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

In most Western countries hepatitis C virus (HCV) is a common risk factor for hepatocellular carcinoma (HCC). Many HCCs are multifocal in origin, but HCC may also grow as a single hepatic nodule for years before generating satellite or distant tumours. HCV may promote cancer through cirrhosis, which is often associated with HCV-related HCC, but it might also have oncogenic properties by interacting with cellular genes that regulate cell growth and differentiation. Treatment of patients with chronic hepatitis C using interferon might attenuate HCC risk, particularly in those who respond to therapy. Many patients whose cancer is detected early have been successfully treated by liver transplantation and have shown significantly prolonged survival. This is less often achieved with hepatic resection or regional therapies, which may indeed destroy small tumours, without affecting the complications of portal hypertension. Screening remains the only realistic approach for improving the treatment of HCC patients, but its cost-effectiveness is uncertain.
Baillieres Best Pract Res Clin Gastroenterol 2000 Apr
PMID:Hepatocellular carcinoma in patients with HCV. 1089 Mar 25

Hepatitis C virus (HCV) infection may occur in infants and children, although it is much less common than it is in adults. The main transmission routes include mother-to-infant transmission, use of HCV infected blood products, unsterile needles or syringes and other invasive procedures. The natural course of HCV infection in children is variable: some (20-40%) develop an acute resolving infection and spontaneous regression occurs in approximately one-third of infants of HCV infected mothers before 2 years of age. Approximately 60-80% of HCV infected children develop a chronic infection with varying degrees of activity and fibrosis, mostly mild during childhood. However, the potential risks of liver cirrhosis and hepatoma during later life are obvious. Interferon is the main agent used to treat HCV infection in children. The response to interferon at the end of 4-12 months of therapy ranges from 25-90%. A sustained response was found in 36-56% of children 6-36 months after the end of therapy. The duration of therapy is recommended to be 12 months. At the end of 3 months, an evaluation of the response is indicated in the majority of children, except those with thalassemia, in whom evaluation of response should be conducted at the end of 6 months of therapy. The benefit of other therapies, such as combination therapy with interferon and ribavirin in children with hepatitis C is currently under investigation.
Baillieres Best Pract Res Clin Gastroenterol 2000 Apr
PMID:Treatment of chronic hepatitis C virus infection in children. 1089 Mar 26

The incidence of hepatocellular carcinoma is increasing world-wide. Although there are no randomized controlled trials showing benefits from surveillance programmes, these strategies have been widely practised by hepatologists, and most early tumours are diagnosed in the setting of such a policy. In this chapter we summarize the surveillance schedule and recall the policy applied in our Unit. Diagnosis at an early stage is crucial to allow the application of curative treatments that are the only hope for increasing the life expectancy of the patient. Surgical resection and liver transplantation are considered the first-line options for early tumours, although there is no agreement on which is the best approach. Resection is limited by the high recurrence rate, whereas the increasing waiting times have decreased the intention-to-treat outcomes of transplantation. Percutaneous treatments are reserved for patients with single non-surgical tumours. Clinical trials assessing treatments for patients with advanced tumours have not shown any survival benefits.
Baillieres Best Pract Res Clin Gastroenterol 2000 Dec
PMID:Early diagnosis and treatment of hepatocellular carcinoma. 1113 51

Ageing of the liver mainly affects the sinusoids and the Kupffer cells. Pseudocapillarization, manifested by reduced sinusoidal fenestration and subendothelial collagen deposition, causes a reduction in oxygen-dependent hepatocyte functions such as oxidative drug metabolism. The liver mass in old people is somewhat reduced and the liver blood flow is diminished. This causes a reduction in the clearance of rapidly cleared drugs, but the clearance of slowly cleared drugs is not affected. The overall capacity of the liver to regenerate is maintained in old people. Therefore, hepatic resections for hepatocellular carcinoma can be carried out in non-cirrhotic elderly people. For liver transplantations, biological age is more important than calendar age. Transplantations in frail old people and in elderly people with very poor liver function are associated with increased morbidity and limited survival. In relatively healthy old people, the results are as good as those in younger age groups. An increased prevalence of hepatitis C associated cirrhosis and hepatocellular carcinoma in the elderly population is to be expected, at least in the next 20 years. There is a high prevalence of gallstones among old people, in particular among females. For symptomatic choledocholithiasis in elderly patients, endoscopic bile duct clearance does not necessarily need to be followed by cholecystectomy.
Best Pract Res Clin Gastroenterol 2002 Feb
PMID:Liver disease in the elderly. 1197 34

