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 principal indication for transjugular intrahepatic portosystemic shunts (TIPS) continues to be rescue therapy for variceal hemorrhage that cannot be controlled by endoscopic or medical therapy. TIPS provide no survival advantage in prevention of rebleeding or refractory ascites. The indications for TIPS continue to expand, however, especially for Budd-Chiari syndrome and hydrothorax. Other more novel indications include bleeding portal hypertensive gastropathy or ectopic varices, Budd-Chiari syndrome, veno-occlusive disease, hepatorenal syndrome, hepatopulmonary syndrome, hepatocellular carcinoma, and polycystic liver disease. Great strides have been made recently in models to predict mortality and complications following TIPS placement. Graft stents hold promise based on early studies. Finally, complications are common and may be life threatening.
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PMID:Current use of transjugular intrahepatic portosystemic shunts. 1253 Sep 46

Risk factors for the development of hepatocellular carcinoma (HCC) were investigated in 397 patients who underwent non-shunt operation for esophageal varices due to underlying cirrhosis or pre-cirrhosis between September 1979 and May 1995. Ninety-five of these patients developed HCC. The clinical characteristics of patients at the time of surgery for varices, stages (F0-F4) of the progression of fibrosis, and grades (A0-A3) of necroinflammatory activity in liver biopsy tissue obtained at surgery in 170 patients based on the New Inuyama Classification (Int. Hepatol. Commun. 6 (1996) 112), were analyzed to investigate their relationship with the development of HCC. In addition, the levels of AST and ALT were followed every 3 months after surgery in 116 patients, and were divided into 2 groups at 80 IU/ml to compare the level of risk for the development of HCC. In liver biopsy tissue, group F4 (n=68/152, 45%) showed a significantly higher (P=0.0224) rate of appearance of HCC than group F3 (n=3/18, 17%). Group F4 also tended to show a higher cumulative HCC appearance rate of 55% compared with 37% for group F3 at 10 years after surgery (P=0.097). In regard to activity, the appearance rate of HCC in group A2+A3 (n=52/112, 51%) was significantly higher (P=0.0008) than that of HCC in group A1 (n=14/58, 25%). The cumulative appearance rate (60%) of HCC in group A2+A3 was significantly higher than that (31%) in group A1 at 10 years after surgery (P=0.0003). The appearance rate of HCC was significantly higher in the group (n=33/44, 75%) with a mean AST level >/=80 IU/ml than in the group (n=41/72, 57%) with a mean AST level <80 IU/ml (P=0.0496). A multivariate analysis of the risk factors for the development of HCC showed that necroinflammatory activity was a risk factor. These results suggested that the histopathologic classification (the New Inuyama Classification) of liver biopsy tissue from patients who underwent non-shunt operation for esophageal varices due to underlying cirrhosis or pre-cirrhosis is useful for predicting the development of HCC, to which the grades of necroinflammatory activity in particular are more closely related.
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PMID:Clinicalpathological analysis of risk factors for the development of hepatocellular carcinoma after surgery for esophageal varices due to underlying cirrhosis or pre-cirrhosis in the 397 patients. 1264 40

