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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endoscopic sclerotherapy has emerged as an effective and safe mode of treatment for long-term management of esophageal varices due to cirrhosis of liver and extrahepatic portal venous obstruction. There are few studies that have evaluated the role of sclerotherapy in the management of esophageal varices in patients with noncirrhotic portal fibrosis (NCPF). We report our results of long-term sclerotherapy in patients with NCPF. Seventy-two consecutive patients (men 29, women 43; age 32.9 +/- 11.8 years) with recurrent variceal bleeding due to NCPF were entered into the sclerotherapy program. Forty-eight patients received intravariceal absolute alcohol and 24 patients received intravariceal sodium tetradecyl sulfate (STD). Variceal obliteration was achieved in 65 (90.3%) patients with a mean of 5.7 +/- 3.0 (range 1-14) sessions. These patients were followed-up for a mean of 21.4 +/- 20.4 (range 1-96) months. Thirteen (17.3%) patients had episodes of upper gastrointestinal bleeding during sclerotherapy. Rebleed after obliteration was seen in 6 (9.2%) patients. Sclerotherapy was associated with a significant reduction in bleeding rate (bleeds per month per patient) during sclerotherapy and after obliteration of varices as compared to presclerotherapy period (P < 0.000001 for both). Recurrence of esophageal varices after obliteration was seen in 9 (13.9%) patients with reobliteration of varices in five patients in whom sclerotherapy was attempted. Complications including esophageal ulcer and stricture formation were seen in 18 (25%) and 4 (5.6%) patients respectively; strictures were restricted to patients who received absolute alcohol. Two (2.77%) patients died of massive upper gastrointestinal bleed during follow-up. We conclude that sclerotherapy is an effective and safe modality in the prevention of variceal bleeds in patients with NCPF.
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PMID:Sclerotherapy in noncirrhotic portal fibrosis. 924 45

This study tests the hypothesis that administration of an oral amino acid load mimicking hemoglobin in patients with cirrhosis of the liver causes deterioration in neuropsychological function and a reduction in regional cerebral perfusion. Eight overnight fasted, metabolically stable cirrhotic patients with no evidence of overt hepatic encephalopathy were studied prior to and 4 h after simulating an upper gastrointestinal bleed by oral administration of 75 g of a solution mimicking the amino acid composition of hemoglobin. Neuropsychological function was measured using a test battery. Peripheral venous blood was collected for the measurement of ammonia and amino acid concentrations. Regional cerebral perfusion was measured using a head SPECT scanner following intravenous administration of technetium-99m hexamethyl propylamineoxime. The amino acid solution resulted in significant deterioration in the immediate and delayed story recall tests. Ammonia concentration increased from a median of 87 (range 67-94) micromol/L to 105 (98-112) micromol/L at 4 h after the simulated bleed (p < 0.01). The concentration of almost all amino acids increased; only isoleucine levels decreased following the upper gastrointestinal bleed. SPECT analysis showed a significant reduction in cerebral perfusion after the simulated bleed in both temporal lobes, left superior frontal gyrus, and right parietal and cingulate gyrus. An oral amino acid load mimicking hemoglobin in cirrhotic patients produces hyperammonemia and hypoisoleucinemia and causes a significant deterioration in memory tests, probably due to a reduction in regional cerebral perfusion. The model of simulating the metabolic effects of an upper gastrointestinal bleed in patients with cirrhosis of the liver seems to be useful in studying the metabolism of hepatic encephalopathy.
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PMID:Oral amino acid load mimicking hemoglobin results in reduced regional cerebral perfusion and deterioration in memory tests in patients with cirrhosis of the liver. 1260 81

A POTENTIALLY SEVERE EVENT: Upper gastrointestinal haemorrhage in a cirrhotic patient is always extremely serious, particularly in the case of rupture of the oesophageal varices, which is the most frequent cause. THE TWO POLES OF TREATMENT: Early vasoactive treatment permits elastic ligature in optimal conditions using an endoscope. The prevention of other complications of cirrhosis is an essential element in the management of these patients.
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PMID:[The place of endoscopic treatment in portal hypertension]. 1261 Apr 67

