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)

Alcoholic liver disease evolves from fatty change through alcoholic hepatitis to alcoholic cirrhosis. Its development is associated with an excess mortality both in relation to the presence of liver disease and to other complications of alcohol abuse. In the majority of patients fatty liver is a benign lesion which will reverse completely following abstinence from alcohol. Continued drinking is associated with the eventual development of cirrhosis in approximately 20% of individuals. Survival rates of 70% are reported both at 2 years and at 10 years. Alcoholic hepatitis is a precirrhotic lesion; progression to cirrhosis is observed more commonly in women, in individuals with severe disease and in those who continue to drink. Thirty-day mortality rates of less than 20% are observed in patients with mild to moderate disease but exceed 40% in individuals with severe liver injury. Corticosteroids may improve short term survival in a small subgroup of patients with severe alcoholic hepatitis. Survival rates of 55 to 60% are reported both at 2 years and at 10 years. Survival is significantly reduced in women and in the elderly and is adversely affected by the presence of severe liver injury, evolution to cirrhosis and continued drinking. Two-thirds of patients with alcoholic cirrhosis present with decompensated disease; 15% will develop hepatocellular carcinoma. Survival rates at 5 years vary from zero to 80%; 60 to 90% of individuals die of their liver disease. Survival is adversely affected by the presence of decompensated disease, superimposed alcoholic hepatitis, continued drinking and the development of hepatocellular carcinoma. The advent of hepatic transplantation, which has a 5-year survival rate in excess of 70%, will influence these survival figures.
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PMID:The prognosis and outcome of alcoholic liver disease. 897 53

The CD95 receptor is a death receptor capable of transducing apoptotic cell death upon ligation with the CD95 ligand (CD95L). The CD95/CD95L system plays a physiological role in apoptosis of lymphocytes and liver cells. In addition, the striking finding of acute hepatic failure in mice upon CD95 triggering has stimulated general interest in the involvement of CD95 mediated apoptosis in human liver disease. The currently available data point to a deregulated CD95 system in viral hepatitis, alcoholic hepatitis, acute hepatic failure of different etiology, diseases of the bile ducts, and hepatocellular carcinoma. Animal experiments suggest a causative relationship between CD95 activation and liver cell death, which, however, still has to be proven for liver disease in man. This review summarizes our present knowledge on CD95 mediated human liver disease.
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PMID:CD95-induced apoptosis in human liver disease. 960 11

It is well accepted that many patients with alcoholic hepatitis have an audible bruit over the liver (hepatic bruit) in western countries. However, this sign has not been discussed in Japan. The aim of this study was to assess the significance of the hepatic bruit in Japanese patients with alcoholic hepatitis. Hepatic bruit was specifically searched for on auscultation by two physician in consecutive patients (6 alcoholic hepatitis, 58 other alcoholic liver disease, 128 nonalcoholic liver disease including 16 hepatocellular carcinoma). Hepatic bruit was detected in 5 of 6 (83%) patients with alcoholic hepatitis, and in 1 of 16 (6%) patients with hepatocellular carcinoma. In any of other liver diseases, hepatic bruit was not detected. We conclude that hepatic bruit may be an important diagnostic finding in Japanese patient with alcoholic hepatitis as it is in western countries.
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PMID:[Clinical evaluation of hepatic bruit audible in patients with alcoholic hepatitis]. 961 1

We performed a case-control study to assess the role of hepatitis B virus (HBV), hepatitis C virus (HCV), GB virus C/hepatitis G virus (HGV), TT virus, alcohol intake, and tobacco smoking as risk factors for hepatocellular carcinoma (HCC) in the presence or absence of cirrhosis. We prospectively recruited 174 patients with a first diagnosis of HCC admitted to the main hospitals in Brescia, North Italy. On the basis of histological, clinical, and radiological criteria, the presence of cirrhosis was established in 142 cases, excluded in 21 cases, and remained undefined in 11 cases. Among the HCC cases without cirrhosis, a histological picture of normal liver was found in a single patient, chronic viral hepatitis was found in 11 patients, alcoholic hepatitis was found in 5 patients, nonspecific reactive hepatitis was found in 3 patients, and hemochromatosis was found in 1 patient. As controls, we also included 610 subjects unaffected by hepatic diseases and admitted to the same hospitals as cases. The odds ratios for having HCC according to positivity for HCV RNA, HBsAg and/or HBV DNA, and alcohol intake > 80 g/day (95% confidence interval) were as follows, in the presence and absence of cirrhosis, respectively: (a) 33.5 (17.7-63.4) and 19.7 (6-64.8) for HCV RNA; (b) 17.6 (9.0-34.4) and 20.3 (5.7-72.6) for HBsAg; and (c) 5.5 (3.1-9.7) and 4.6 (1.5-13.8) for alcohol intake. No association was found with HGV or TT virus infections or tobacco. This study has shown that most HCC cases arising in the area are due to HBV, HCV, or alcohol intake, in both the presence and absence of cirrhosis.
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PMID:Etiology of hepatocellular carcinoma in Italian patients with and without cirrhosis. 1069 84

