID:Hepatitis B virus infection in southern African blacks with hepatocellular cancer. 8 90

A short review of alpha-1-fetoprotein (AFP), is followed by a presentation of the serum AFP concentrations obtained in healthy subjects and in patients with hepatoma, cirrhosis of the liver or metastatic liver cancer, measured by radioimmunoassay (RIA). A calculation is made from these results of the upper limit of normal (9 ng/ml), a limit which is suggestive of hepatoma (215 ng/ml) and a limit which is pathognomonic for hepatoma (7500 ng/ml). It is concluded that the quantitative determination of AFP by RIA represents a sensitive method which provides valuable clinical information for the early diagnosis of hepatoma.
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PMID:[Serum concentrations of alpha-1-fetoprotein suggestive of, or pathognomonic for hepatoma (author's transl)]. 8 72

The proportions of T and B lymphocytes in the liver infiltrates of 23 patients with chronic active hepatitis have been determined. The results were compared with the values obtained from peripheral blood and with the presence of HB virus markers and alpha-fetoprotein in liver tissue. A group of patients with chronic liver disease other than chronic active hepatitis were studied as controls. In chronic active hepatitis the percentage of hepatic T cells was 49 +/- 8 SD (control patients 61 +/- 8) (P less than 0.01), whereas the percentage of B cells was 40 +/- 10 (control patients 18 +/- 8) (P less than 0.01). No correlation was observed between hepatic T and B cells and the presence of HB virus. The numbers of T cells in liver tissue was significantly higher, the numbers of B cells lower, in patients whose biopsies were positive for alpha-fetoprotein than in those whose biopsies were negative. In peripheral blood, only the patients with chronic active hepatitis and established cirrhosis presented lower absolute values of T cells, whereas surface immunoglobulin-positive lymphocytes were within the normal range.
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PMID:Evaluation of T and B lymphocytes in liver infiltrates of patients with chronic active hepatitis. 8 2

Serum alpha-fetoprotein (AFP) levels were measured by radioimmunoassay in 89 healthy adult Chinese, 170 patients with histologically verified non-malignant liver diseases, and 14 hepatitis B surface antigen (HBsAg) carriers with normal liver histology. In 97% of the healthy adults, AFP levels were under 20 ng/ml, which is then regarded as the normal upper limit. Cases with supranormally elevated AFP levels ranged from 15-51% in chronic hepatic disorders and were 33% in acute hepatitis. None of the healthy HBsAg carriers had abnormal AFP level. HBs antigenemia was found to be related to AFP elevation in chronic active hepatitis, cirrhosis, and acute hepatitis but not in chronic persistent hepatitis and healthy HBsAg carriers. The correlation could be demonstrated only when the sensitive third generation test was employed to define seropositivity of HBsAg. Events after hepatic injury induced by hepatitis B virus, rather than the HBs antigenemia itself, are probably responsible for the association. Whether the association of HBsAg and elevated serum AFP in these nonmalignant hepatic disorders contributes to the higher risk of subsequent development of hepatocarcinoma in Taiwan is unknown and requires further long-term longitudinal study.
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PMID:Relationship of hepatitis B surface antigen to serum alpha-fetoprotein in nonmalignant diseases of the liver. 8 92

The immunocellular response to fetal antigens was studied in ten patients with hepatocarcinomas. Homogenized extracts of human fetal liver and purified human alpha-fetoprotein were used as antigen substances. The control group included 15 patients with cirrhosis of the liver. The level of circulating T lymphocytes (E-rosettes) was also registered. Patients with hepatocarcinoma showed a definite response to both antigens, determined by the degree of inhibition of leukocyte migration. The migration indices were as follows: x = 0.65 +/- 0.16 for homogenized fetal liver antigen, and x = 0.79 +/- 0.13 for alpha-fetoprotein antigen. These values were 0.93 +/- 0.13 and 0.95 +/- 0.15 respectively in the cirrhotic patients. The differences in the migration indices for the two groups were statistically significant with both antigens (p less than 0.0005 and p less than 0.005). The decrease of the number of T lymphocytes in patients with hepatomas was also significant (p less than 0.005). The determination with homogenized fetal antigen was more sensitive than with alpha-fetoprotein (p less than 0.01). A significant relationship between the severity of the tumor and the immunocellular response could also be seen (r = 0.84; p less than 0.001). Response tended to diminish as the tumor progressed. The disappearance of immunocellular response seemed to depend at least in part on the decreasing number of T lymphocytes, since there was a significant inverse correlation between the two parameters (r = -0.75; p less than 0.01).
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PMID:[Immunocellular response to fetal antigens in patients with hepatoma (author's transl)]. 9 78


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