Upper gastrointestinal (UGI) bleeding in cirrhosis is associated with enhanced ammoniagenesis, the site of which is thought to be the colon. The aims of this study were to evaluate interorgan metabolism of ammonia following an UGI bleed in patients with cirrhosis. Study 1: UGI bleed was simulated in 8 patients with cirrhosis and a transjugular intrahepatic portasystemic stent-shunt (TIPSS) by intragastric infusion of an amino acid solution that mimics the hemoglobin molecule. We sampled blood from the femoral artery and a femoral, renal, portal, and hepatic vein for 4 hours during the simulated bleed and measured plasma flows across these organs. Study 2: In 9 cirrhotic patients with an acute UGI bleed that underwent TIPSS insertion, blood was sampled from an artery and a hepatic, renal, and portal vein, and plasma flows were measured. Study 1: During the simulated bleed, arterial concentrations of ammonia increased significantly (P =.002). There was no change in ammonia production from the portal drained viscera, but renal ammonia production increased 6-fold (P =.008). In contrast to an unchanged ammonia removal by the liver, a significant increase in muscle ammonia removal was observed. Study 2: In patients with an acute UGI bleed, ammonia was only produced by the kidneys (572 [184] nmol/kg bw/min) and not by the splanchnic area (-121 [87] nmol/kg bw/min). In conclusion, enhanced renal ammonia release has an important role in the hyperammonemia that follows an UGI bleed in patients with cirrhosis. During this hyperammonemic state, muscle is the major site of ammonia removal.
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PMID:The kidney plays a major role in the hyperammonemia seen after simulated or actual GI bleeding in patients with cirrhosis. 1277 5

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

Two-stage total hepatectomy and liver transplantation has been reported for acute liver disease such as fulminant hepatic failure, primary graft failure, severe hepatic trauma, and spontaneous hepatic rupture secondary to hemolysis, elevated liver function tests, low platelets syndrome, and preeclampsia. This is the first report of patients with cirrhosis to undergo a 2-stage total hepatectomy and liver transplantation. From 1984 to 2002, our institution performed 2008 orthotopic liver transplantations. We identified 4 patients with chronic liver disease who underwent a 2-stage hepatectomy and liver transplantation. This is a retrospective review of these 4 patients and a review of the literature on this procedure. All 4 patients were young men with an age range of 29-31 years and had underlying cirrhosis as well as a previous transjugular intrahepatic portosystemic shunt (TIPS)procedure. Acute decompensation fulfilling Ringes' criteria for toxic liver syndrome secondary to an upper gastrointestinal bleed occurred in all patients. The approximate average time between hepatectomy and liver transplantation was 20 hours (range: 8-42 hours). In all cases, the explanted liver showed histological changes of acute hepatic necrosis within the background of cirrhosis. After hepatectomy, vasopressor requirements were well documented in 2 patients. For 1 patient, there was a clear improvement in their hemodynamic status. The mean hospital stay of the 4 patients was 63 days. All patients were discharged from the hospital and are alive and well with adequate liver function at 6 to 37 months follow-up. Two-stage total hepatectomy and liver transplantation may be a life-saving procedure in highly selected cirrhotic patients with acute hepatic decompensation and multiorgan dysfunction.
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PMID:Two-stage total hepatectomy and liver transplantation for acute deterioration of chronic liver disease: a new bridge to transplantation. 1504 3

Upper gastrointestinal bleeding (UGIB) is a life-threatening complication of cirrhosis that develops from esophageal varices in almost 70% of patients. The mortality rate from the bleeding episodes is reported to be 30% [1-4]. Standard management of UGIB of cirrhotic patients is vasoactive therapy combined with endoscopic procedures such as endoscopic sclerotherapy and band ligation [5]. Currently, it is reported that recombinant activated fVIIa (Novoseven, NovoNordisc) can correct the prothrombin time in decompensated cirrhotic patients and also can be used safely in Child's B and C cirrhotic patients with UGIB [6-8]. Herein, we describe the first case report in the literature of a cerebrovascular event after the administration of a single dose of fVIIa in a cirrhotic patient with esophageal variceal bleeding.
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PMID:A cerebrovascular event after single-dose administration of recombinant factor VIIa in a patient with esophageal variceal bleeding. 1692 52

