Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 57 year-old woman was admitted to our hospital because of large hepatocellular carcinoma (HCC). Laboratory data showed hypercholesterolemia, thrombocytosis and hypoglycemia. Based on several examinations and the clinical course, we diagnosed HCC with paraneoplastic syndrome. It is rare that 3 paraneoplastic phenomena occur in a patient with HCC. In particular, paraneoplastic thrombocytosis is very rare in paraneoplastic syndrome associated with HCC.
 ...
PMID:[A case of hepatocellular carcinoma with paraneoplastic hypercholesterolemia, thrombocytosis and hypoglycemia]. 1767 26

The deficiency of glucose-6-phosphatase (G6Pase) underlies glycogen storage disease type Ia (GSD-Ia, von Gierke disease; MIM 232200), an autosomal recessive disorder of metabolism associated with life-threatening hypoglycemia, growth retardation, renal failure, hepatic adenomas, and hepatocellular carcinoma. Liver involvement includes the massive accumulation of glycogen and lipids due to accumulated glucose-6-phosphate and glycolytic intermediates. Proteomic analysis revealed elevations in glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and other enzymes involved in glycolysis. GAPDH was markedly increased in murine G6Pase-deficient hepatocytes. The moonlighting role of GAPDH includes increasing apoptosis, which was demonstrated by increased TUNEL assay positivity and caspase 3 activation in the murine GSD-Ia liver. These analyses of hepatic involvement in GSD-Ia mice have implicated the induction of apoptosis in the pathobiology of GSD-Ia.
 ...
PMID:Activation of glycolysis and apoptosis in glycogen storage disease type Ia. 1941 92

One hundred and ninety-three Sprague-Dawley (SD) rats (average body weight being 100-120 g) were randomly divided into 5 groups (I-V). Animals in group I and group II served as the negative control and positive control, respectively, and both received 0.1 mg/kg selenium (Se) from sodium selenite. Animals in groups III-V were fed with Se from Se-enriched malt (SEM) supplemented diets (0.3, 1 and 3 mg/kg, respectively). Simultaneously, hepatocarcinoma were induced in groups II-V by diethylnitrosamine (DEN) solution (100 mg/L) at the dosage of 10 mg/kg body weight every day as drinking water for 16 weeks, then sterilized water for a further two weeks. Rats of group I drank sterilized water during the whole experimental time. At 4th, 8th, 12th, 16th week, five rats in each group were then sacrificed by cervical decapitation. At the termination of the study, at 18th week, the surplus rats were sacrificed by cervical decapitation. Feed was withheld from the rats for 12h before sampling. The values of plasma glucose at different sampling times were measured. The values of the hormones in plasma related to plasma glucose metabolism, including insulin, glucagon, insulin-like growth factors-II (IGF-II), and the ratios of insulin/glucose (IGR(1)), insulin/glucagon (IGR(2)) and glucagon/glucose (GGR) were determined. At the same time, the correlation of plasma glucose concentrations related to hormones was statistically analyzed. The results indicated that the values of plasma glucose, insulin, glucagon and GGR in the groups treated with DEN were decreased significantly as compared with that of the negative control group, however, the values of IGF-II and IGR(2) were increased significantly. SEM showed a significant effect in suppressing the decreased of plasma glucose and glucagons, and delaying the increased of IGF-II and IGR(2) in the DEN-induced hepatocarcinoma rats. The plasma glucose concentrations revealed a significant relation to the hormones. In conclusion, SEM could reduce the development of hypoglycemia in the DEN-induced hepatocarcinoma rats by regulating the relative levels and balances or proportions of hormones.
 ...
PMID:Effect of selenium-enriched malt on hypoglycemia and regulatory hormones in diethylnitrosamine-induced hepatocarcinoma SD rats. 1952 Apr 6

Uip to 20% of patients with liver cirrhosis develop hepatogenous diabetesdue to the hepatocellular functional loss and insulin resistance. Optimizing diabetic metabolic conditions is not only important to avoid typical late complications of diabetes, but also cirrhosis-associated complications e.g. gastrointestinal bleeding, hepatic encephalopathy or the occurence of hepatocellular carcinoma. So far there have beenno recommendations orguidelines for the diagnosis and treatmentof hepatogenous diabetes. The medical teatment of a diabetic condition is mainly influenced by its side effects. The risk of hypoglycemia must be considered carefully during drug treatment, especially in patients with chronic alcohol abuse. Suitable oral antidiabetics are glinides and short-acting sulfonylureas or possibly meal-related insulin administration with short-acting insulins or rapid-acting insulin analogues. Biguanide and PPAR-gamma agonists are contraindicated because of side effects in liver cirrhosis. Regarding basic treatment, an adequate daily energy and protein supply should be ensuredbecause the majority of patients with liver cirrhosis are malnourished.
 ...
PMID:[Metabolic disturbances in liver cirrhosis (part 2), hepatogenous diabetes: diagnostic aspects and treatment]. 2035 3