It is very difficult to predict new developments in hepatology so we have decided to analyse the most important issues related to three clinical conditions in hepatology. The first is chronic hepatitis. Here, we discuss the relevance of occult forms of hepatitis B virus infection in the development of cryptogenic liver disease and hepatocellular carcinoma. In addition, the role of genotyping in hepatitis B is analysed, indicating that patients with genotype A have a better prognosis than those with genotype D. The treatment of hepatitis B virus infection is also reviewed, and it has been suggested that research should be directed towards the development of new anti-viral agents to suppress virus replication. The natural history of hepatitis C virus infection is considered, emphasizing the need to know the progression of fibrosis in these patients. The chapter also suggests that treatment of hepatitis C virus infection with pegilated interferon and ribavirin is currently relatively effective. New therapeutic strategies will be required in the future, the most important challenge being the development of a hepatitis C virus vaccine. The second section is on chronic cholestasis. The role of anti-mitochondrial antibodies in primary biliary cirrhosis is considered. The possible infectious agents implicated as potential triggers of primary biliary cirrhosis are also discussed, suggesting that several infections may play a role in the pathogenesis of this condition. Other aetiopathogenic factors, for example organic compounds, drugs and chemicals, are indicated. It is possible that, in the near future, the precise sequence and molecular basis by which infectious agents or xenobiotics may initiate the cascade of the autoimmune response will be defined. One of the most important challenges in primary sclerosing cholangitis concerns the mechanisms that may induce the development of this disease. Up until now, genetic factors have been suggested, recent data reporting a clear-cut association between primary sclerosing cholangitis and the tumour necrosis factor-alpha(2) allele. The third part of this chapter includes recent progress achieved in hepatocellular carcinoma, discussing developments in the knowledge of hepatocellular carcinogenesis. Hepatocellular carcinomas appear so far to be genetically heterogeneous neoplasms, and this heterogeneity may correlate with the variety of aetiological factors involved. The risk factors and primary, secondary and tertiary prevention of the condition are also analysed. Finally, the development of new therapeutic strategies for hepatocellular carcinoma is evaluated by evidence-based studies.
Best Pract Res Clin Gastroenterol 2002 Dec
PMID:Expected developments in hepatology. 1247 1

Chronic viral hepatitis is a common disease. More than 500 million people have chronic viral hepatitis worldwide. These diseases are due to chronic infection with hepatitis B virus, hepatitis D virus or hepatitis C virus. Chronic viral hepatitis is responsible for severe complications: cirrhosis and hepatocellular carcinoma, which are responsible for major morbidity and mortality worldwide. The prognosis of chronic viral hepatitis depends on the rate of progression of fibrosis, which varies widely from one patient to another. Some factors, such as gender, age, alcohol consumption and immune status, influence the progression of fibrosis. In recent years, treatment of chronic viral hepatitis has markedly improved-especially in chronic hepatitis C, with more than 50% of patients having a sustained response with the combination of pegylated interferon and ribavirin. Also, in chronic hepatitis B, new drugs are available, or being evaluated, and combination therapy could dramatically change future therapeutic strategies.
Best Pract Res Clin Gastroenterol 2003 Apr
PMID:Transition of care between paediatric and adult gastroenterology. Chronic viral hepatitis. 1267 18

