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)

Tumor cell marker antibodies were used to analyze ten cases of hepatocellular carcinoma associated with cirrhosis. Clinically, eight of these cases gave a history of chronic alcoholism and the other two of hepatitis B virus infection. Formalin-fixed, paraffin-embedded sections from these cases were screened with antibodies against alpha fetoprotein (AFP), hepatitis B surface antigen (HBsAg) and carcinoembryonic antigen (CEA) using the peroxidase antiperoxidase and avidin-biotin immunoperoxidase procedures. Three cases were positive for AFP, four for HBsAg, and three for CEA; two cases had both HBsAg and CEA. Alpha fetoprotein was present only in the cytoplasm of tumor cells in three cases. Hepatitis B surface antigen, on the other hand, was present in the cytoplasm of hepatocytes in cirrhotic areas and, in one out of the four cases, was also present in hepatocellular carcinoma cells. Carcinoembryonic antigen was seen in three cases; it was present on the surface and in the cytoplasm of proliferating ducts within the cirrhotic areas and between cell surfaces of individual tumor cells in two cases. The presence of different markers was not related to the microscopic appearance of the tumors. In one case, positivity for AFP was of diagnostic help in a tissue sample obtained by needle biopsy. The avidin-biotin immunoperoxidase procedure was more sensitive than the peroxidase antiperoxidase (PAP technique in the pathological assessment of autopsy specimens. Our findings are in agreement with those of other reports and indicate that AFP and HBsAg are the most commonly found markers in hepatoma associated with cirrhosis, and that CEA staining is variable and hepatoma associated with cirrhosis, and that CEA staining is variable and probably non-contributory.
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PMID:Immunohistochemistry of hepatocellular carcinoma associated with cirrhosis. 621 34

Thirty-four patients from the Philadelphia area with hepatocellular carcinoma (HCC) were matched with colon cancer patients, lung cancer patients and blood donors according to age and sex. Sera from the four groups were tested to determine the prevalence of hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), and antibody to hepatitis B core antigen (anti-HBc). Five of the HCC patients (14.7%) and none of the controls were positive for HBsAg. At least one of the three serologic markers of hepatitis B virus (HBV) infection was found in 51.5% of the HCC patients, 5.3% of the colon cancer patients, 11.1% of the lung cancer patients, and 10.7% of the blood donors. Twelve of the seventeen seropositive HCC patients (70.6%) were positive for anti-HBc alone, while all of the seropositive lung cancer patients and donors were positive for anti-HBs alone. Sera positive for any HBV marker were also tested for e antigen (HBeAg) and its antibody (anti-HBe). Four of the HCC patients (23.5% of the seropositives) had anti-HBe, while none of the sera tested had HBeAg. A history of alcoholism did not appear to influence HBV seropositivity in the HCC patients. This study supports the hypothesis that HBV infection is closely associated with HCC even in areas where both conditions are uncommon. The wide disparity between seropositivity for HBsAg and anti-HBc in the HCC patients is an unusual feature, for which an age effect may be the best explanation.
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PMID:Association of hepatitis B virus infection with hepatocellular carcinoma in American patients. 626 Jun 95

Six main types of histopathological changes were found in 463 patients with chronic alcoholism admitted during the 10-year period from 1966 to 1975: group I, normal liver in 2.6%; group II, fatty liver in 8.4%; group III, acute alcoholic hepatitis (AAH) in 7.6%; group IV, cirrhosis with or without steatosis in 68.7%; group V, cirrhosis with AAH in 12.8%; group VI, liver cell carcinoma (LCC) in 1.9% (all of the latter patients were also included in group IV). Seventy-three % were males and 27% were females. Females tended to be older than males. Cirrhosis was found in 68% of the group between 21 and 30 yr and in 85% between 51 and 60 yr. Normal histology or steatosis was less frequent after the age of 50 yr. Ascites and jaundice were more frequent in patients with AAH than in patients with steatosis. The majority of patients had SGOT under 100 karmen units/ml; SGPT was normal in 80% of patients with cirrhosis and higher than 100 karmen units/ml in 10%. SGPT was higher than SGOT in only 11.9% of the patients. Mortality was 46.7% according to the followup until 1978. Survival was 38.4% at the end of the first year and decreased very slowly afterwards to 32.8% in males and 11.5% in females after a 5-yr period.
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PMID:Alcoholic liver diseases in Portugal. Clinical and laboratory picture, mortality, and survival. 704 74

