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)

Between March 1982 and September 1983, 40 inpatients (25 men and 15 women, mean age 53 years) with alcoholic cirrhosis and total serum bilirubin greater than or equal to 5 mg per dl were studied. Those with hepatocellular carcinoma, renal failure, hyponatremia, septicemia, spontaneous bacterial peritonitis, gastrointestinal bleeding, and hepatic coma were excluded. Patients were studied for 28 days. The two groups were offered an oral diet containing 40 kcal per kg per day. Patients in the supplementary parenteral nutrition group received 40 kcal per kg per day and 200 mg nitrogen per kg per day using a central catheter. The major endpoint was total serum bilirubin on Day 28. On admission, serum bilirubin was not significantly different in the two groups: oral group, 12.5 +/- 6.6 mg per dl; supplementary parenteral nutrition group, 12.3 +/- 8.5 mg per dl. On Day 28, serum bilirubin was lower in the supplementary parenteral nutrition group (2.5 +/- 1.4 mg per dl) than in the oral group (4.1 +/- 2.2 mg per dl) (p less than 0.02). Serum bilirubin was also lower in the supplementary parenteral nutrition group than in the oral group on Days 7, 14 and 21 (p less than 0.05). Analysis of covariance, considering serum bilirubin on admission and at randomization and time between admission and randomization, confirmed these results. On Day 28, anthropometric parameters, serum transferrin, prealbumin and retinol-binding protein were higher in the supplementary parenteral nutrition group, but the differences were not significant. Serum albumin was significantly lower in the supplementary parenteral nutrition group. The incidence of encephalopathy and sepsis was not significantly different between the two groups.
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PMID:A randomized clinical trial of supplementary parenteral nutrition in jaundiced alcoholic cirrhotic patients. 308 33

Endoscopic injection sclerotherapy was given to 155 patients with esophageal varices mainly related to non-alcoholic liver cirrhosis. The formation of a superficial ulcer in the lower esophagus was achieved in 141 (91.0%) of the 155 patients, with an average of 4.1 sessions of endoscopic injection sclerotherapy during an average time of 4.9 weeks. The average volume of 5% ethanolamine oleate sclerosant used was 24.8, 19.2, 12.3 and 6.5 ml for the initial to fourth sessions of endoscopic injection sclerotherapy, respectively. For 14 patients, a sufficient number of sessions of endoscopic injection sclerotherapy could not be given: 10 early deaths (5 hepatoma, 4 liver failure and 1 gastric bleeding), and 4 refused further sessions. When the esophageal mucosa had been eliminated and a superficial ulcer had formed, episodes of recurrent bleeding or recurrence of esophageal varices were nil over a median follow-up of 14.6 months, with a range of 1 to 27 months. In seven patients, bleeding recurred before elimination of the mucosa could be achieved, but these bleeding episodes were well controlled with an additional session of endoscopic injection sclerotherapy. At the time of analysis, there were 36 deaths (20 hepatoma, 14 liver failure and 2 gastric bleeding) among these 155 patients. Thus, the mean follow-up was 16.3 months (range: 7 to 27 months) in the 119 survivors, with no recurrence of the varices. We propose that removal of the esophageal mucosa may well be the endpoint of repeated endoscopic injection sclerotherapy in the management of patients on injection sclerotherapy.
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PMID:Prevention of recurrence of esophageal varices after endoscopic injection sclerotherapy with ethanolamine oleate. 349 73

