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)

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

We have reported here 38 cases of hepatoma observed over a period of 3 1/2 years in a Paris hospital, and recall the main circumstances of discovery of this primary tumour of the liver. Clinically, hepatomegaly with a hard, painful border, increasing rapidly in volume in a patient with a past history of alcoholism and with a poor general condition, remains the best sign. More often, decompensated cirrhosis is the only sign and may lead to the wrong diagnosis, until alphafoetoprotein estimation and laparoscopy are carried out. Unfortunately, the almost constant presence of cirrhosis, usually diffuse, and the pluricentric character of the hepatoma, make any attempt at removal immpossible. Treatment consists simply of the administration of analgesics whilst awaiting a fatal issue within 3 to 4 months. We believe that it is useful to have constantly in mind this terminal complication of cirrhosis as, at present, among the direct or associated causes of death from cirrhosis, hepatomas seem to account for about 20%.
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PMID:[Clinical and developmental aspects of hepatoma]. 18 Aug 63

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.
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PMID:[Fever and liver cirrhosis]. 22 38

Among 7763 autopsies performed in Greater Copenhagen in 1973, there were 309 cases of cirrhosis of the liver and 52 cases of primary carcinoma of the liver (PCL). Of the latter, 45 were hepatocellular carcinoma (HCC), 4 combined HCC and cholangiocarcinoma (CCC) and 3 CCC. HCC was found in 7.8 per cent of the cirrhotic livers and was in 57.1 per cent accompagnied by cirrhosis. The criteria of WHO, Peters (modified) and Anthony were used for classification. The degree of differentiation of the tumours was estimated using the criteria of WHO and Edmondson. The apparently small number of CCC may be due to the fact that this tumour is often overdiagnosed at the expense of HCC. The incidence of combined tumours is probably higher than generally assumed. The reticulin stain was found very valuable in HCC, both for descriptive and diagnostic purposes. In contrast to the situation in sub-Saharan Africa where hepatitis B virus is incriminated as the most important etiologic factor of HCC, it was found in the present study that alcoholism was a very essential cause of cirrhosis and thereby of HCC.
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PMID:Primary carcinoma of the liver. A histological study of 52 cases from Denmark. 22 41

Alcohol and tobacco appear to act synergistically in the pathogenesis of epithelial cancers of the oropharynx (excluding lip), larynx, and esophagus. For the subsites within the upper aerodigestive tract, over 10,000 deaths in United States men during 1978 may be attributed to tobacco and alcohol consumption. The cancer sites for which tobacco and alcohol are major determinants occur with greater frequency in men, blacks, lower socioeconomic groups, and with increasing urbanization and increasing age (35--70 years). Because primary hepatocellular carcinoma occurs more commonly in patients with cirrhosis, chronic alcohol abuse is an important risk mechanism for carcinoma of the liver parenchyma. Although experimental animal studies have failed to demonstrate whether ethanol can independently initiate tumorigenesis, various alternative or associated biochemical and immunological mechanisms of action have been proposed.
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PMID:Alcohol as a co-factor in the etiology of cancer. 44 84

Our knowledge of the cellular changes that lead to liver cell carcinoma in humans is limited by proper and necessary ethical restriction on clinical research. We know rather more about risk factors, the most important of which is cirrhosis, it seems that both the causative agent and the time of duration of the cirrhotic process are relevent to the magnitude of this risk. According to present knowledge, alpha1-antitrypsin deficiency, alcoholism, naturally occurring carcinogens, drugs, and the hepatitis B virus seem to carry the greatest risk of cancer developing in a cirrhotic patient. Cirrhosis, however, is not an essential prerequisite, and some or possibly all of these agents can also induce cancer without cirrhosis. Bile duct carcinoma commonly follows infestation with liver flukes. Cirrhosis is usually absent but duct epithelial hyperplasia is present prior to the development of cancer. Many cellular changes have been observed in patients and among populations considered to be at risk from liver cancer. Of these, liver cell dysplasia is the most striking and studies of its prevalence, natural history, and association with cirrhosis suggest that it is a precancerous change.
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PMID:Precursor lesions for liver cancer in humans. 77 94