Clinical and laboratory observations were made on 220 chronic alcoholics, regularly taking at least 150 g of alcohol daily. Haematological data concerning white blood cells, platelets and red cells counts, mean corpuscolar volume, hemoglobin and serum iron in these patients were compared with control values obtained from 150 healthy teetotal subjects. Hematological changes in chronic alcoholics were correlated with histological liver damages in transcutaneous needle-biopsies. No statistical differences were evident for white cells and platelets counts and for serum iron content; however, in chronic alcoholics, serum iron content showed a great dispersion around the mean. Mean corpuscolar volume (MCV) was significantly increased (P less than 0,001) in chronic alcoholics (even in those with a normal liver biopsy) but there was no significant difference in the degree and the incidence of macrocytosis between patients showing normal liver appearances or fatty changes only, and those showing more severe damage, i.e, acute alcoholic hepatitis (with or without steatosis), central hyaline-sclerosing necrosis and or hepatofibrosis, cirrhosis and hepatocarcinoma. No significant difference was seen between male and female alcoholics. Macrocytosis may be considered as an early marker for alcoholism but it does not correlate with the type of histological liver damage. Hemoglobin levels were significantly reduced in chronic alcoholics (P less than 0,01): the degree and incidence of anemia were more severe in those patients with advanced liver diseases and in female alcoholics. There is no statistically significant correlation between macrocytosis and anemia.
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PMID:[Macrocytosis and anemia in chronic alcoholism. Correlation with the results of hepatic needle biopsy]. 724 21

Iron was systematically studied in the nontumorous liver of 24 patients with hepatocellular carcinoma (HCC) developed on a noncirrhotic liver compared with 4 control groups (cirrhosis with and without HCC, liver metastasis, and normal liver) matched according to age, sex, and presence of chronic alcoholism. Assessment of liver iron was made by (1) histology according to iron distribution and quantification (total iron score: 0 to 60), and (2) biochemistry (liver iron concentration-N < 36 mumol/g) with calculation of the hepatic iron index (liver iron concentration/age). Patients with hepatocellular carcinoma developed on a noncirrhotic liver presented with (1) histological iron in 83%; (2) parenchymal iron excess significantly more frequent (90%) than in controls; (3) total iron score (15 +/- 12) and liver iron concentration (81 +/- 96) significantly greater than in controls; and (4) hepatic iron index significantly increased (1.4 +/- 1.5) when compared with control groups, except for the hepatocellular carcinoma complicating cirrhosis group (0.9 +/- 1.1). This study (1) shows a mild but unquestionable parenchymal iron excess in the nontumorous liver of most patients presenting with hepatocellular carcinoma developed on a noncirrhotic liver and, at a lesser extent, on cirrhosis, (2) should incite others to study the putative role of iron in the development of liver cancer both in patients with cirrhosis and those without it, whatever the cause of the underlying liver disease, and (3) add argument to take into account and to treat any liver iron excess, even when mild.
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PMID:Increased liver iron stores in patients with hepatocellular carcinoma developed on a noncirrhotic liver. 763 11

