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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Significant liver disease including fatty metamorphosis, alcoholic hepatitis, cirrhosis, and hepatoma occur in two thirds of subjects who consume alcoholic beverages in sufficient quantities to interfere with work and social responsibilities; this is of major importance in the rapidly escalating morbidity and mortality from alcoholism. Chronic alcoholics should be routinely evaluated for the presence of altered liver function and structure. Clearance of indocyanine green using dichromatic ear densitometry and computer and analysis provides a simple and sensitive method for mass screening of such patients. Clinical studies of lymphocyte reactivity to purified alcoholic hyaline may be valuable in recognizing alcoholic hepatitis, the precursor of cirrhosis. Ethanol toxicity, malnutrition and constitutional factors contribute to the development of hepatic fibrosis and cirrhosis in alcoholics. Ethanol and/or acetaldehyde and the supernatant from lymphocytes stimulated by alcoholic hyaline cause a significant increase in the incorporation of proline into collagen of the damaged liver. Abstinence and correction of nutrient deficits are the cornerstones of treatment for alcoholic liver disease; a daily meal and dietary supplements should be provided for those with liver injury who continue to imbibe. Alcoholics with progressive liver disease despite supportive therapy may be aided by pharmacologic agents which suppress immunologic response and reduce fibrogenesis.
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PMID:Liver disease of the alcoholic. 16 41

Basal energy expenditure was measured by indirect calorimetry in 12 cirrhotic patients with hepatocellular carcinoma. Values were compared to those observed in 12 cirrhotic patients without hepatocellular carcinoma but with similar nutrition status. Energy expenditure was also predicted in each patient by the Harris-Benedict equation. Basal energy expenditure, whether expressed as kilocalorie per day or corrected for kilogram body weight or for kilogram fat-free mass, was found increased in cirrhotic patients with hepatocellular carcinoma. These patients expended an average of 250 kcal/day more than was expected given their body size. The highest values were observed in the patients who experienced a recent significant weight loss. Our study demonstrates that the presence of hepatocellular carcinoma on liver cirrhosis increases the metabolic rate of patients. This factor could contribute to progressive malnutrition in patients with hepatocellular carcinoma and should be taken into consideration when these patients are given nutritional support.
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PMID:Increased energy expenditure in cirrhotic patients with hepatocellular carcinoma. 142 84

Progressive degrees of metabolic alterations are frequent in cirrhosis impairing peripheral tissue and body composition. Hepatocellular carcinoma worsens protein wasting and malnutrition. A normal energy production rate and an abnormal substrate oxidation rate are well-known findings in cirrhosis; however, no data are available on cirrhotic patients with hepatocellular carcinoma. The aim of this study was to measure oxidative metabolism in cirrhotic patients with and without hepatocellular carcinoma and to investigate the correlation between energy production rate, respiratory quotient and nutritional state. Thirteen male cirrhotic patients with hepatocellular carcinoma (8 well-nourished and 5 malnourished) were compared with 17 cirrhotic patients without hepatocellular carcinoma (11 well-nourished and 6 malnourished) and six controls who were age and sex matched. A diagnosis of malnutrition was made if the fat mass percentage was reduced to less than 20% of the patient's body weight. Indirect calorimetry was performed between 8 and 10 AM, after a 12-hr fast, for 30 min (with a 10-min steady-state period), and measured energy production rate was calculated according to Weir's formula. Body composition was assessed by means of the Durnin and Womersley formula. Anthropometry and bioelectric impedance analysis showed no variations in kilograms of fat-free mass in our malnourished patients. Our data show that, when the energy production rate is measured while the patient is at rest and corrected for fat-free mass, the energy requirements of cirrhotic patients and cirrhotic patients with hepatocellular carcinoma matched that of the controls, regardless of nutritional state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxidative metabolism in cirrhotic patients with and without hepatocellular carcinoma: effects of malnutrition. 133 Aug 66