BACKGROUND: Endoscopic injection sclerotherapy (EIS) for treatment of esophagogastric varices is well established in Japan. However, varices may still recur unpredictably following EIS. We studied this problem using endoscopic color Doppler ultrasonography (ECDUS) and specifically examined esophagogastric blood flows. METHODS: Prophylactic EIS was performed by intravariceal injection of 5% ethanolamine oleate (EO) in 49 patients with esophageal varices secondary to liver cirrhosis. No patient had documented hepatocellular carcinoma (HCC) before EIS, and patients who developed HCC during follow-up were excluded. We performed ECDUS before EIS, and 2 weeks and 2 years later. The esophagogastric intra- and extramural venous blood flows, including flow in the azygos vein, were compared between these observations. Gastric intramural blood flow and changes in extramural gastric blood flow, including the azygos vein flow, were scored. Dynamic computer tomography (CT), ultrasonography (US), and color Doppler-ultrasonography (CDUS) were also performed before EIS and 1 month following the procedure. Thereafter, patients underwent CT and US examinations every 6 months for 2 years to detect any development of porto-systemic shunts or HCC. RESULTS: The average number of EIS procedure per patient was 3.1+/-0.8 (mean+/-SD), and the total amount of sclerosant injected was approximately 33.5+/-6.5 ml. The overall recurrence rate over the 2-year follow-up was 36.7%. The gastric intra- and extramural blood flows did not differ between those patients with or without major shunts before EIS. In patients with recurrent variceal formation, the gastric intramural blood flow score following EIS (2.1+/-0.5) was significantly higher than that in patients without recurrence (0.8+/-0.6) (P<0.01). In addition, gastric extramural blood flow score following EIS (0.8+/-0.6) was significantly lower in patients with recurrence than that in those without recurrence (1.7+/-0.5) (P<0.01). The same differences held after exclusion of patients with major shunts. The gastric intramural blood flow score in patients with recurrent variceal formation (2.1+/-0.4) was significantly higher than that in patients without recurrence score (P<0.01). Moreover, gastric extramural blood flow score in patients with recurrent variceal formation (1.0+/-0.7) was significantly lower than in patients without recurrence (1.6+/-0.5) (P<0.01). CONCLUSIONS: Two characteristics were observed in patients with recurrent cases of esophageal varices 2 weeks following EIS. The first was the maintenance of gastric intramural blood flow. The second was the absence of dilation of the gastric extramural blood vessels. These observations may enable us to predict the recurrence of esophagogastric varices using ECDUS within 2 weeks following EIS.
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PMID:Endoscopic color Doppler ultrasonographic evaluation of recurrent esophagogastric varices following endoscopic injection sclerotherapy. 1285 Jun 88

DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of abdominal pain or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal varicose veins or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric varicose veins. In the case of large oesophageal-gastric varicose veins that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
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PMID:[Portal vein thrombosis]. 1453 80

Bacterial infection may adversely affect the hemostasis of patients with gastroesophageal variceal bleeding (GEVB). Antibiotic prophylaxis can prevent bacterial infection in such patients, but its role in preventing rebleeding is unclear. Over a 25-month period, patients with acute GEVB but without evidence of bacterial infection were randomized to receive prophylactic antibiotics (ofloxacin 200 mg i.v. q12h for 2 days followed by oral ofloxacin 200 mg q12h for 5 days) or receive antibiotics only when infection became evident (on-demand group). Endoscopic therapy for the GEVB was performed immediately after infection work-up and randomization. Fifty-nine patients in the prophylactic group and 61 patients in the on-demand group were analyzed. Clinical and endoscopic characteristics of the gastroesophageal varices, time to endoscopic treatment, and period of follow-up were not different between the two groups. Antibiotic prophylaxis decreased infections (2/59 vs. 16/61; P <.002). The actuarial probability of rebleeding was higher in patients without prophylactic antibiotics (P =.0029). The difference of rebleeding was mostly due to early rebleeding within 7 days (4/12 vs. 21/27, P =.0221). The relative hazard of rebleeding within 7 days was 5.078 (95% CI: 1.854-13.908, P <.0001). The multivariate Cox regression indicated bacterial infection (relative hazard: 3.85, 95% CI: 1.85-13.90) and association with hepatocellular carcinoma (relative hazard: 2.46, 95% CI: 1.30-4.63) as independent factors predictive of rebleeding. Blood transfusion for rebleeding was also reduced in the prophylactic group (1.40 +/- 0.89 vs. 2.81 +/- 2.29 units, P <.05). There was no difference in survival between the two groups. In conclusion, antibiotic prophylaxis can prevent infection and rebleeding as well as decrease the amount of blood transfused for patients with acute GEVB following endoscopic treatment.
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PMID:Antibiotic prophylaxis after endoscopic therapy prevents rebleeding in acute variceal hemorrhage: a randomized trial. 1499 93