Meta-analysis is increasingly used in hepatogastroenterology. Meta-analysis is of value to provide a systematic review of related trials and to display their results in an objective, easily understandable manner. When the trials are sufficiently homogeneous, meta-analysis can document the superiority, (a), or the lack of superiority (b) of a treatment with respect to another (e.g., (a) Interferon plus ribavirin vs Interferon for chronic hepatitis; (b) 5-ASA vs sulfasalazine for maintaining remission in ulcerative colitis). However the interpretation of meta-analysis requires caution. Meta-analysis can be unreliable or unstable if based on a few, small trials (e.g., Tamoxifen vs non-active treatment for hepatocellular carcinoma), or if distorted by confounding variables and publication bias (e.g., glucocorticoids vs standard treatment in alcoholic hepatitis). Eventually, qualitative heterogeneity makes the pooled results of meta-analysis meaningless or questionable (e.g., endoscopic sclerotherapy for prevention of first variceal bleeding in cirrhosis) and should prompt the search for its sources to plan future studies. Finally, meta-analysis of trials measuring the treatment effect of a drug vs a placebo when an active drug is available for comparison provides the limited informative content for the physician of the individual trials (e.g. 5-ASA vs placebo for maintaining remission in ulcerative colitis).
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PMID:Meta-analysis as a source of evidence in gastroenterology: a critical approach. 1073 May 66

The constellation of histopathologic lesions that characterize alcoholic and nonalcoholic steatohepatitis has been well described and has served as the basis for clinical diagnosis, natural history studies, and experimental models for analyses of etiopathogenesis. The lesions common to both entities include, to varying degrees, steatosis, liver cell ballooning, lobular inflammation with a notable component of polymorphonuclear leukocytes, and a characteristic form of fibrosis that is initially located in the perisinusoidal regions of acinar zone 3. Cirrhosis with or without steatosis or steatohepatitis may occur in both entities. Mallory's hyaline is common but not necessary; megamitochondria and varying amounts of iron may be observed in either process. Hepatocellular carcinoma is a recognized complication of both processes, albeit with greater frequency in the former. Alcoholic hepatitis may present with more severe clinical and histologic manifestations than the nonalcoholic counterpart, including significant morbidity and mortality. The perivenular lesions collectively referred to as sclerosing hyaline necrosis are markers of severity, and are not common in nonalcoholics. In many instances, however, the microscopic lesions of these two processes are similar, likely as a reflection of common pathogenetic pathways, and the distinction between the two is ultimately clinically derived.
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PMID:Alcoholic and nonalcoholic steatohepatitis. 1212 63

The role of reactive oxygen species (ROS) in liver disease is controversial. This mostly reflects the difficulties to quantify ROS in vivo, particularly in humans. We aimed to measure the presence of ROS in diseased human liver and identify possible relations between ROS levels and etiology, histology and hepatocyte proliferation. Liver biopsy specimens from 102 individuals: 18 healthy controls and 84 patients (42 HCV chronic hepatitis (CHC), 19 HBV chronic hepatitis (CHB), 7 PBC, 4 PSC, 4 HCV relapsing hepatitis after liver transplantation, 3 autoimmune hepatitis, 3 hepatocellular carcinoma, 2 alcoholic hepatitis) underwent analysis by radical-probe electron paramagnetic resonance (EPR). ROS in patients (median = 5 x 10(-6) mmol/mg) were higher than in controls (median = 3 x 10(-11) mmol/mg) (p < 0.001). Progressively increasing levels of ROS were recorded passing from control values to CHB (median = 4 x 10(-7) mmol/mg), CHC (median = 3 x 10(-6) mmol/mg) and PBC (median = 2 x 10(-5) mmol/mg), the differences being significant (p < 0.001). ROS in CHC positively correlated with histological disease activity (r = 0.92; p < 0.001). No correlation was found between ROS and hepatocyte proliferation rate, presence/degree of steatosis, serum ferritin levels and aminotransferases. ROS overproduction in liver appears to be a common thread linking different pathologic conditions and seems to be influenced by diseases' etiologies.
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PMID:Oxidative stress EPR measurement in human liver by radical-probe technique. Correlation with etiology, histology and cell proliferation. 1244 19