Chylous ascites is a rare complication of cirrhosis. We report 20 cirrhotic patients with chylous ascites seen between 1976 and 1989. Hepatocellular carcinoma was associated in 2 cases and, in 5 cases, chylous ascites followed surgery (portosystemic shunt in 4 cases). Chylous ascites was spontaneous in the 13 other cases. Prevalence of chylous ascites was 1.1 p. 100 in the cirrhotic population with ascites observed between 1983 and 1988. Chylous ascites, whether spontaneous or postoperative, was almost always refractory to medical treatment (16 of 18 patients). Treatment by Le Veen shunt was unsuccessful in 4 patients and lead to infection in 2 cases. Four of 6 patients treated by portocaval shunt died during the first postoperative month. Repeated paracentesis should be preferred, but this can be complicated by malnutrition. Seven of 10 alcoholic cirrhotics with spontaneous chylous ascites and 2 of 4 patients with postoperative chylous ascites died during the year following diagnosis. In view of this poor prognosis, hepatic transplantation should be considered early in selected patients.
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PMID:[Chylous ascites in cirrhosis. Retrospective study of 20 cases]. 217 27

The feeding for 10 or 11 weeks of young male Fischer-344 rats, a diet devoid of choline and low in methionine, leads to the appearance of gamma-glutamyltransferase-positive foci of altered hepatocytes in the liver and to the induction of initiated resistant hepatocytes. The latter are known to contain the primary precursor cells for the ultimate development of hepatocellular carcinoma. This initiation of carcinogenesis with the choline-devoid diet is prevented by added choline. These observations indicate that a dietary deficiency may, by itself, without known contaminating or added carcinogens, initiate the carcinogenic process.
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PMID:Initiation of carcinogenesis by a dietary deficiency of choline in the absence of added carcinogens. 288 29

The cancers consistently associated with ingestion of alcohol, the head and neck cancers, are also associated with tobacco use and arise from epithelia that are in direct contact with both agents. Tobacco smoking-related cancers at sites not directly in contact with alcoholic beverages, that is, lung, bladder, and perhaps pancreas, do not consistently show a relationship to alcohol consumption, although lung and pancreatic tumors are associated in some studies. Liver cancer was thought to be strongly related to alcohol consumption on epidemiological grounds and because of its relationship to cirrhosis. As knowledge of the viral etiology of some cirrhoses has evolved and as methods to detect viruses have developed, the significant association between hepatitis B virus and hepatocellular carcinoma has become clear. Alcohol and hepatitis B virus may interact in the etiology of the disease and have important separate roles as well. There are epidemiologic and experimental data showing that malnutrition (resulting from poor food choice), economic deprivation, or alcoholism contributes to the risk for head, neck, and liver cancers. Colon cancers occur about equally in men and women, are found in well-nourished populations, and are not associated with tobacco smoking. Rectal cancers show a preponderance of cases in men but are frequently found in women as well and are not thought to be associated with smoking or malnutrition. The association between colorectal cancers and alcohol consumption, when it is found, apparently occurs at even relatively low alcohol intakes and is often stronger for consumption of beer than of other beverages. Nutritional and metabolic mechanisms proposed for the influence of alcohol on carcinogenesis are supported by studies in human subjects and laboratory animals. Animal models are needed in which effects of ethanol on carcinogenesis can be consistently demonstrated and which can then be used to examine mechanisms.
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PMID:Alcohol and cancer. 303 1

