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)

Until now, the hepatitis B virus has been thought to play a minor role in the aetiology of chronic liver disease in Australia. This is a report of 21 patients with cirrhosis and/or primary hepatocellular carcinoma with hepatitis B antigenaemia. Primary hepatocellular carcinoma occurred in six patients, five of whom had underlying cirrhosis. The disease occurred mainly in non-Australian born males, and was not often associated with a previous history of hepatitis. The death of 16 patients within 12 months of presentation is in contrast to previous concepts of the benign nature of hepatitis B associated cirrhosis.
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PMID:Emerging patterns of hepatitis B chronic liver disease in Australia. 22 47

Serologic tests for evidence of hepatitis B virus (HBV) infection were performed on family members of Asian and non-Asian patients with either hepatitis B surface antigen (HBsAg)-positive hepatocellular carcinoma or chronic HBV infection. Asian family members had a significant increase of HBsAg (34% higher) and of antibody to HBsAg or of antibody to hepatitis B core antigen (50% higher) when they were compared with non-Asian family members. In the Asian group, viral markers were detected more frequently in blood relatives than in nonblood relatives of the index cases. Within this group, birthplace did not influence the frequency of antigenemia, since HBsAg was positive in 55 (44%) of 125 Asians born in Asia and in 36 (38%) of the 94 Asians who were born in the United States. Also, HBsAg positivity frequently was seen in offspring from HBsAg-positive carrier mothers as well as from HBsAg-positive carrier fathers whose spouses were either HBsAg-negative or who had antibody. The e antigen was found more often in individuals 30 years of age or younger than in older individuals. This study indicates that intrafamilial spread of HBsAg in Asian families plays an important role in the perpetuation of HBV infection and in the eventual development of chronic liver disease in this ethnic group.
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PMID:A comparative study of hepatitis B viral markers in the family members of Asian and non-Asian patients with hepatitis B surface antigen-positive hepatocellular carcinoma and with chronic hepatitis B infection. 22 73

Six patients with hepatitis B surface antigen-positive (HBsAg-pos) chronic liver disease have been treated with transfer factor (TF) prepared from leucocytes of normal blood donors with no history of hepatitis, and with TF from subjects recently recovered from type B hepatitis. In three patients there were transient elevations of aspartate transaminase (AsT) after 'specific' TF, representing damage or destruction of hepatocytes, and in two of these patients there was coincidental complement consumption, suggesting that TF had stimulated production of antibody. In one other patient there was an increase in E-rosetting lymphocyte (ERL) concentration representing a change in T-lymphocyte reactivity. One of the two patients who had no measured response to TF had a primary liver cell carcinoma and was receiving prednisolone therapy. TF prepared from subjects who have recently recovered from type B hepatitis may have temporarily altered the immunological status of patients with HBsAg-pos chronic liver disease, but it did not have a beneficial therapeutic effect.
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PMID:Transfer factor in the attempted treatment of patients with HBsAg-positive chronic liver disease. 60 32

The sensitivities of three technqiues used to detect serum hepatitis B surface antigen (HBsAg) were compared in 411 patients with various types of chronic liver disease. Counterimmunoelectrophoresis proved an unreliable test. Two haemagglutination technqiues were slightly less sensitive than radioimmunoassay but were more rapidly performed. Less sensitive techniques were particularly unreliable in active liver disease where HBsAg titres were low. HBsAg was detected in patients with chronic persistent hepatitis, alcoholic liver disease, chronic active liver disease with or without cirrhosis, and primary liver cell carcinoma. Forty-six of the 68 (68%) HBsAg positive subjects were males coming from outside the United Kingdom. The HBsAg titres in 13 subjects with chronic persistent hepatitis were significantly higher (P less than 0-001) than those in 43 subjects with chronic active liver disease. Corticosteroid therapy did not alter the HBsAg titre significantly. None of the 28 HBsAg positive subjects studied serially for up to two years cleared HBsAg from the serum. Anti-HBs was examined by passive haemagglutination and found in 35 subjects, 26 of whom had no evidence of liver disease, 80% came from abroad. Anti-HBs was believed to be of epidemiological rather than of pathological importance.
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PMID:Detection, by three techniques, of hepatitis B surface antigen (HBsAg) and determination of HBsAg and anti-HBs titres in patients with chronic liver disease. 83 98

Fifty Kenyan patients with chronic liver disease or hepatocellular carcinoma were tested for hepatitis B surface antigenaemia by radioimmunoassay. The hepatitis B surface antigen was detected in 77% of the patients with chronic persistent or chronic aggressive hepatitis, or cirrhosis confirmed by liver biopsy, compared with 15% in a control group. All six patients with hepatocellular carcinoma had detectable hepatitis B surface antigen or antibody. 50% of the controls had hepatitis B surface antibody in their plasma detectable by haemagglutination. Auto-immune associated liver disease appeared infrequent. The possibility that the hepatitis B virus is an important cause of cirrhosis in Kenya is discussed.
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PMID:Hepatitis B surface antigenaemia in Kenyans with chronic liver disease. 84 49

In all of 12 patients with chronic liver disease, whose platelet dynamics were investigated by the 51Cr-labelling technique in association with surface counting, platelet survival was reduced and in 11 the splenic platelet pool was increased. Surface counting showed high initial spleen liver ratios in eight patients, and in four there was evidence of progressive destruction of platelets in the spleen. In one patient, subsequently shown to have a hepatoma, progressive accumulation of platelets was noted at the tumour site.
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PMID:Platelet dynamics in chronic liver disease with special reference to the role of the spleen. 85 32