Nine hundred and ninety nine patients were admitted in our Department (the Third Department of Internal Medicine, School of Medicine, UOEH) during the five years more since the opening date of the University Hospital (July, 9, 1979), and 864 cases in them (86.2%) suffered from the various digestive diseases. Most of the in-patients with digestive diseases in our Department are resident in Kitakyushu city and its suburbs, especially in Yahatanishi-ku, Wakamatsu-ku and Onga county, therefore, it may be possible to investigate the ecological characteristics of the in-patients of our Department in the relation to the outbreak, clinical course and outcome of the digestive diseases. Namely, it may be assumed that the incidence and prevalence of the idiopathic inflammatory bowel disease (IBD) including ulcerative colitis and Crohn's disease are relatively high in this area (Kitakyushu city and its suburbs) as compared with the average of all Japan. Although the true causes of these illness are still unknown, the inclination of haptoglobin phenotypes (HP) which include 2-2, 2-1 & 1-1 type 1-1 strongly suggests to the association with some genetical factors on the high incidence of these diseases (IBD). In this connection, Hp type 1-1 were recognized 4 in 11 cases (36.4%) with ulcerative colitis, and 3 in 7 cases (42.9%) with Crohn's disease in our Department whereas only 3-5% in normal controls. Secondly, the patients with carcinoma of the biliary tree (bile duct and gall bladder) are relatively more, namely, 17 cases of bile duct cancer and 3 cases of gall bladder cancer were admitted in our Department during this term. It is interesting to note that hepatohilar type of the bile duct cancer was observed comparatively high (4 in 17 cases, 52.9%) in the past five years-more although the etiology is unknown. Finally, several characteristics in liver diseases particularly in viral hepatitis were illustrated in this study, namely, the ratio of transient HBV infection to whole (transient and persistent) HBV infection in the patients with acute viral hepatitis (due to HBV) is high (80.9%), HBeAg positivity is high in chronic B-hepatitis (44.9%), the ratio of alcoholic cirrhosis to whole liver cirrhosis is relatively high (34.9%) and HBsAg positivity is lower in liver cirrhosis due to non-alcoholic origin (mainly due to hepatitis virus) than the average of this country, and also, hepatocellular carcinoma (HCC) without liver cirrhosis is higher (23.0%) than the average of whole Japan (less than 15%) statistically.
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PMID:[Ecological approach to the patients with digestive diseases in Kitakyushu City and its suburbs]. 372 13

Carcinoembryonic antigen (CEA) was measured in whole serum and in serum extracted with perchloric acid by microradioimmunoassay in patients with benign and malignant diseases of the liver and pancreas. The level of detectability was 5 ng per ml. This level or greater was present in the serum of 50% of patients with chronic diffuse liver disease, 64% with pancreatitis, 94% with cancer of the digestive system, and 3% of controls. The incidence of levels of CEA of 5 ng/ml or more differed for various categories of chronic liver disease: from 22% in active chronic hepatitis, 46% in primary biliary cirrhosis, 63% in hepatoma, 78% in cryptogenic cirrhosis, and 88% in alcoholic cirrhosis; levels of CEA correlated with degrees of impairment of liver function as judged by bromsulphalein retention and serum levels of alkaline phosphatase and transaminase. In pancreatitis, 64% of cases had levels of CEA ranging from 5 to 20 ng/ml and in cancer of the pancreas 94% had levels above 5 ng/ml and 50% above 20 ng/ml.
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PMID:Carcinoembryonic antigen in serum in diseases of the liver and pancreas. 472 56

The precise nature of the relationship between cirrhosis and HCC remains to be elucidated. However, it seems likely that no single explanation will cover the various forms the association takes in different parts of the world. In the high HCC incidence regions of sub- Saharan Africa and the Far East, an etiology common to the two disorders, HBV and possibly other hepatitis viruses, seems to account for the majority of cases. The role of aflatoxin in these areas is uncertain because it appears not to cause cirrhosis in man. In populations in which HCC is uncommon, alcoholic cirrhosis is the most frequent association of HCC. There is no convincing evidence to support a shared etiology in this situation because alcohol has not thus far been proved to be directly oncogenic for the liver. Possibly, cirrhosis renders the hepatocytes more susceptible to environmental carcinogenic factors. The same explanation may apply to hemochromatosis. There is at present little evidence for the postulate that HCC is an inevitable consequence of the hyperplasia of cirrhosis.
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PMID:Relationship between hepatocellular carcinoma and cirrhosis. 608 59

The aetiological associations of hepatocellular carcinoma in 25 White South African patients were assessed. The most frequent association was cirrhosis, which was present in 13 out of 23 patients (56,5%)--7 had alcoholic cirrhosis, 5 (including 1 of those with alcoholic cirrhosis) markers of current or past hepatitis B virus infection, 1 idiopathic haemochromatosis, and 1 no obvious cause. Two further patients in whom the presence or absence of cirrhosis could not be ascertained with certainty also drank to excess. Markers of current hepatitis B virus infection were detected in 24,5% of the patients and evidence of current or past infection in 45,5%. These prevalences are lower than those in matched South African Blacks with hepatocellular carcinoma, but are significantly higher than those in White blood donors. Two young female patients had taken oral contraceptives and another had taken conjugated equine oestrogens.
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PMID:Hepatocellular carcinoma in white South Africans--aetiological considerations. 609 67