To aid understanding of markers of disease and predictors of outcome in alcohol-exposed systems, we undertook a literature survey of more than 700 articles to view the morphological characteristics and the clinical and experimental epidemiology of the Mallory body. Mallory bodies are filaments of intermediate diameter that contain intermediate filament components (e.g., cytokeratins) observable by conventional light microscopy or immunohistochemical methods, identical in structure regardless of initiating factors or putative pathogenesis. Although three morphological types can be identified under electron microscopy (with fibrillar structure parallel, random or absent), they remain stereotypical manifestations of hepatocyte injury. A summary of the conditions associated with Mallory bodies in the literature and their validity and potential etiological relationships is presented and discussed, including estimates on the combined light microscopic and immunohistochemical prevalences and kinetics. Emphasis is placed on proper confounder control (in particular, alcohol history), which is highly essential but often inadequate. These conditions include (mean prevalence of Mallory bodies in parentheses): Indian childhood cirrhosis (73%), alcoholic hepatitis (65%), alcoholic cirrhosis (51%), Wilson's disease (25%), primary biliary cirrhosis (24%), nonalcoholic cirrhosis (24%), hepatocellular carcinoma (23%), morbid obesity (8%) and intestinal bypass surgery (6%). Studies in alcoholic hepatitis strongly suggest a hit-and-run effect of alcohol, whereas other chronic liver diseases show evidence of gradual increase in prevalence of Mallory bodies with severity of hepatic pathology. Mallory bodies in cirrhosis do not imply alcoholic pathogenesis. Obesity, however, is associated with alcoholism and diabetes, and Mallory bodies are only present in diabetic patients if alcoholism or obesity complicates the condition. In addition, case studies on diseases in which Mallory bodies have been identified, along with pharmacological side effects and experimental induction of Mallory bodies by various antimitotic and oncogenic chemicals, are presented. Mallory bodies occur only sporadically in abetalipoproteinemia, von Gierke's disease and focal nodular hyperplasia and during hepatitis due to calcium antagonists or perhexiline maleate. Other conditions and clinical drug side effects are still putative. Finally, a variety of experimental drugs have been developed that cause Mallory body formation, but markedly different cell dynamics and metabolic pathways may raise questions about the relevance of such animal models for human Mallory body formation. In conclusion, the Mallory body is indicative but not pathognomonic of alcohol involvement. A discussion on theories of development and pathological significance transcending the clinical frameworks will be presented in a future paper.
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PMID:The Mallory body: morphological, clinical and experimental studies (Part 1 of a literature survey). 792 9

To identify factors that might be useful as prognostic indexes for the risk of hepatocellular carcinoma in Italian patients with genetic hemochromatosis, 152 homozygotes were studied prospectively for 1 to 229 mo. Factors that were considered in estimating the risk of developing hepatocellular carcinoma were age, sex, cirrhosis (Child class), HBsAg, antibodies to HBsAg, antibodies to HBcAg, hepatitis C antibodies, alcohol abuse and the amount of iron removed during therapeutic phlebotomy to produce iron depletion. At diagnosis, cirrhosis was present in 97 patients and absent in 55. During follow-up, hepatocellular carcinoma developed in 28 of the 97 patients with cirrhosis but in none of those without. Among patients with cirrhosis, the cumulative probability of being free of hepatocellular carcinoma at 10 yr was 70%. For patients with and without HBsAg the probabilities of being free of liver cancer at 10 yr were, respectively, 54% and 75%; for those with and without history of alcoholism, 58% and 78%; and for those younger and older than 55 yr, 90% and 54%. In patients with cirrhosis, multivariate analysis using proportional-hazards (Cox) regression found that the only factors contributing significantly to the estimation of a prognostic index were age, presence of HBsAg and alcohol abuse. Age over 55 yr increased the relative risk of hepatocellular carcinoma 13.3-fold (p < 0.001), the presence of HBsAg increased it 4.9-fold (p < 0.02) and alcohol abuse increased it 2.3-fold (p < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic factors for hepatocellular carcinoma in genetic hemochromatosis. 798 40

