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)

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiologic processes, including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In Part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In Part II of this review, we will review oxidative stress in common pathophysiologic conditions, including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis, and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.
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PMID:Nitric oxide and redox regulation in the liver: part II. Redox biology in pathologic hepatocytes and implications for intervention. 2040 Jan 12

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiologic processes, including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In Part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In Part II of this review, we will review oxidative stress in common pathophysiologic conditions, including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis, and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.
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PMID:Nitric oxide and redox regulation in the liver: Part I. General considerations and redox biology in hepatitis. 2044 70

A 37-year-old Japanese man was diagnosed with liver cirrhosis due to Wilson's disease in 2001 and treated with D-penicillamine. Thereafter, he was admitted to our hospital for further examination of a space occupying lesion in the liver. The patient was diagnosed with hepatocellular carcinoma (HCC) (7th segment, 2.5 cm in diameter) in May 2010 and treated with radiofrequency ablation therapy. Biopsy findings from a non-cancerous area revealed a fatty liver, though cirrhotic nodules were not found. Long-term treatment for Wilson's disease may improve hepatic fibrosis, and careful screening for HCC by abdominal imaging is needed in such cases.
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PMID:Hepatocellular carcinoma in a case of Wilson's disease treated with radiofrequency ablation therapy. 2172 66

Copper is an essential trace element required by all living organisms. Excess amounts of copper, however, results in cellular damage. Disruptions to normal copper homeostasis are hallmarks of three genetic disorders: Menkes disease, occipital horn syndrome, and Wilson's disease. Menkes disease and occipital horn syndrome are characterized by copper deficiency. Typical features of Menkes disease result from low copper-dependent enzyme activity. Standard treatment involves parenteral administration of copper-histidine. If treatment is initiated before 2 months of age, neurodegeneration can be prevented, while delayed treatment is utterly ineffective. Thus, neonatal mass screening should be implemented. Meanwhile, connective tissue disorders cannot be improved by copper-histidine treatment. Combination therapy with copper-histidine injections and oral administration of disulfiram is being investigated. Occipital horn syndrome characterized by connective tissue abnormalities is the mildest form of Menkes disease. Treatment has not been conducted for this syndrome. Wilson's disease is characterized by copper toxicity that typically affects the hepatic and nervous systems severely. Various other symptoms are observed as well, yet its early diagnosis is sometimes difficult. Chelating agents and zinc are effective treatments, but are inefficient in most patients with fulminant hepatic failure. In addition, some patients with neurological Wilson's disease worsen or show poor response to chelating agents. Since early treatment is critical, a screening system for Wilson's disease should be implemented in infants. Patients with Wilson's disease may be at risk of developing hepatocellular carcinoma. Understanding the link between Wilson's disease and hepatocellular carcinoma will be beneficial for disease treatment and prevention.
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PMID:Inherited copper transport disorders: biochemical mechanisms, diagnosis, and treatment. 2183 3

Peroxiredoxin (Prx)-4, a secretable endoplasmic reticulum (ER)-resident isoform of the mammalian Prx family, functions as a thioredoxin-dependent peroxidase. It is acknowledged that Prx-4 plays a role in the detoxification of hydrogen peroxide, and potentially other peroxides, which may be generated during the oxidative folding of proteins and oxidative stress in the ER. The present study was undertaken in order to specifically quantify the tissue levels of Prx-4. To accomplish this, an enzyme-linked immunosorbent assay was developed using a specific polyclonal antibody produced by immunizing a rabbit with native recombinant rat Prx-4 protein. The assay was used to detect Prx-4 in the range of 0.1 and 10 ng/ml, and to investigate tissue distribution in rats. Using this immunoassay, we found that the serum levels of Prx-4 were substantially lower in asymptomatic Long-Evans Cinnamon rats, a rat model of Wilson's disease, compared to normal rats. In addition, the treatment of rat hepatoma cells with N-acetylcysteine led to a significant increase in the release of Prx-4 protein into the medium; thus, it appears likely that the secretion of Prx-4 is associated with the redox state within cells. These results suggest that serum Prx-4 has potential for use as a biomarker for hepatic oxidative stress.
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PMID:Measurement of peroxiredoxin-4 serum levels in rat tissue and its use as a potential marker for hepatic disease. 2268 88