To assess the natural history of non-alcoholic liver cirrhosis, one hundred and eighty medically treated Japanese cases, including 110 accompanied by esophageal varices were investigated retrospectively. Among those patients with varices fifty-one (46.4%) bled from the upper gastrointestinal (GI) tract and thirty-two (29.1%) from esophageal varices, while GI bleeding was found in only six out of 70 patients without varices. The GI bleeding rate was the highest in patients with varices and concomitant hepatoma (76.5%). The mortality rate of the GI bleeders was 68.6% in patients with varices and 33.3% in patients without varices. The mortality on the first variceal bleeding episode was 65.6%, and another 25.0% had rebleeding from varices, resulting in a one-year survival of 9.4%. The ten-year cumulative percentage of variceal bleeding was 61.2% in patients with varices, and that of occurrence of hepatoma was 50.7% in total of 180 patients. This study revealed that the non-alcoholic cirrhotic patients have a highly rate of complication by hepatoma and that the development of hepatoma doubles the risk of varix rupture.
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PMID:The natural history of non-alcoholic cirrhosis. 609 96

The authors report the case of a patient with alcoholic cirrhosis in whom the appearance of a hepatocarcinoma coincided with the appearance of an "asymptomatic" monoclonal gammaglobulinopathy and hypercalcaemia attributed to a probable paraneoplastic syndrome. The authors discuss the hypotheses which have been proposed to explain the link between monoclonal gammaglobulinopathy and cancer and they stress the particular case of hepatocarcinoma in which the association has been rarely reported. They also review the diagnostic criteria of paraneoplastic hypercalcaemia.
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PMID:[Hepatoma manifesting monoclonal gammapathy and hypercalcemia]. 609 84

In most cases, primary liver carcinoma in tropical areas remains an hepatoma. The high incidence of this malignant tumor of the liver in some regions, and especially in black Africa, is still unexplained. As compared with the form found either in the European or in the North-African, this hepatoma shows special features since it occurs in younger people (35 years), follows a bursting-out course and is precipitously associated not to an alcoholic cirrhosis but to a post-hepatitic one. An humoral syndrome leading to a presomptive diagnosis consists of hypoglycemia, hypercholesterolemia, hyperlipemia, and high blood level of alcaline phosphatases. In 85% of the cases, these tumors secrete an alpha fetoprotein determined by radioimmunoassay. A major etiologic factor is the oncogenous activity of hepatitis virus B which could be either an induction factor or a "co-factor" which would initiate, facilitate or increase the activity of the carcinogen. In this respect, aflatoxin has to be regarded as a "co-factor" too. The best treatment, when it is possible, is an exeresis carried out through a partial hepatectomy. If such a surgical intervention is unadvisable, chemotherapy is the only possibility. Immunization against viral hepatitis has raised hope for the prophylaxis of hepatoma. But it will not be possible to evaluate it before the year 2.000.
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PMID:[Primary liver cancer in the tropical environment. Classical and current data]. 619 92

A review of 180 patients with either chronic hepatitis or hepatocellular carcinoma (HCC) indicate a significant association. 40 patients with chronic hepatitis were seen between 1975-79. 6/25 of chronic active hepatitis and 7/15 with chronic persistent hepatitis were HBsAg positive (RIA). In the 41 patients with HCC, 15 (37%) were alcoholic, 10 cirrhosis (HBsAg positive), 5 haemochromatosis 5 cryptogenic cirrhosis, 2 probably due to sex steroids and in 4 no aetiological factor was apparent. HBsAg was present in 10/22 (45%) of HCC with cirrhosis, 15/256 (6%) for alcoholic cirrhosis, 5/16 (33%) for haemachromatosis and 5/30 (16%) cryptogenic cirrhosis. 8/80 (10%) who had acute viral hepatitis (B) are antigen positive at 6 months. This report shows that Hepatitis B virus infection is now a significant causes of liver injury in 180 patients studied. The majority of patients who have HBsAg positive cirrhosis do not have a history of acute hepatitis.
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PMID:An Australian experience of hepatitis B infection, cirrhosis and hepatocellular carcinoma. 625 12


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