Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The relationship between the past history of selected diseases and the risk of dying from hepatocellular carcinoma (HCC) was analyzed using 110,792 cohort members (46,465 males and 64,327 females) recruited between 1988 and 1990 by the JACC Study (the Japan Collaborative Cohort Study for Evaluation of Cancer Risk). Significantly elevated hazard ratios (HRs) were observed in both genders for the past history of kidney diseases, liver diseases, gallstones or cholecystitis, diabetes mellitus, and blood transfusion. Further, when analyzed by age group (those 40-59 years of age were "younger" and those 60-79 years of age were "older"), although the significant associations were generally maintained, the magnitude of the HRs for liver diseases and diabetes mellitus seemed to be considerably different between the younger and older age groups for male cohort members. When the analyses were limited to cohort members without the past history of liver diseases, the past histories which had significantly elevated HRs were hypertension (HR = 3.14, 95% confidence interval (CI): 1.25-7.89), diabetes mellitus (HR = 4.17, 95% CI: 1.22-14.25), and blood transfusion (HR = 7.69, 95% CI: 3.09-19.15) in the younger male age group and gallstone or cholecystitis (HR = 2.58, 95% CI: 1.11-5.98) in the older male age group. On the other hand, for females, the significantly elevated HRs were gastric or duodenal ulcer (HR = 4.33, 95% CI: 1.09-17.25) in the younger age group and diabetes mellitus (HR = 6.16, 95%CI: 2.25-16.90) and blood transfusion (HR = 3.86, 95%CI: 1.58-9.41) in the older age group. However, since the evidence from our univariate analyses might not be decisive, multivariate Cox proportional hazards models controlling for potential confounders and effect modifiers will be required to obtain more valid or unbiased hazard ratios.
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PMID:Past medical history and risk of death due to hepatocellular carcinoma, univariate analysis of JACC study data. 1476 73

Nonalcoholic fatty liver disease (NAFLD) is being increasingly recognized as a common liver disorder that represents the hepatic manifestation of the metabolic syndrome, a variably defined aggregate of disorders related to obesity, insulin resistance, type II diabetes, hypertension and hyperlipidemia. Nonalcoholic steatohepatitis (NASH) is the progressive form of liver injury that carries a risk for progressive fibrosis, cirrhosis, and end-stage liver disease. Hepatocellular carcinoma (HCC) is a documented complication in an as yet unknown percentage of cases of NASH cirrhosis. The diagnosis of nonalcoholic steatohepatitis requires histopathologic evaluation because the lesions of parenchymal injury and fibrosis cannot be detected by imaging studies or laboratory tests. This article will briefly discuss prevalence studies and the pathophysiology of NAFLD and focus on current discussions related to the specific lesions in the pathology of NASH, including the challenges of pediatric NASH and NASH-related cirrhosis.
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PMID:Nonalcoholic steatohepatitis. 1508 83

Nonalcoholic steatohepatitis and chronic viral hepatitis C are the two dominant liver diseases in the Netherlands. Hepatic steatosis is usually innocuous but in twenty percent of patients it develops into steatohepatitis. One-fifth of these patients develop liver cirrhosis and hepatocellular carcinoma can also be a consequence of the disease. Nonalcoholic steatohepatitis is characterized by macrovesicular steatosis, necroinflammation, loss ofhepatocytes and fibrosis. Nonalcoholic steatohepatitis often is associated with type 2 diabetes mellitus, hypertension, dyslipoproteinemia and obesity. Insulin resistance plays a major role in the pathogenesis of this disease. Drugs against insulin resistance can ameliorate nonalcoholic steatohepatitis. Gradual weight loss, a diet including polyunsaturated fatty acids and exercise are other important treatment components of this condition.
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PMID:[Nonalcoholic steatohepatitis: diagnosis, pathogenesis, treatment and prognosis]. 1583 33

