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)

Portal vein thrombosis, except in hepatocellular carcinoma and severe cirrhosis, is due to one or several prothrombotic disorders with or without a local precipitating factor. We report a case of a portal and splenic vein thrombosis, without cavernoma and varices which occurred in a 72-year-old man with abdominal pain and weakness. Three prothrombotic states including latent myeloproliferative disorder, antiphospholipid syndrome, and factor II G202101 mutation, were observed. Anticoagulant treatment resulted in complete repermeation of the portal and splenic veins without a hemorrhagic event. This illustrates that several prothrombotic states may occur in a single patient with portal vein thrombosis. Early anticoagulant therapy, in recent portal vein thrombosis, can result in repermeation.
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PMID:[Portal vein thrombosis associated with a myeloproliferative disorder, prothrombin G20210A mutation, antiphospholipid syndrome, with repermeation during anticoagulant therapy]. 1152 Nov 10

The case of a 77-year-old woman with hepatitis C virus infection with a 5-year history of muscle weakness and mild disturbance of gait is reported. Steroid therapy did not improve her symptoms. She developed HCV-related liver cirrhosis and hepatocellular carcinoma, and muscle biopsy revealed inclusion body myositis. Immunohistochemistry showed that the nonstructural region of HCV and 8-hydroxy-2'-deoxyguanosine, a marker of DNA damage by reactive oxygen species, were present in striated muscle cells of this patient.
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PMID:Inclusion body myositis associated with hepatitis C virus infection. 1158 73

An 80-year-old white woman who presented with fatigue, weakness, weight loss, constipation and polydipsia is reported. The patient was given a diagnosis of severe hypercalcemia and was subsequently found to have clinical, roentgenographic and pathological evidence of hepatocellular carcinoma. Further studies revealed a low parathyroid hormone level, excluding the possibility of primary hyperparathyroidism, and a negative bone survey, precluding metastatic bone disease. The patient's hypercalcemia was believed to emanate from the humoral secretion of a parathyroid hormone-related peptide, which was found to be elevated, and was abated with conservative management while her cancer was being treated with chemotherapy. The details of this rarely documented presentation, which can easily be mistaken for hepatic encephalopathy, are provided.
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PMID:Severe hypercalcemia as an initial presenting manifestation of hepatocellular carcinoma. 1236 13

Hepatocellular carcinoma is one of the most common malignancies reported in Korean adult males. Hepatocellular carcinoma usually spreads to regional lymph nodes around porta hepatis via lymphatics and to distant metastasis via hematogenous spread. The lung is most common distant metastatic site, followed by the adrenal glands, local lymph nodes and bones. But metastasis to the spinal cord of hepatocellular carcinoma is very rare. Recently we experienced a patient with hepatocellular carcinoma who had suffered from lower leg weakness for 10 days. The patient was proved to have hepatocellular carcinoma with metastasis to the spinal cord. MRI showed an ovoid intracordal mass between the twelfth thoracic and first lumbar vertebra level. After emergency irradiation, the patient could recover.
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PMID:[A case of primary hepatocellular carcinoma with metastasis to the spinal cord]. 1249 8

Congenital myasthenic syndromes are caused by different genetic defects affecting proteins expressed at the neuromuscular junction. Recently, the first molecular genetic defect resulting in a presynaptic congenital myasthenic syndrome has been reported: Recessive loss-of-function mutations in CHAT, the gene encoding choline acetyltransferase, were described in five congenital myasthenic syndrome families. In this study, we investigated three patients from two independent Turkish kinships. Clinically, all patients presented with moderate myasthenic symptoms including ptosis and muscle weakness with increased fatigability. Multiple episodes of sudden apnea were reported for all patients. One child suffering from a second, unrelated disorder, i.e. hepatocellular carcinoma, showed a severe myasthenic phenotype, requiring permanent ventilation. Genetically, we identified a novel missense mutation (I336T) in the CHAT gene homozygously in all three patients. Haplotype analysis revealed that the mutant allele cosegregates with the clinical phenotype in both families (maximum combined two-point LOD-score of 2.46 for D10S1793). In summary, we confirm that CHAT mutations are responsible for a clinically distinct form of congenital myasthenic syndrome, characterized by episodic apnea. Infections and stress may lead to a life-threatening failure of neuromuscular transmission in congenital myasthenic syndrome with episodic apnea. The observation of the same mutation (I336T) in two independent Turkish kinships may suggest a common origin, i.e. founder.
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PMID:Congenital myasthenic syndrome due to a novel missense mutation in the gene encoding choline acetyltransferase. 1260 6

Hepatocellular carcinoma represents the 8th most frequent malignancy worldwide. The World Health Organization recognizes five histologic patterns and four cytologic variants of hepatocellular carcinoma. Clear cell carcinoma of the liver is a well-defined variant of hepatocellular carcinoma in which a large number of cells show clear cytoplasm that does not stain with hematoxylin and eosin. It can be confused with other clear-cell malignancies. A 52-year-old man presented with mild dyspeptic symptoms, right-sided upper abdominal pain, weakness, weight loss, abdominal mass and jaundice symptoms for nearly six weeks. After diagnostic procedures, an ultrasonography-guided liver biopsy was performed. In microscopic examination, malignant cells with vacuolated foamy to clear cytoplasm and central and eccentric nuclei, tumor composed of solid mass and cords, and clear cells were observed, and hepatocellular carcinoma, clear cell variant, is diagnosed. We report this rare case of primary clear cell carcinoma in the cirrhotic liver. The case was discussed in detail regarding histological presentation, with particular attention to histopathologic differential diagnosis.
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PMID:Clear cell carcinoma of the liver: a case report. 1465 70