Early stage hepatocellular carcinoma is a symptom-free disease. Local and general symptoms occur due to the growth of the tumor tissue and the infiltration of the surrounding blood vessels. Illness progression is indicated by the development of abdominal discomfort, cachexia, therapy-resistant decompensation of previously compensated cirrhosis and in severe cases, the thrombosis of the portal vein or the hepatic veins. Characteristic laboratory findings are the quickly deteriorating blood and liver function tests results, the occurrence of haemostatic disorders and occasional hypoglycemia and/or hypercalcemia. To clarify the etiology and to identify high risk patients, we need to differentiate alcohol-, drug- or chemical-induced hepatic disorders, viral hepatitis B, C and Delta, metabolic disorders and non-alcoholic steatohepatitis. In the case of focal hepatic lesions, persistently elevated alfa fetoprotein levels have a high diagnostic value. At levels over 200 ng/ml, the positive predictive value is >90%. Other, less commonly measured biomarkers are the glycosilated alfa fetoprotein-L3 and the vitamin K-deficiency induced des-gamma-carboxy prothrombin. The risk of tumor occurrence is multiple in patients with HbeAg positive chronic hepatitis B if the virus is of genotype C with mutations in the 1762 and 1764 locations of the core promoter region. Abdominal ultrasound and measurement of alfa fetoprotein is recommended every 6 months for high risk individuals, or every 3-4 months over an 18-24 months period for patients with hepatic lesions of <1cm and of unknown malignancy.
 ...
PMID:[Symptoms of hepatocellular carcinoma. Laboratory tests used for its diagnosis and screening]. 2071 15

We report a case of splenic tumor associated with severe hypoglycemia. The patient was a 69-year-old man with a large splenic tumor. He had suffered from relapsing hypoglycemic attacks and the lowest serum glucose level (4 mg/dl). He died 34 months after the onset of symptoms of left abdominal pain. Autopsy revealed large tumors in the spleen, 3 medium sized tumors in the lungs, and several small tumors in the liver. Microscopic studies of the splenic tumors revealed a hepatocellular carcinoma which showed a strongly positive reaction against anti-PIVKA-II and anti-"hepatocyte" antibodies. Several bile ductules thought to be heterotopic remnants of the liver tissues were found in the capsule of the spleen, adjoining the splenic tumor. It was suggested that the tumor originated from one of these ductules. Electron microscopic analysis showed numerous endocrine-like granules of every tumor cell, and 87-165 times stronger mRNA expression of insulin-like growth factor-II was measured in the tumor tissues when compared with normal liver tissue. Owing to these results, we believe that this is the first report of hepatocellular carcinoma that had developed from a liver tissue in the spleen.
 ...
PMID:Hepatocellular carcinoma arising from ectopic liver tissue in the spleen producing insulin-like growth factor II. 2094 27

Here we describe an experimental tumor, hepatocarcinoma-29: transplantable strain of this tumor is maintained in an ascitic form in CBA/LacYIcgn mice in Institute of Cytology and Genetics of SD of RAS. After inoculation into the thigh muscles, the tumor induces anorexia, progressing loss of fat and muscle tissues, and physiological changes specific for cachexia: leukocytosis, hypoglycemia, and hypercorticism. The tumor metastasizes to all vital viscera and leads to animal death from renal failure.
 ...
PMID:Hepatocarcinoma-29, a metastasizing transplantable mouse tumor inducing cachexia. 2111 3

Patients with hepatocellular carcinoma may manifest paraneoplastic syndromes such as hypercholesterolaemia, hypoglycaemia, hypercalcaemia and erythrocytosis. An exceptional case of hepatocellular carcinoma associated with polymyositis, a rheumatic paraneoplastic syndrome, is reported. A 72-year-old male complained for a recent muscular weakness mainly in the proximal limb muscles. The clinical course, a raised level of serum creatine kinase and electromyographic findings suggested polymyositis, and the pathological findings on muscle biopsy were compatible with this diagnosis. Computed tomography of the upper abdomen revealed a mass lesion in segment IV, V and VII of the liver, and alpha foetoprotein level was high, resulting in the diagnosis of hepatocellular carcinoma.
 ...
PMID:Hepatocellular carcinoma with polymyositis as an initial symptom: a case report. 2148 65