Hepatic steatosis is the hallmark of nonalcoholic fatty liver disease (NAFLD), which is the consequence of multiple metabolic derangements among which insulin resistance plays a pivotal role. Steatosis is, also, a feature of hepatitis C virus (HCV) infection. However, in chronic hepatitis C, the prevalence of steatosis is 2.5-fold more elevated than that expected by a chance concurrence with NAFLD, suggesting that HCV may be implied in the development of steatosis. As observed in NAFLD, in patients infected with HCV genotype 1 steatosis is associated with an increased body mass index. On the other hand, in patients infected with genotype 3 the extent of steatosis strictly correlates with the viral load indicating that steatosis is mainly "virus-related". Regardless of the "metabolic" or "viral" etiology, hepatic steatosis in HCV contributes to the progression of liver fibrosis, to the development of hepatocellular carcinoma and to an impaired response to interferon treatment. Features such as obesity, insulin resistance and type 2 diabetes mellitus are shared by NAFLD and HCV-associated steatosis. In addition, HCV infection, directly or through steatosis, favors the development of type 2 diabetes mellitus. Hyperlipidemia is an independent predictor of the development of NAFLD, but not of HCV-associated steatosis. Arterial hypertension is common in nonalcoholic steatohepatitis patients, and HCV infection has recently been acknowledged as an independent risk factor for atherosclerosis. The role of iron in the progression of both NAFLD and HCV-associated steatosis remains controversial while lipoperoxidation and oxidative stress are pathogenic mechanisms shared by both. Some metabolic risk factors may be shared by both HCV-associated steatosis and NAFLD although the disease progression and pathophysiological background may be different. Preliminary data suggest that the therapeutic options for NAFLD may also be useful to improve HCV-associated steatosis.
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PMID:[Hepatitis C virus-associated and metabolic steatosis. Different or overlapping diseases?]. 1585 90

We studied acception of cholesterol from Fu5AH hepatoma cells by blood serum from subjects with normal level of high-density lipoprotein cholesterol and hyperlipidemia (alone or in combination with other risk factors for coronary heart disease). Cholesterol-binding activity of high-density lipoproteins decreased in subjects with hyperlipidemia alone or in combination with excess body weight and/or arterial hypertension. Impairment of high-density lipoprotein activity was associated with changes in their phospholipid composition.
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PMID:Impaired antiatherogenic function of high-density lipoproteins in the presence of various risk factors for coronary heart disease. 1602 33

Right ventricular hypertension (RVH) is an entity that could be expected in various cardiopulmonary diseases. Mechanical obstruction to the right ventricle outflow tract is a cause of RVH. We present the case of a 69 year-old male with a history of hepatocarcinoma previously treated. The developed RVH due to mechanical obstruction secondary to metastatic infiltration of the right ventricle. The clinical syndrome was characterized by systemic venous hypertension. Non-invasive studies, such as electrocardiogram and computed tomography scan limited the metastasis to the right ventricle; the diagnosis was confirmed by cardio-angiography and endocardial biopsy. The studies did not demonstrate neoplastic activity at any other level.
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PMID:[Severe right ventricular hypertension secondary to metastatic obstruction due to hepatocarcinoma]. 1613 1

Metabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity. The liver is a target organ in metabolic syndrome patients in which it manifests itself with non-alcoholic fatty liver disease spanning steatosis through hepatocellular carcinoma via steatohepatitis and cirrhosis. Given that metabolic syndrome and non-alcoholic fatty liver disease affect the same insulin-resistant patients, not unexpectedly, there are amazing similarities between metabolic syndrome and non-alcoholic fatty liver disease in terms of prevalence, pathogenesis, clinical features and outcome. The available drug weaponry for metabolic syndrome includes aspirin, metformin, peroxisome proliferator-activated receptor agonists, statins, ACE (angiotensin I-converting enzyme) inhibitors and sartans, which are potentially or clinically useful also to the non-alcoholic fatty liver disease patient. Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non-alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance-related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non-alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non-alcoholic fatty liver disease.
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PMID:Review article: the metabolic syndrome and non-alcoholic fatty liver disease. 1622 69