Acute alcoholic hepatitis is an anatomical (fatty liver with sclerosing hyaline necrosis) and a clinical (hepatomegaly with a variety of symptoms of hepatic failure) entity arising out of chronic alcoholism, and of a typically 'pre-cirrhotic' state. Although fatal in 25% of acute cases due to failure of homeostasis, it often leaves a centrilobular scarring necrosis which in more than 60% of cases progresses to nodular cirrhosis. Continued alcoholism worsens the prognosis. Alcoholic hepatitis may be confused with acute abdominal catastrophes or with a hepatoma. The characteristic Mallory bodies found on liver biopsy are found rarely in non-alcoholic hepatitis. There is no effective treatment for this disease except reduction of alcohol intake; indeed, the disease may become self-perpetuating.
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PMID:[Acute alcoholic hepatitis]. 92 58

Alcoholism is the most common form of drug abuse and alcoholic liver disease is a major health problem which in terms of increasing incidence is only rivaled by viral hepatitis. Cirrhosis of the liver, most of which is probably alcoholic, is among the leading causes of morbidity and mortality between the ages of 25 to 65 in Western countries. Alcoholic liver disease includes adaptive and toxic ultrastructural alterations, alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis, later accompanied by hepatoma.
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PMID:[Biochemical and clinical aspects of alcoholic liver damage]. 100 21

To clarify the relationship between hepatitis C virus (HCV) infection and hepatocellular carcinoma (HCC), frozen serum samples from 213 patients with histologically proven liver cirrhosis alone (96 alcoholics, 59 HBsAg positive, 29 non-A, non-B hepatitis, 29 cryptogenic) and 40 patients with liver cirrhosis and HCC (12 alcoholics, 7 HBsAg positive, 7 non-A, non-B hepatitis, 14 cryptogenic) were analyzed for antibodies to hepatitis C virus (anti-HCV) with the ortho-HCV-ELISA. The results were as follows. 50 of 253 (20%) patients were anti-HCV positive. The prevalence of anti-HCV was significantly higher in patients with HCC than in patients without HCC (14 of 40 [35%] vs 36 of 213 [17%]; p less than 0.001). In anti-HCV-positive patients HCC were significantly more frequent than in anti-HCV-negative patients (14 of 50 [28%] vs 26 of 203 [13%]; p less than 0.001). The significantly higher occurrence of HCC in anti-HCV-positive patients was not related to other known risk factors such as alcoholism or chronic hepatitis B virus (HBV) infection. Patients with HCV infection as the only risk factor also had a significantly higher occurrence of HCC (12 of 38 [32%] vs 26 of 203 [13%]; p less than 0.001). Our data suggest that chronic HCV infection plays an important role in the pathogenesis of HCC, in particular in patients with cirrhosis unrelated to alcohol or HBV infection.
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PMID:[Hepatitis-C virus and hepatoma]. 131 Nov 25

The presence of antibody to the hepatitis C virus was determined in 254 alcoholic patients with non-B chronic hepatitis and a titre of antinuclear antibodies of 1/40 or lower. Alcoholic hepatitis was present in 12 patients, steatohepatitis in 20, active chronic hepatitis in 22, cirrhosis in 181, and hepatocarcinoma in 19. Twenty patients had previously received blood transfusion alone or during surgery, 49 had undergone previous surgery without transfusion, a clinical episode of hepatitis could be traced in 14, 4 patients were drug addicts, 41 had received blood transfusion after the diagnosis was made, and 128 presented with alcoholism alone. Anti-hepatitis C antibody was found in 20 out of 2,000 blood donors (1%) in our hospital. Anti-hepatitis C antibody was found in 87 patients (34.2%) in our series, a figure unaltered by past medical history. Patients with anti-HC antibody had higher levels of AST, ALT, total proteins, gamma-globulin, and IgG. The incidence of active chronic hepatitis was higher among patients with anti-HC antibody, whereas the incidence of steatohepatitis was higher among patients without anti-HC. Regarding findings on liver biopsy, the incidence of anti-HC was significantly higher (p less than 0.001) among patients with active chronic hepatitis (72.7%) than in any other group; no significant differences were found between patients with cirrhosis (33.3%), hepatocarcinoma (31.5%), steatohepatitis (15%), or alcoholic hepatitis (16.7%). Among HBsAg-negative patients, the incidence of anti-HC was similar between those with (39.7%) and without other serum markers of HB (32.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence and significance of the C virus antibody in chronic hepatopathy not related to B virus in alcoholics]. 131 33


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