The treatment of portal hypertension in children has undergone considerable evolution in the past decade. The treatment offered depends on the cause of the hypertension and the underlying health of the liver. The diagnosis of portal hypertension often can be made by the history and physical examination. Upper gastrointestinal bleeding in the presence of splenic enlargement is pathognomonic for portal hypertension. Bleeding and hypersplenism are the principal symptoms. Treatment of bleeding starts with confirming the diagnosis with esophageal and gastric endoscopy. The patient is admitted to an intensive care unit and started on intravenous octreotide. Banding or sclerosis of esophageal varices will result in cessation of the bleeding but not a permanent cure. A careful investigation for the cause of the portal hypertension should be done. This includes imaging studies of intra-abdominal arteries and veins, a liver biopsy, and liver function tests, including coagulation studies. For patients with extrahepatic portal vein thrombosis, early consideration should be given to surgical treatment with a meso-Rex bypass. Patients with liver disease should be treated for the underlying disorder and undergo regular endoscopic monitoring for recurrence of varices. Patients with well-compensated cirrhosis should be considered for selective surgical shunting, and those with advanced disease for liver transplantation. The benefit of long-term beta blockers in children has not been proven by clinical trials.
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PMID:Medical and surgical management of portal hypertension in children. 1694 69

Upper gastrointestinal hemorrhage carries significant morbidity and mortality in patients with portal hypertension and cirrhosis. The optimal prevention strategy for rebleeding in these patients remains controversial with respect to the safety and efficacy of transjugular intrahepatic portosystemic shunt (TIPS) versus a portocaval surgical shunt (PC). We sought to determine the long-term cost-effectiveness of these two treatments. A Markov state transition decision analysis was created and Monte Carlo sensitivity analysis performed to follow patients with early cirrhosis who have an upper gastrointestinal bleed despite medical therapy into either TIPS or PC. Patients were followed throughout the transition states until either death or survival. Probabilities of gastrointestinal rebleed, hepatic encephalopathy, surgical and TIPS-related complications as well as death were obtained from an extensive literature review. Costs were derived from average Medicare reimbursements. The main outcome was dollars per life-year saved. For patients with mild to moderate cirrhosis with upper gastrointestinal variceal bleed, the average cost per life year saved was $17,771 (SD = 471) and $21,438 (SD = 308) for TIPS and PC, respectively. The average life expectancy was 5.0 years and 7.0 years for TIPS and PC, respectively. This yielded an incremental cost-effectiveness rate for portocaval shunt of $3,299 per life year saved. Compared with TIPS, surgical PC shunt resulted in improved survival with minimal increase in cost. Therefore, given the low incremental cost of PC, it should be adopted as a cost-effective strategy in managing this patient population.
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PMID:Cost-effective analysis of transjugular intrahepatic portosystemic shunt versus surgical portacaval shunt for variceal bleeding in early cirrhosis. 2133 74

Massive bleeding hemobilia occurs rarely in patients with hepatocellular carcinoma (HCC) without any invasive procedure. Upper gastrointestinal bleeding in patient with cirrhosis and abdominal pain with progressive jaundice in patient with HCC were usually thought as variceal bleeding and HCC progression respectively. We experienced recently massive bleeding hemobilia in patient with HCC who was a 73-year old man and showed sudden abdominal pain, jaundice and hematochezia. He had alcoholic cirrhosis and history of variceal bleeding. One year ago, he was diagnosed as HCC and treated with transarterial chemoembolization periodically. Sudden right upper abdominal pain occurred then subsided with onset of hemotochezia. Computed tomography showed bile duct thrombosis spreading in the intrahepatic and extrahepatic ducts, while an ampulla of vater bleeding was observed during duodenoscopy. Hemobilia could be one of the causes of massive bleeding in patients with cirrhosis and HCC especially when they had sudden abdominal pain and abrupt elevation of bilirubin.
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PMID:[Massive bleeding hemobilia occurred in patient with hepatocellular carcinoma]. 2335 50


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