Liver transplantation has been an accepted treatment for end-stage liver disease since the 1980s. The development of living donor liver transplantation (LDLT) was driven by limited deceased donor organ donation and a response to the growing demand for the option of liver replacement. LDLT is now performed with high rates of success due to judicious donor and recipient selection, careful preoperative planning, excellent anesthesia management, and prompt detection and treatment of complications. The first successful liver transplantation in Asia was performed in 1984, in Chang Gung Memorial Hospital in a Taiwanese adolescent with Wilson's disease, complicated by end-stage liver cirrhosis. The longest Asian liver transplant survivor has now been living for 26 years and that patient's transplant was also performed in Chang Gung Memorial Hospital. Through December 31, 2011, a total of 924 (783 living donor, 141 deceased donor) liver transplants have been performed at the Kaohsiung Chang Gung Memorial Hospital, where both graft and patient survivals are excellent. For biliary atresia, hepatitis B virus cirrhosis, and hepatocellular carcinoma recipients, our 5-year LDLT survival rates are 98%, 94%, and 90%, respectively. Our overall (deceased and living donor) actuarial 3-year survival rate is 91%. Innovative techniques in LDLT represent technical refinements in hepatic vein, portal vein, hepatic artery, and biliary reconstruction approaches. Hepatic vein reconstruction is highlighted by venoplasty reconstructions in both graft hepatic vein orifices and recipient hepatic veins, to ensure adequate outflow and decrease ischemia times during implantation. Vascular interposition to reconstruct middle hepatic vein tributaries with either fresh or cryopreserved vessels is used when the middle hepatic vein is not routinely harvested with the graft. We have extended the routine use of microsurgical techniques, initially for hepatic artery reconstruction, to biliary reconstruction where the possibility of duct-to-duct reconstruction is performed with accuracy and precision in pediatric non-biliary atresia and in multiple, small bile ducts. Long-term survival has always been related to the immunosuppression regimen, which influences outcome. Newer drugs do not equate to lesser complications. Rather, improvement in how we can find new uses for old drugs is now the norm. Less immunosuppression, as long as hepatic function is maintained at an acceptable level, decreases the chances of long-term complications related to immunosuppression use.
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PMID:More than a quarter of a century of liver transplantation in Kaohsiung Chang Gung Memorial Hospital. 2275 15

We report the exceptional case of hepatocellular carcinoma in a non-cirrhotic patient, whose Wilson's disease was diagnosed at the unusual age of 58 years. The liver histology revealed macrovesicular steatosis with fibrosis, but no cirrhosis. The disease was treated with D-penicillamine for 3 years until acute discomfort in the right upper quadrant led to detection of multifocal hepatocellular carcinoma, which was successfully resected. The histological examination confirmed the malignant nature of the 4 lesions, which were classified according to Edmondson and Steiner as poorly differentiated hepatocellular carcinoma grade 3. The non-tumoral parenchyma showed 80% steatosis with ballooned cells, lobular inflammation, septal fibrosis but no cirrhosis. Hepatocellular carcinoma is rare in Wilson's disease, especially in the absence of cirrhosis. The literature's 28 published cases are reviewed and the contributory role of copper in the hepatocarcinogenic process is discussed.
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PMID:Hepatocellular carcinoma in a non-cirrhotic patient with Wilson's disease. 2359 33

Wilson's disease (WD) is an autosomal recessive inherited disorder of copper metabolism that results in the accumulation of copper in the body and primarily in the liver, brain, and cornea. Copper is a toxic metal and might be associated with cancer induction. Most malignancies associated with WD are hepatocellular carcinoma and cholangiocarcinoma. Other intra-abdominal malignancies have been only rarely reported. To our knowledge, this is the first report to suggest that patients with WD may be vulnerable to a malignant change in the colonic mucosa during long-term copper chelating therapy. We report a case of colonic adenocarcinoma in a patient with WD and review the related literature.
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PMID:A Case of Colonic Adenocarcinoma in a Patient with Wilson's Disease. 2389 95

A 25-year-old man who was normally fit and well, presented with a 2-year history of progressively worsening tremor. His tremor was generalised, affecting head, neck and all four limbs. One of the patient's brothers had suffered from similar problems, but never sought medical attention. Examination revealed a generalised tremor, of greater amplitude on the patient's left side, which increased in its amplitude upon exertion. Slit-lamp examination revealed bilateral Kayser-Fleischer rings and serum caeruloplasmin was found to be low, while 24 h urinary copper excretion was elevated. A diagnosis of Wilson's disease was made and an abdominal ultrasound was performed, revealing evidence of portal hypertension and a hyperechoic hepatic nodule, later confirmed to be hepatocellular carcinoma. The patient underwent partial hepatic resection and was started on D-penicillamine.
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PMID:Hepatocellular carcinoma in a young man with resting and postural tremors. 2408 1

Pregnancy is a special clinical state with several normal physiological changes that influence body organs including the liver. Liver disease can cause significant morbidity and mortality in both pregnant women and their infants. Few challenges arise in reaching an accurate diagnosis in light of such physiological changes. Laboratory test results should be carefully interpreted and the knowledge of what normal changes to expect is prudent to avoid clinical misjudgment. Other challenges entail the methods of treatment and their safety for both the mother and the baby. This review summarizes liver diseases that are not unique to pregnancy. We focus on viral hepatitis and its mode of transmission, diagnosis, effect on the pregnancy, the mother, the infant, treatment, and breast-feeding. Autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson's disease, Budd Chiari and portal vein thrombosis in pregnancy are also discussed. Pregnancy is rare in patients with cirrhosis because of the metabolic and hormonal changes associated with cirrhosis. Variceal bleeding can happen in up to 38% of cirrhotic pregnant women. Management of portal hypertension during pregnancy is discussed. Pregnancy increases the pathogenicity leading to an increase in the rate of gallstones. We discuss some of the interventions for gallstones in pregnancy if symptoms arise. Finally, we provide an overview of some of the options in managing hepatic adenomas and hepatocellular carcinoma during pregnancy.
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PMID:Liver diseases in pregnancy: diseases not unique to pregnancy. 2428 52


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