There have been few studies and case-reports of bone metastases from hepatocellular carcinoma. To determine the characteristics of these metastases, we retrospectively studied 22 patients in whom the diagnosis was established either on the basis of concomitant occurrence of malignant bone lesions and hepatocellular carcinoma in the absence of other detectable malignant disease (n = 15) or on the basis of histological evidence of bone metastasis from an hepatocellular carcinoma (n = 7). There were 21 males and one female. Mean age was 62.5 years. Most patients (88.2%) had chronic alcohol abuse. The bone metastases occurred as the first manifestation of the liver cancer in half the cases (11/22). Time interval between onset of bone symptoms and admission was less than one month in 6 of 11 patients; mean interval was 7.4 weeks. Hepatomegaly was found upon initial physical evaluation in 9 of 11 patients. Pain was the main symptom of bone disease (18/22). Palpable bone masses were found in 6 of 22 patients. Purely osteolytic lesions were seen on roentgenograms in every case; rupture of the cortex and spread to adjacent soft tissues were common findings. The radionuclide bone scan was normal in four of 12 patients. An advanced primary hepatic tumor was found in 84.2% of cases. Histologic examination of bone specimens established the diagnosis of metastasis from a hepatocellular carcinoma in 7 of 9 patients (77.8%). Severe bleeding occurred during one of the nine biopsy procedures. Patients were given symptomatic treatment. Systemic chemotherapy was used in five patients, unsuccessfully. Median survival was three months.
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PMID:[Bone metastasis of hepatocellular carcinoma. Apropos of 22 cases]. 801 16

Between 1979 and 1991, 156 patients with histologically proven liver cirrhosis, good liver function, and bleeding portal hypertension underwent operation with portal blood flow preserving procedures (selective shunts: 101; Sugiura-Futagawa: 55). Long-term results of the procedures and the quality of life of the 145 patients who survived the operation were studied. During the observation period (range 3 to 156 months), 28 patients died. The main causes of death were liver failure and hepatoma. Twenty-three patients were lost for follow-up. Twenty-six patients (18%) developed 1 or more encephalopathic episodes. Four patients (3%) experienced rebleeding. One hundred eight patients (74%) had a good quality of life, and 26 (18%) had a poor quality of life. Eleven (15%) of 73 patients with a history of alcoholism continued drinking. Five-year survival for the selective shunt group was 81% and for the devascularization group was 83%. In 81% of the patients, portal blood flow was maintained. It is concluded that both procedures are effective in the long-term. Most patients are able to rehabilitate from the use of alcohol, and most of them have a good quality of life. For patients with good liver function (whose main problem is bleeding), surgery is the best choice of treatment.
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PMID:Survival and quality of life after portal blood flow preserving procedures in patients with portal hypertension and liver cirrhosis. 802 91

A variety of specific conditions often stimulate controversy regarding candidacy for liver transplantation. We review the published experience with liver transplantation for alcoholic liver disease, fulminant and chronic hepatitis B, and hepatocellular carcinoma and transplantation in older subjects. Liver transplantation for alcoholic liver disease and in subjects older than 60 years is becoming less controversial because recent data demonstrate that these patients have excellent survival and good quality of life after transplantation. Only 10% to 15% of persons with alcoholism return to drinking after transplantation, and most do so only transiently. Liver transplantation for patients with hepatitis B virus infection or primary liver cancer is more problematic because recurrent disease is common in both conditions. After transplantation for chronic hepatitis B, 80% to 90% of patients have reinfection of the allograft and long-term survival is 45% to 50%. Patients receiving transplants for hepatocellular carcinoma have only 20% to 30% long-term survival, but these survivors are cured of malignancy. Data are presented to support continued liver transplantation for chronic hepatitis B and hepatocellular carcinoma; however, patients must be selected based on factors that predict a favorable outcome, and experimental therapies should be employed to explore ways to improve the existing survival rates.
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PMID:Controversies in patient selection for liver transplantation. 827 56


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