Non Alcoholic Fatty Liver Disease (NAFLD), with prevalence of 10-51% in general population involving all ages, is the major cause of elevation of ALT and a common finding by ultrasound screening and may range from simple steatosis, to Non Alcoholic Steatohepatitis (NASH) and its clinical consequences as cirrhosis and hepatocellular carcinoma. In this review will be analyse factors influencing the onset of the disease. NAFLD, primarly associated with insulin resistance, is in fact considered the hepatic manifestation of the metabolic syndrome: a cluster of disorder that includes obesity, diabetes mellitus, dyslipidaemia, arteriosclerosis and hypertension. The increased incidence and prevalence of obesity and diabetes may explain growing interest in NAFLD. Racial, ethnic, enviromental and behaviour models are also reviewed.
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PMID:Nonalcoholic fatty liver disease: defining a common problem. 1623 86

A 70-year-old man had been obese since youth. He had been treated for hypertension and diabetes mellitus. An abdominal ultrasound showed a mass in the liver. He was admitted to St Marianna University School of Medicine Hospital for further evaluation. There was no history of alcohol use, and hepatitis viral markers and autoantibodies were all negative. Several imaging studies showed overt hepatocellular carcinoma (HCC). Transcatheter arterial embolization was performed, followed by surgical resection. Histopathological examination revealed moderately differentiated HCC. The non-tumor areas had pseudolobules in a diffuse pattern similar to alcoholic cirrhosis. The histological findings in the ectopic liver tissue attached to the gallbladder, which was also resected during surgery, were that there was no cirrhosis, but fine fibrosis with inflammatory cell infiltration of sinusoids. These findings were consistent with non-alcoholic steatohepatitis (NASH). There was probably a progression of similar findings that had developed into cirrhosis. These findings confirmed a diagnosis of HCC, cirrhosis, and underlying NASH in this patient. The present case is important for investigation of the development into cirrhosis and carcinogenesis of NASH. The present case demonstrates the importance of evaluating obese patients with fatty liver for underlying NASH and ongoing follow up for development of cirrhosis and HCC.
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PMID:Hepatocellular carcinoma with silent and cirrhotic non-alcoholic steatohepatitis, accompanying ectopic liver tissue attached to gallbladder. 1639 79

Tetrandrine (TET), a bis-benzylisoquinoline alkaloid isolated from the dried root of Hang-Fang-Chi (Stephania tetrandra S. Moore), is well known to possess activities including antioxidant, anti-inflammation, anti-fibrotic and anticancer. It is used clinically to treat hypertension and silicosis. In the present study, the anti-proliferative and apoptotic effects of TET were evaluated on three different hepatoma cell lines, namely Hep G2, PLC/PRF/5 and Hep 3B. Using XTT assay, results showed that the IC50 values of TET were 4.35 microM for Hep G2, 9.44 microM for PLC/PRF/5 and 10.41 microM for Hep 3B cells. The CC50 of TET against BNL-CL.2 mouse normal liver cells was 31.12 microM. Interestingly, TET exhibited a lower IC50 value and better selectivity against Hep G2 and PLC/PRF/5 cells than cisplatin. Microscopic observation study, DNA fragmentation assay and flow cytometric analysis further supported apoptotic effect of TET on both PLC/PRF/5 and Hep 3B cells. The cell cycle of PLC/PRF/5 treated with TET appeared to arrest at G2/M phase in a dose-dependent manner, whereas no effect was noted on the cell cycle of Hep 3B cells. The present study concludes that TET exhibited anti-proliferative effect on Hep G2, PLC/PRF/5 and Hep 3B cells in a dose-dependent manner. TET also possesses a lower IC50 and better SI value than cisplatin against Hep G2 and PLC/PRF/5 cells. The effect of TET on cell cycle progression was found to vary with the type of hepatoma cells, suggesting the genetic make-up of the cells play an important role in the response to drug treatment.
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PMID:Antiproliferative and apoptotic effects of tetrandrine on different human hepatoma cell lines. 1643 45


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