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 23-year-old man was admitted to our department due to hemorrhage from gastric varices. He had been diagnosed as having Wilson's disease at the age of 17. Abdominal ultrasonography and computed tomography (CT) showed portal thrombosis and a large mass occupying most of the right lobe in the liver. The tumor was diagnosed as hepatocellular carcinoma (HCC) by image views and tumor markers. He died 3 months after the diagnosis, and an autopsy was performed. Histologic examination of the tumor showed moderately to poorly differentiated HCC. The nontumorous lesion of the liver revealed cirrhosis. HBX-DNA sequence was not detected in the liver. Hepatic cirrhosis is a well-recognized complication of Wilson's disease, but HCC is extremely rare. We describe the clinical findings of this patient and discuss the relationship of the development of HCC with a review of the relevant literature.
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PMID:Hepatocellular carcinoma associated with Wilson's disease. 1560 92

Nonalcoholic steatohepatitis (NASH) is a liver disease characterized by the histological features of steatohepatitis in the absence of significant alcohol consumption. The natural history of NASH is poorly defined. Here we report our experience with a patient to illustrate the clinical course of cirrhotic NASH. A 67-year-old woman was admitted with hematemesis due to the rupture of esophageal varices. Her varices were treated by endoscopic ligation and endoscopic sclerotherapy. Her medical history was unremarkable. Both the patient and her family members were asked about alcohol intake several times during her illness, but all of them denied a history of alcohol intake. She had insulin resistance, as determined by homeostasis model assessment. Serological tests for viral hepatitis were all negative. Viral hepatitis, autoimmune liver disease, iron overload, and metabolic liver disorders were all excluded. Imaging tests failed to reveal any steatosis, because of the presence of severe fibrosis. Liver biopsy showed moderate steatosis, moderate inflammation, ballooning degeneration, and Mallory bodies. We diagnosed NASH associated with cirrhosis based on the clinicopathological features. Almost 2 years later, she developed hepatocellular carcinoma (HCC) and she died of multiple HCCs. At autopsy, tumor invasion was seen throughout liver segment 8. The noncancerous liver showed burnt-out NASH; the steatosis, necroinflammation, ballooning degeneration, and Mallory bodies had all disappeared. In Japan, the prevalence of nonalcoholic fatty liver disease will increase as obesity has been increasing, so it is important to understand how to diagnose NASH. When a patient has NASH, careful follow-up should be performed.
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PMID:Nonalcoholic steatohepatitis: cirrhosis, hepatocellular carcinoma, and burnt-out NASH. 1562 89

In cirrhotic patients, esophageal and esophagogastric varices are the most common sites of bleeding, often responsible for hypovolemic shock. Hepatocellular carcinoma, blunt abdominal trauma and postprocedural complications are classical causes of hemoperitoneum in hepatic cirrhosis. Rupture of omental varices is another and rarely reported cause of shock in cirrhosis. We report a case of hypovolemic shock caused by ruptured omental varices. Selective review of literature regarding presentation, diagnosis and management of ruptured intraabdominal varices is also part of presentation.
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PMID:Spontaneous rupture of omental varices: an uncommon cause of hypovolemic shock in cirrhosis. 1572 80

In Germany, liver diseases are the leading cause of death through illness among 30 to 45 year olds. Most are chronic diseases and timely preventative or therapeutic measures could avert their manifestation or at least the following complications. Currently, screening for liver diseases is focused on specific groups at risk such as patients with alcohol abuse, relatives of patients with a genetic disease or individuals at risk of an infection with a viral hepatitis. For some diseases, studies have been started to test the practicability of population screening, which has already been successfully implemented for Hepatitis B and C in blood donors. Screening is also recommended for advanced liver disease. It helps to detect the development of cirrhosis and its complications namely varices and hepatocellular carcinoma.
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PMID:[Early diagnosis of liver diseases]. 1574 12


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