Glucose-6-phosphatase deficiency (G6P deficiency), or glycogen storage disease type I (GSDI), is a group of inherited metabolic diseases, including types Ia and Ib, characterized by poor tolerance to fasting, growth retardation and hepatomegaly resulting from accumulation of glycogen and fat in the liver. Prevalence is unknown and annual incidence is around 1/100,000 births. GSDIa is the more frequent type, representing about 80% of GSDI patients. The disease commonly manifests, between the ages of 3 to 4 months by symptoms of hypoglycemia (tremors, seizures, cyanosis, apnea). Patients have poor tolerance to fasting, marked hepatomegaly, growth retardation (small stature and delayed puberty), generally improved by an appropriate diet, osteopenia and sometimes osteoporosis, full-cheeked round face, enlarged kydneys and platelet dysfunctions leading to frequent epistaxis. In addition, in GSDIb, neutropenia and neutrophil dysfunction are responsible for tendency towards infections, relapsing aphtous gingivostomatitis, and inflammatory bowel disease. Late complications are hepatic (adenomas with rare but possible transformation into hepatocarcinoma) and renal (glomerular hyperfiltration leading to proteinuria and sometimes to renal insufficiency). GSDI is caused by a dysfunction in the G6P system, a key step in the regulation of glycemia. The deficit concerns the catalytic subunit G6P-alpha (type Ia) which is restricted to expression in the liver, kidney and intestine, or the ubiquitously expressed G6P transporter (type Ib). Mutations in the genes G6PC (17q21) and SLC37A4 (11q23) respectively cause GSDIa and Ib. Many mutations have been identified in both genes,. Transmission is autosomal recessive. Diagnosis is based on clinical presentation, on abnormal basal values and absence of hyperglycemic response to glucagon. It can be confirmed by demonstrating a deficient activity of a G6P system component in a liver biopsy. To date, the diagnosis is most commonly confirmed by G6PC (GSDIa) or SLC37A4 (GSDIb) gene analysis, and the indications of liver biopsy to measure G6P activity are getting rarer and rarer. Differential diagnoses include the other GSDs, in particular type III (see this term). However, in GSDIII, glycemia and lactacidemia are high after a meal and low after a fast period (often with a later occurrence than that of type I). Primary liver tumors and Pepper syndrome (hepatic metastases of neuroblastoma) may be evoked but are easily ruled out through clinical and ultrasound data. Antenatal diagnosis is possible through molecular analysis of amniocytes or chorionic villous cells. Pre-implantatory genetic diagnosis may also be discussed. Genetic counseling should be offered to patients and their families. The dietary treatment aims at avoiding hypoglycemia (frequent meals, nocturnal enteral feeding through a nasogastric tube, and later oral addition of uncooked starch) and acidosis (restricted fructose and galactose intake). Liver transplantation, performed on the basis of poor metabolic control and/or hepatocarcinoma, corrects hypoglycemia, but renal involvement may continue to progress and neutropenia is not always corrected in type Ib. Kidney transplantation can be performed in case of severe renal insufficiency. Combined liver-kidney grafts have been performed in a few cases. Prognosis is usually good: late hepatic and renal complications may occur, however, with adapted management, patients have almost normal life span. DISEASE NAME AND SYNONYMS: Glucose-6-phosphatase deficiency or G6P deficiency or glycogen storage disease type I or GSDI or type I glycogenosis or Von Gierke disease or Hepatorenal glycogenosis.
 ...
PMID:Glucose-6-phosphatase deficiency. 2159 42

Hypoglycemia is a well-known complication of insulinoma and other non-islet-cell tumors like hepatic tumor. In the emergency unit of neurology department, hypoglycemia is an uncommon cause of convulsive status epilepticus. We report a rare case with hypoglycemia-induced convulsive status epilepticus as the initial presentation of primary hepatic carcinoma. The previously healthy 57-year-old male peasant presented with persistent unconsciousness and repeated convulsive seizures. He was later found to have hepatoma related hypoglycemia. This case highlights the importance of blood sugar test in unexplained status epilepticus in the emergency room of neurology department. Intravenous glucose infusion rather than anti-epileptic drugs might be safer and more effective in treating status epilepticus caused by hepatoma related hypoglycemia.
 ...
PMID:Hypoglycemia-induced convulsive status epilepticus as the initial presentation of primary hepatic carcinoma. 2238 39


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>