Mallory bodies (MBs) are aggresomes, composed of cytokeratin and various other proteins, which form in diseased liver because of disruption in the ubiquitin-proteasome protein degradation pathway. Heat shock proteins (hsp's) are thought to be involved in this process because it was discovered that MB formation is induced by heat shock in drug-primed mice. It has been reported that ubiquitin and a mutant form of ubiquitin (UBB(+1)) are found in aggresomes formed in the neurons in Alzheimer's disease and in the liver MBs in various liver diseases. In addition, hsp 70 has been found in aggresomes in Alzheimer's and in MBs in drug-primed mice. Therefore, we hypothesized that hsp's might be involved in MB formation in human liver diseases. Liver biopsy sections were double-stained using ubiquitin and hsp 70 or 90b antibodies. Both hsps 70 and 90b were found in MBs in all liver diseases investigated including primary billiary cirrhosis, nonalcoholic steatohepatitis, hepatitis B and C, idiopathic cirrhosis, alcoholic hepatitis, and hepatocellular carcinoma. Ubiquitin and the hsp's colocalized in all MBs in the diseased liver sections. These results indicate that hsp involvement in MB formation is similar to that seen in aggresome formation in other conformational diseases.
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PMID:Heat shock proteins are present in mallory bodies (cytokeratin aggresomes) in human liver biopsy specimens. 1271 Sep 48

Non alcoholic fatty liver disease (NAFLD) and its more agressive form, non alcoholic steatohepatitis (NASH) are entities that are becoming subject of interest of the medical community in general, especially because of the increased prevalence of diabetes and obesity in the world population. There is solid evidence linking NAFLD with the so called metabolic syndrome or syndrome X, to the point of accepting hepatic steatosis and its spectrum as one more element of the latter, along with diabetes, hipertension, hypertriglyceridemia and obesity. Insulin resistance seems to be the common link between these entities. Clinical evaluation of every patient with abnormal aminotransferase levels should take into account non alcoholic fatty liver and its spectrum, especially if the subject is obese or diabetic. Despite the important developments in the field of imaging, currenty the only way to differentiate NASH from simple NAFLD is by performing a liver biopsy, which should be discussed extensively with the patient. The prognosis of simple NAFLD is generally benign, but if there is fibrosis, ballooning of the hepatocytes, inflammation and Mallory bodies there is risk to progression to cirrhosis. Liver histology in NAFLD is indistinguishable from alcoholic hepatitis, although the clinical course is generally more benign. Despite this long and protracted clinical course, an important number of subjects have complications of cirrhosis including hepatocellular carcinoma, and many patients require a liver transplantation. There is no specific treatment for this condition, although every therapeutic regimen should include a gradual and supervised weight reduction, a balanced diet and exercise, as well as correction of precipitant factors. There is currently no specific pharmacologic treatment for NASH or NAFLD. Current body of evidence and some pilot studies suggest that the future might be concentrated in agents improving insulin resistance. Meanwhile, we should do our best to study the prevalence of NAFLD in our country and, when clinically pertinent, study histologically those patients with high risk of fibrosis.
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PMID:[Non-alcoholic fatty liver]. 1276 15

Recently incidence of alcoholic liver disease (ALD) has been increasing in Japan associated with an increase in alcoholic beverage consumption. There have been a large number of reports about the relationship between alcohol and hepatocarcinogenesis, but it remains controversial. In this review, we addressed 1) the recent trend in incidence of ALD including severe alcoholic hepatitis (SAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) in heavy drinkers in Japan, and 2) the characteristics of HCC in heavy drinkers with negative serum markers for viral hepatitis. We carried out nation-wide survey by asking for the hospitals that are approved by the Japanese Society of Gastroenterology for recent aspects of in-patients with ALD. Except for HCC, percentage of ALD without viral hepatitis is more than 70%, which is increased when compared to the national survey carried out in 1992. Percentage of alcoholic LC without positive markers for viral hepatitis was 61% and alcohol plus virus group was 39%. Furthermore, in alcoholic LC patients without HCC, those who did not have viral hepatitis were 80%. However, the percentage of HCC without viral hepatitis was 27% of all of the heavy drinkers with HCC. Regarding our own cases, subjects were 432 HCC patients who were admitted to our hospital since 1995. There were 296 cases (68.5%) of HCV-positive, 70 cases (16.2%) of HBV-positive, 27 cases (6.3%) of both HCV- and HBV-positive. Thirty-nine cases (6.7%) were negative for serum markers for viral hepatitis. Among them, 13 cases (3.0%) were not heavy drinkers (non-B, non-C, non-alcohol) and 26 cases (6.0%) were heavy drinkers (non-B, non-C, heavy drinkers). Twenty-five of these 26 (96.2%) cases had cirrhosis. In conclusion, since the consumption of alcohol is increasing in Japan, the frequency and number of cases of alcoholic liver cirrhosis are increasing. Viral hepatitis infection, however, still plays an important role in hepatocarcinogenesis in heavy drinkers. Radiographic examinations at an appropriate interval for HCC are recommended, even in cases with alcoholic liver cirrhosis who are negative for serum markers of viral hepatitis, to ensure the early diagnosis of HCC.
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PMID:[Alcoholic liver diseases in Japan and modification by hepatitis virus]. 1463 19


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