Orthotopic liver transplantation began in Brisbane in January 1985. During the first two years of the programme an assessment committee evaluated 55 patients (38 adults, 17 children). Patients were either accepted for transplantation, rejected as unsuitable or deferred for elective reassessment. All of the 10 adults who were rejected for transplantation because they had "too advanced" disease died within four months of assessment. Six children who were accepted for transplantation died before a suitable donor liver could be found. In the first two years, 21 orthotopic liver transplantations were performed on 18 patients (adults, 13 patients; children, five patients). Fifteen of 21 grafts were procured from within Queensland. Twelve (67%) patients are alive at three to 23 months and all have been discharged from hospital. Deaths in adults were due to sepsis (three patients), aspiration pneumonitis (one patient), rejection and hepatic artery thrombosis (one patient) and the recurrence of a hepatocellular carcinoma five months after discharge from hospital (one patient). Two patients underwent a second transplantation procedure because of chronic rejection at four months and at 11 months, respectively, after the initial operation. One patient received a second transplant for primary graft failure at four days after the operation. A scoring system which considered the presence of pre-operative patient factors, such as coma, ascites, malnutrition and previous abdominal surgery, partly predicted the operative blood loss and patient survival. In conclusion, orthotopic liver transplantation is being performed in Australia with survival rates that are comparable with those of established overseas units.
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PMID:The Queensland Liver Transplant Programme: the first two years. 330 93

HCC occurs in a higher incidence in some subsets of human populations residing in specific geographic areas around the world. These include black populations residing south of the Sahara, particularly in South and East Africa; in populations of Southeast Asia and the Western Pacific; in India, China, and in some other circumscribed areas. These epidemiologic observations strongly suggest that environmental factors are involved in the etiology of HCC. Evidence from human and animal data point toward a multicausal etiology, including dietary or environmental contamination with mycotoxin carcinogens, acting in concert with hepatitis B viral infection and, in some areas, with malnutrition. Dietary factors that appear to influence susceptibility to HCC include fat, protein and amino acids, vitamin A, selenium, and zinc. In addition, alcohol consumption, environmental chemicals that are natural or man made, and genetic predisposition must also be considered. It seems likely that identification of etiologic agents (hepatitis B infection, aflatoxin, malnutrition) and correction or prevention of these are the most promising means for controlling HCC in man.
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PMID:Chemical carcinogenesis: mycotoxins and other chemicals to which humans are exposed. 608 58

The conversion of alcoholic hepatitis into cirrhosis and the eventual development of hepatocellular carcinoma (HCC) has been documented by serial biopsies in patients with uncomplicated alcoholism. Ethanol toxicity, nutritional deficiency and immunological abnormalities in a genetically predisposed individual appear to account for this sequence which can be accelerated by the hepatitis B virus and other noxious agents. Immune deficiency in malnourished alcoholics with liver disease diminishes response to the hepatitis B vaccine and may contribute to the development of HCC. Antigenic moieties in Mallory bodies appear to contribute directly to cytotoxicity and fibrosis in alcoholics, and may act like proto-oncogens. Available Mallory-body-specific monoclonal antibodies will hopefully facilitate diagnosis and treatment. Studies of DNA and collagen synthesis by in vitro perfusion of percutaneous liver biopsies provide information on precursor lesions of HCC. Abstinence, nutrient therapy and drug-induced anabolism lead to repair of liver damage and correction of immunological abnormalities, both of which may contribute to development of HCC in alcoholics with cirrhosis.
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PMID:Hepatocellular carcinoma in the alcoholic. 610 Feb 66

The important factors in the causation of hepatocellular carcinoma (HCC) in Africa include hepatitis B virus (HBV), aflatoxin and possibly malnutrition. The evidence in support of an association of HBV with HCC is mainly epidemiological and includes: (a) the similarity between the geographical distribution of chronic carriers of hepatitis B surface antigen (HBsAg) and that of HCC; (b) the increased prevalence of HBV markers in the serum of patients with HCC when compared with the general population; and (c) the observation that HBV infection precedes the general development of the tumour and that HBV infection increases the risk of HCC over 200-fold. Laboratory evidence has shown that HBV DNA is integrated in the host tissue in patients with HCC. A vaccination programme in Senegal showed that hepatitis B vaccine reduced HBV infection and it is hoped that it will eventually lead to a reduction in HCC. Studies in East Africa have shown a correlation between aflatoxin contamination and the incidence of HCC. The possible roles of malnutrition and/or alcohol are discussed.
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PMID:Etiology of hepatocellular carcinoma in Africa. 610 Feb 89


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