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)

Liver cell dysplasia was noted on histological examination of nontumorous liver from 24 of 50 (48%) black southern African males with hepatocellular carcinoma (HCC). Macronodular cirrhosis was present in 40 (80%). There was no statistically significant difference between the frequency of dysplasia in 50% of 40 cirrhotic and 40% of 10 noncirrhotic livers, or in 52.6% of 38 hepatitis B antigen (HBAg) positive and 33.3% of 12 HBAg negative HCC patients. HBAg positivity was present in 80% of 40 cirrhotic and in 60% of 10 noncirrhotic HCC patients. This lack of significant correlation between liver cell dysplasia, and both cirrhosis and HBAg positivity in HCC patients in contrast to findings in Uganda and the United States, suggests a different pathogenetic mechanism for dysplasia in southern Africa. Liver cell dysplasia in man appears to be analogous to preneoplastic experimentally-induced hyperplastic foci or areas.
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PMID:Liver cell dysplasia: association with hepatocellular carcinoma, cirrhosis and hepatitis B antigen carrier status. 22 74

Hereditary tyrosinemia type I presents with either acute hepatic failure in the neonatal period or later in infancy with progressive liver dysfunction secondary to cirrhosis. The inevitably fatal outcome in those children with the chronic form has been transformed with the advent of liver transplantation. Native livers from five children who received allografts were studied pathologically and compared with earlier hepatic biopsies in two of these patients that had been performed several years before transplantation. Our findings support the conclusion that a sequence of morphologic changes from the initial micronodular cirrhosis through an intermediate mixed cirrhotic pattern to macronodular cirrhosis occurs. The micronodular phase is transitory, over a period of only a few months, since mixed micronodular macronodular cirrhosis was already present in the livers of children who received transplants by 11 months of age. Focal hepatocellular dysplasia was present in one of the livers with mixed cirrhosis but was not identified in the other two cases. Macronodular cirrhosis accompanied two cases of hepatocellular carcinoma in this study. In order to preclude the latter complication, liver replacement is necessary before the age of 2 years.
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PMID:Hereditary tyrosinemia type I (chronic form): pathologic findings in the liver. 253 31

Non-neoplastic morphologic changes in various types of cirrhosis were evaluated in relationship to the presence or absence of hepatocellular carcinoma (HCC), using autopsy livers from Hokuriku (Japan) and Los Angeles (USA). Macronodular cirrhosis was closely related to HCC in B-viral cirrhosis, alcoholic cirrhosis and cirrhosis of uncertain type. Liver cell dysplasia was most frequently seen in cases with and without HCC in B-viral cirrhosis but was significantly more frequent with HCC in cases of alcoholic cirrhosis and cirrhosis of uncertain type. Nodular bulging activity within regenerative nodules was closely related to HCC in alcoholic cirrhosis. A positive relationship between HCC and Mallory bodies was found in non-alcoholic cirrhosis. These data suggest that patients with macronodular cirrhosis, liver cell dysplasia, nodular bulging activity and Mallory bodies may have an increased risk of developing, or having HCC dependent on the etiology of cirrhosis. The geography and race differences had some relationship to the incidence of HCC.
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PMID:Risk lesions in cirrhosis and development of hepatocellular carcinoma: an autopsy study. 254 32

Hepatocellular carcinoma has a lower prevalence and presents at a later age in urban Blacks than in rural Blacks. These differences have previously been shown not to be attributable to differences in serum hepatitis B virus markers. In the present study, the average age of patients with hepatocellular carcinoma in a developing urban Black population is shown to have risen from 38.9 to 56.5 years (p less than 0.0001) over a 20-year interval, while the prevalence of co-existing cirrhosis has declined from 66 to 44% (p less than 0.05) and tissue HBsAg positivity has fallen from 44 to 17.7% (p = 0.002). The lower prevalence of tissue HBsAg in the recent patients may be explained by their older age. Macronodular cirrhosis was present in 56% of cases in the earlier period but declined to 18.9% in the later period, with micronodular cirrhosis becoming the dominant nontumor pathology (p = 0.002). Liver damage attributable to the abuse of alcohol is now found in more than half of the cases (48/90) of hepatocellular carcinoma occurring in this population. The remainder show no changes (12 cases) or show macronodular or incomplete septal cirrhosis (30 cases), presumed to be of viral origin. The latter cases are more likely to have serum markers of current hepatitis B virus infection than those with evidence of alcohol abuse. We conclude that alcohol is increasing in importance as an etiologic association of hepatocellular carcinoma in urban South African Blacks. At the same time, the prevalence of macronodular cirrhosis (and of cirrhosis as a whole) in urban patients with this tumor has declined. The reason for this decline is not known.
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PMID:Liver morphology in southern African blacks with hepatocellular carcinoma: a study within the urban environment. 298 64

Two hundred thirty-four autopsy cases of liver cirrhosis were examined to correlate the tissue HBV markers and excess alcohol intake with the type of liver cirrhosis, and the incidence of hepatocellular carcinoma (HCC). The following four groups were classified as follows: (1) HBV marker-positive alcoholic group A, (2) HBV marker-negative alcoholic group B, (3) HBV marker-positive non-alcoholic group C, and (4) HBV marker-negative non-alcoholic group D. Macronodular cirrhosis predominated in groups, A, C, and D, while in group B macronodular and micronodular cirrhosis were almost of the same frequency. The mean age at death of the patients with macronodular cirrhosis of HBV-positive alcoholic group A was similar to that of HBV-positive non-alcoholic group C but lower than that of HBV-negative alcoholic group B, suggesting a longer survival of alcoholics without HBV infection than that with HBV infection, when patients had macronodular cirrhosis at autopsy. In HBV-negative alcoholic group B, patients with macronodular cirrhosis had a higher mean age than those with micronodular cirrhosis, while in HBV-positive alcoholic group A, the mean age of patients with either cirrhosis was similar. This suggested that in the absence of HBV infection, macronodular cirrhosis in alcoholics may be related to the increased life span that allows a conversion of micronodular cirrhosis into macronodular one, and in HBV-positive alcoholics it may arise in relation to HBV infection. HCC was frequently associated with macronodular cirrhosis, regardless of the presence or absence of alcohol abuse or HBV infection, but rare in micronodular cirrhosis.
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PMID:Correlation of morphologic subtypes of liver cirrhosis with excess alcohol intake, HBV infections, age at death, and hepatocellular carcinoma. A study on 234 autopsy cases in Japan. 301 43

A high incidence of primary hepatocelluar carcinoma in the Orient and Africa has been reported. It is also seen frequently in Saudi Arabia. In a series of 54 consecutive patients diagnosed histologically, the male to female ratio was 10:1--the highest reported. The peak age was between 40-60 years and the mean survival was eight months. This is in contrast to hepatocelluar carcinoma in Africa where the age is between 25-35 years and the disease runs a quick downhill course simulating an abscess. Macronodular cirrhosis was diagnosed histologically or suggested clinically in 80% of the cases. Serum was positive for HBsAg in 55% of the patients, compared with 8% in healthy blood donors. These figures are as significant as reports from high incidence areas and point strongly to a possible causal relationship between HBV infection and the development of primary hepatocellular carcinoma.
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PMID:Primary hepatocelluar carcinoma in Saudi Arabia. A clinicopathological study of 54 cases. 625 76