The prevalence of hepatitis C is 7-10-fold higher in alcoholics than it is in the general population. Among alcoholics, the prevalence of hepatitis C is higher in alcoholics with advanced liver disease. Serum ALT and hepatitis C viral load may improve if alcoholic patients with hepatitis C stop drinking for more than 4 months.Up to 60% of patients with hepatitis C have a past history of alcohol use. In patients with hepatitis C, chronic alcohol consumption of more than 5 drinks per day increases the rate of liver fibrosis. Hepatitis C patients who ingest more than 5 alcoholic drinks per day are at increased risk for cirrhosis, hepatocellular carcinoma and, possibly, death from liver disease. Recent alcohol use decreases the response rate to interferon treatment. The detrimental effects of small amounts (3 or fewer drinks per day) of alcohol consumption in patients with hepatitis C are not known.
Best Pract Res Clin Gastroenterol 2003 Aug
PMID:Liver disease in alcohol and hepatitis C. 1282 60

The consumption of excess alcohol in patients with liver iron storage diseases, in particular the iron-overload disease hereditary haemochromatosis (HH), has important clinical consequences. HH, a common genetic disorder amongst people of European descent, results in a slow, progressive accumulation of excess hepatic iron. If left untreated, the condition may lead to fibrosis, cirrhosis and primary hepatocellular carcinoma. The consumption of excess alcohol remains an important cause of hepatic cirrhosis and alcohol consumption itself may lead to altered iron homeostasis. Both alcohol and iron independently have been shown to result in increased oxidative stress causing lipid peroxidation and tissue damage. Therefore, the added effects of both toxins may exacerbate the pathogenesis of disease and impose an increased risk of cirrhosis. This review discusses the concomitant effects of alcohol and iron on the pathogenesis of liver disease. We also discuss the implications of co-existent alcohol and iron in end-stage liver disease.
Best Pract Res Clin Gastroenterol 2003 Aug
PMID:Effect of alcohol on iron storage diseases of the liver. 1282 61

Non-alcoholic fatty liver disease (NAFLD) is a frequent syndrome encompassing fatty liver alone and steatohepatitis (NASH). Often asymptomatic, the suspicion arises because of abnormal aminotransferases or a bright liver on abdominal ultrasound. It should be suspected during evaluation of associated conditions as obesity, diabetes or dyslipidaemia. The diagnostic evaluation must exclude other potential causes of liver disease and may include a liver biopsy, the only method able to confirm features of necroinflammation and fibrosis that define NASH and its prognostic implications. Indeed, the presence of necroinflammation has been associated with a significant risk of progression to cirrhosis and eventually hepatocellular carcinoma. Age >45 years, obesity and diabetes have also been associated with an increased risk of liver fibrosis and progression to cirrhosis. Given the high prevalence of NAFLD, general measures of life-style changes, focusing on exercise, diet, and total alcohol abstinence, should be implemented before a liver biopsy is considered.
Best Pract Res Clin Gastroenterol 2004 Dec
PMID:Non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH): diagnosis and clinical course. 1556 40

Hepatocellular carcinoma (HCC) is a major contributor to cancer incidence and mortality. There is a wide variation, however, in the global distribution of HCC. Eighty percent of the burden is borne by countries in Asia and sub-Saharan Africa. In most high-risk countries, principal risk factors include infection with hepatitis B virus and dietary exposure to aflatoxin B(1). In contrast, hepatitis C virus and alcohol consumption are more important risk factors in low-risk countries. In recent years, the incidence of HCC has decreased in some high-risk countries and increased in some low-risk countries. Reasons for both trends are not completely understood, but are likely related to public health efforts in Asia and the increase in hepatitis C virus infection in low-risk countries. Vaccination programs against hepatitis B virus will likely decrease the HCC rate even further in decades to come.
Best Pract Res Clin Gastroenterol 2005 Feb
PMID:Epidemiology and natural history of hepatocellular carcinoma. 1575 2


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