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death in Taiwan. In order to delineate the unique demographic features and clinical profile of terminal HCC, we conducted a retrospective study in a hospital-based hospice in Taiwan. Of a total of 991 terminally ill cancer patients (654 men and 337 women, mean age 66.1 years) admitted to our palliative care unit during a three-year period, 110 patients (11.1%) were diagnosed as having HCC (93 men and 17 women, mean age 60.5 years). The most common metastatic sites were bone and lung. Eighty-five HCC patients (77.3%) also had associated liver cirrhosis. The most common symptoms of HCC patients upon admission to the hospice ward were pain, fatigue or weakness, anorexia/vomiting, peripheral edema, cachexia, and ascites. Hypoalbuminemia, anemia, hyponatremia and jaundice were common laboratory abnormalities. Eighty-four patients (76.4%) required opiates for pain management. Upper gastrointestinal bleeding or varices bleeding developed in 76 patients (69.1%). Ninety-four patients (85.5%) died at the hospital, and the overall median survival time at hospice ward was 12 days. Because of more severe underlying portal hypertension and deteriorated liver function, terminal HCC patients with decompensated liver cirrhosis (Child-Pugh class C) had a significantly higher prevalence of peripheral edema, ascites, dyspnea, jaundice, thrombocytopenia, and stage III-IV hepatic encephalopathy than noncirrhotic or Child-Pugh class A and B terminal HCC patients. Symptoms and signs resulting from these portal hypertensions frequently complicated the symptomatic management of terminal HCC patients in the hospice ward. The treatment of these complications is mostly empirical in hospice ward, where intensive laboratory or diagnostic tests are usually not performed. In conclusion, symptoms and signs of terminally ill HCC patients in hospice are unique and should be managed appropriately.
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PMID:Hospice palliative care for patients with hepatocellular carcinoma in Taiwan. 1504 5

A 55 yr-old man presented with progressive muscle weakness and oliguria for 5 days. Laboratory findings suggested rhabdomyolysis complicated with acute renal failure. A diagnosis of polymyositis was based upon the proximal muscle weakness on both upper and lower limbs, elevated muscle enzyme levels, muscle biopsy findings and the needle electromyography findings. The muscle biopsy showed extensive muscle necrosis and calcification. Investigations for underlying malignancy demonstrated hepatocellular carcinoma. The patient was managed with hemodialysis and high dose prednisolone. His renal function was fully recovered and his muscle power did improve slightly, but he died of a rupture of the hepatic tumor. In our view, this is an interesting case in that the hepatocellular carcinoma was associated with polymyositis and fulminant rhabdomyolysis-induced acute renal failure requiring hemodialysis.
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PMID:Hepatocellular carcinoma,polymyositis,rhabdomyolysis,and acute renal failure. 1560 4

Disorientation, muscle fasciculations and weakness seen in a 12-year-old neutered female domestic shorthaired cat were attributed to hypoglycaemia associated with a large hepatoma. Glucagon tolerance tests on this cat and a healthy cat showed that their plasma glucose concentrations increased and decreased at about the same rate. Plasma insulin concentrations in the healthy cat increased and decreased in parallel with the plasma glucose concentration. In the affected cat, plasma insulin concentrations increased initially but decreased more rapidly. Reflecting these observations, the amended insulin to glucose ratios in the affected cat were much lower than those of the healthy cat, until the 4-hour sample. Serum somatostatin, somatomedin and gastrin concentrations were measured but no conclusions as to pathogenesis of the hypoglycaemia could be made. The alterations in insulin secretion in the affected cat suggested that altered hormonal control of glucose homeostasis may have occurred with this tumour.
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PMID:Observations on hypoglycaemia associated with a hepatoma in a cat. 1603 47

To analyze the clinical features of hepatocellular carcinoma (HCC) in patients with signs and symptoms of nervous system involvement as the initial presentation. Over a period of 11 years (January 1993 to December 2003), 15,008 HCC patients were identified at the Chang Gung Memorial Hospital in Kaohsiung, Taiwan. Amongst them, 42 cases had nervous system involvement, of which six had nervous system involvement as their initial presentation. These six cases were enrolled in this study and their clinical and laboratory data were analyzed. The clinical features of the other 36 HCC cases with nervous system involvement were also analyzed for comparison. The six cases were all males, aged 36-68 years old. The involved parts of the nervous system were the cerebellar hemisphere (one), the frontal lobe (one), the sphenoid sinus, sellar turcica, and cavernous sinus (one), the cervical spine (one), and the thoracic spine (two). Their corresponding neurologic presentations were back pain, headache, consciousness disturbance, visual disturbance, and limb weakness. Whilst three out of six patients presenting with nervous system manifestations were found to have concurrent systemic metastases in other expected sites (lung, bone), three had isolated nervous system involvement even after extensive work up. The associated medical conditions of the six cases included hepatitis B (three), hepatitis C (one), liver cirrhosis (two), portal vein thrombosis (three), and diabetes mellitus (two). All the six died within 9 months after the detection of nervous system involvement. The prevalence of nervous system involvement in HCC patients is 0.28% (42/15,088), with 0.04% (6/15,088) having this as their initial presentation. The prognosis of HCC with nervous system involvement is grave. Their clinical and laboratory data are not unique but the diagnosis could only be confirmed by hepatic and nervous system imaging studies, histopathologic examination, and serum alpha-fetoprotein detection. This consideration should be emphasized especially in areas that are hyperendemic for HCC and if the original focus of metastatic lesion is obscure.
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PMID:Hepatocellular carcinoma presenting as nervous system involvement. 1738 89


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