A quantitative immunoenzymatic assay has been developed for alpha-fetoprotein which is sensitive and specific. Seventy-eight percent of United States hepatoma patients have detectable serum alpha-fetoprotein elevations over 50 ng/ml, whereas only 2 of 93 other gastrointestinal tumors were positive. Thirteen percent of patients with acute viral hepatitis, 44% of patients with massive hepatic necrosis, and 23% of patients with chronic active hepatitis had measurable serum alpha-fetoprotein concentrations. However, patients with non-viral acute or chronic liver disease were largely alpha-fetoprotein negative and alpha-fetoprotein was undetectable on multiple postoperative samples from 6 patients after hepatic lobectomy in the rapidly regenerating phase. Therefore, alpha-fetoprotein elevations in nonmalignant liver diseases are not due solely to hepatic regeneration but appear to be related to viral injury. The immunoenzymatic assay does not require purified antigen or radioisotope equipment and can detect and quantitate clinically significant alpha-fetoprotein levels greater than 50 ng/ml.
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PMID:Serum alpha-fetoprotein (AFP) in benign and malignant gastrointestinal diseases: evaluation of an immunoenzymatic assay. 112 34

Sera from Japanese patients with chronic liver disease were tested for hepatitis B virus (HBV) markers and antibodies to hepatitis C virus (anti-HCV), and the results were correlated to the presence of hepatocellular carcinoma. In chronic non-A, non-B liver disease, anti-HCV prevalence was high both in patients with hepatocellular carcinoma (78/89, 88%) and without it (66/84, 79%), while previous HBV infection was more common in patients with hepatocellular carcinoma (65/89, 73%) than in those without it (46/84, 55%) (P less than 0.05). Coexistence of anti-HCV and antibodies to HBV was observed frequently in patients with hepatocellular carcinoma (56/89, 63%) compared with patients without it (39/84, 46%) (P less than 0.05). In chronic HBV carriers, anti-HCV was more common in patients with hepatocellular carcinoma (12/38, 32%) than in those without it (3/62, 5%) (P less than 0.01). These results suggest that infection with the two viruses may be a risk factor for more serious liver disease.
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PMID:Hepatitis B virus markers and antibodies to hepatitis C virus in Japanese patients with hepatocellular carcinoma. 130 50

To investigate the prevalence of antibody to hepatitis C virus (anti-HCV) in heavy drinkers with liver disease in Japan, we tested serum samples from 113 heavy drinkers with liver disease and 121 without liver disease. All were negative for HBsAg with no history of blood transfusion. These subjects had consumed more than 80 g of ethanol daily for 5 years or more. Findings for anti-HCV determined by recombinant immunoblot assay testing were positive in 14 (35.9%) of the 39 patients with liver cirrhosis, 14 (58.3%) of the 24 patients with hepatocellular carcinoma and in 8 (53.3%) of the 15 patients with chronic hepatitis. The anti-HCV positive rate in the drinkers with these liver diseases was significantly higher than in those with such disorders as fatty liver (0/10), hepatic fibrosis (0/22), and alcoholic hepatitis (0/3), as well as in the alcoholics without liver disease (5/121, 4.2%). Considering histologic findings in the anti-HCV positive cirrhotics, the occurrence of lymph follicle formation (71.4%), piecemeal necrosis (78.6%) and loose fibrosis (64.3%) were observed to a significantly higher extent than in cirrhotics who were negative for anti-HCV. These findings suggest that advanced chronic liver disease among heavy drinkers in Japan, especially of hepatocellular carcinoma, is closely associated with HCV infection. In the livers of heavy drinkers who were positive for anti-HCV, histologic findings indicated the possibility of viral infection.
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PMID:High prevalence of antibody to hepatitis C virus in heavy drinkers with chronic liver diseases in Japan. 131 67

Homozygous alpha 1-antitrypsin deficiency (PiZZ phenotype) is known to be associated with increased risk of cirrhosis and primary liver cancer. Although a relationship between heterozygous alpha 1-antitrypsin deficiency and chronic liver disease was suggested recently, it is still a matter of controversy whether such patients are at increased risk of liver cancer. The goal of this study was to determine the prevalence of heterozygous alpha 1-antitrypsin deficiency of different phenotypes among patients with primary hepatobiliary cancers. We studied 82 patients with primary hepatobiliary cancer; 59 had hepatocellular carcinoma and 23 had bile duct carcinoma. alpha 1-Antitrypsin quantitation and phenotyping were performed in each patient using standard methods. The distribution of the various Pi phenotypes was compared with that found in a normal population and reported elsewhere. Odds-ratio and chi 2 tests were used to measure the relative risk and the significance of association, respectively, between primary hepatobiliary cancers and heterozygous alpha 1-antitrypsin deficiency. Four patients in each of the cancer groups were heterozygous. Among the hepatocellular carcinoma patients, three had the PiMS phenotype and one had the PiMZ phenotype. Of these four heterozygous patients, only two had cirrhosis; one had cryptogenic cirrhosis and the other had hepatitis B virus-related cirrhosis. One noncirrhotic patient with a PiMZ phenotype had a fibrolamellar carcinoma. Of the four patients with bile duct carcinoma, three had the PiMS phenotype and one had the PiMZ phenotype. Of the four heterozygous patients, two had primary sclerosing cholangitis without associated inflammatory bowel disease and one patient had had previous biliary operations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of increase in heterozygous alpha 1-antitrypsin deficiency phenotypes among patients with hepatocellular and bile duct carcinoma. 131 55


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