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

Using with the newly modified perchloric acid pretreatment method and endotoxin specific assay (Endospecy), the plasma endotoxin in the patients with liver cirrhosis was investigated. The mean value of plasma endotoxin in control (n = 20) was below 9.8 pg/ml. The plasma endotoxin level in liver cirrhosis was 5.7 +/- 5.3 pg/ml (n = 70, mean +/- SD), and 20% of the patients (15 cases) showed above 9.8 pg/ml. Endotoxin level significantly correlated with the severity of liver function based on the Child-Turcotte classification (p less than 0.01). Plasma endotoxin positively correlated with total bilirubin (r = 0.417) and ICG clearance test (r = 0.298) and negatively correlated with prothrombin time (%) (r = 0.497) and HDL-cholesterol (r = 0.578) in the patients with liver cirrhosis. There was no correlation between esophageal varices and plasma endotoxin level. Plasma endotoxin was slightly detected in the patients with decompensated cirrhosis, and these data suggest that plasma endotoxin level in cirrhosis is not so elevated.
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PMID:[Plasma endotoxin measured by the combination of new perchloric acid pretreatment method and endotoxin specific assay in liver cirrhosis]. 132 Jan 42

Clinically, idiopathic portal hypertension (IPH) is characterized by overt splenomegaly with pancytopenia, portal hypertension and relatively mild abnormalities in liver function tests. Although its etiology is still undetermined, the liver pathology is characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, irregularly distributed parenchyma atrophies and absent of regeneration nodules. The disease is relatively benign and does not progress to cirrhosis. Differential diagnosis between IPH and liver cirrhosis is mandatory. We now report a case with histologically proven IPH, including clinical course, laboratory data, roentgenographic findings of hepatic venogram and celiac angiogram, hepatic hemodynamic features and intravariceal pressure of esophageal varix which has never been reported in Taiwan.
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PMID:Idiopathic portal hypertension: a case report. 132 89

A novel, simple, clinically useful quantitative liver function test, called the galactose single point (GSP) method, was developed by measurement of galactose blood concentration 1 h after galactose was administered (0.5 g/kg). It was quickly infused intravenously in 55 normal healthy volunteers, 73 patients with chronic hepatitis (CH), 36 with cirrhosis and 41 with hepatocellular carcinoma (HCC). Patients with CH diagnosis were assessed by liver biopsy. Cirrhosis was diagnosed by histological examination or a chronic hepatitis history with esophageal varices or ascites, whereas HCC was diagnosed either histologically, or cytologically proved, or as implied in the 'one imagine study' being positive with AFP > 300 ng/dl. Highly significant galactose blood levels were observed between normal healthy volunteers and patients 50, 60 and 70 min after galactose was administered. Galactose elimination capacity (GEC), modified GEC (MGEC) and consecutive GSP tests were performed in 6 healthy volunteers for 2 days. 0.64-16.87% variation was observed for each subject. The significant differences (p < 0.001) in average GSP values were 247 +/- 18.1, 422 +/- 27.3, 629 +/- 42.8 and 579 +/- 43.6 micrograms/ml for normal healthy volunteers, CH, cirrhosis and HCC patients, respectively. Highly significant correlations (p < 0.001) were obtained among GSP, GEC and MGEC for all patients. Positive correlations were observed between GSP, GEC, MGEC and AST (serum aspartate aminotransferase), ALT (serum alanine aminotransferase), serum bilirubin, albumin, prothrombin time and r-globulin. According to results obtained from 202 normal healthy volunteers and patients, the GSP method may be a simple, clinically useful quantitative measurement of liver function for the determination of a patient's residual liver function, the prognosis of liver function for patients with cirrhosis, postoperational follow-up and, finally, the timing of a liver transplant.
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PMID:Assessment of liver function using a novel galactose single point method. 133 11

Varices of the colostomy are a rare complication of colostomy performed in patients with portal hypertension. This work is based on 14 cases. The colic stomy is the terminal operation in surgery for cancer in twelve cases, and a bypass stomy in two cases. Portal hypertension is due to cirrhosis in 10 cases and to metastases to the liver in 4 cases. All 14 colostomy varices were expressed by bleeding. In 7 cases, oesophageal varices were detected with fiberendoscopy. Only one of these patients had an upper digestive hemorrhage. Colostomy hemorrhages are the revealing complication and the main sign of the disease. The emergent treatment of bleeding of the colostomy must combine several methods, most often consecutively: local compression, ligation, sclerotherapy. Once bleeding is controlled, the radical treatment must be primarily medical (hygienic and dietary habits, beta-adrenergic blocking agents), but complementary surgery may prove to be necessary, most often to redo the colostomy with additional deconnection. The prognosis mainly depends on the function of the liver, the deterioration of which is accelerated by the successive hemorrhagic accidents. Hepatorenal failure is the main cause of death.
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PMID:[Colostomy-induced varices in portal hypertension]. 133 37

There are different opinions in respect to the main sources in upper gastrointestinal bleeding in hepatic cirrhosis. Some authors claim that ruptured esophageal varices are the cause of most of the hemorrhages. Recently, characteristic lesions have been showed in the gastric mucosa in portal hypertension (congestive gastropathy), and many believe that they are frequently the origin of the bleeding. We reviewed the records of 195 episodes of upper gastrointestinal bleeding in cirrhosis, with endoscopy performed within 12 hours of entry, and report here the endoscopic findings and the bleeding sites. We also investigated the relation between the etiology and functional class of the hepatic disease and the bleeding source. We observed variceal hemorrhage in 52.2% of cases; by gastroduodenal mucosal lesions in 13.8%; by gastric and duodenal ulcers in 13.8%; undetermined origin in 14.8% (due to coexistence of two or more lesions, without active bleeding). We found no differences between alcoholic and nonalcoholic cirrhotics in the bleeding sources. Furthermore, the bleeding sites were not different either in child A, B and C patients. In contrast, in major hemorrhages, esophageal varices were more frequently the origin (73.5%) than in minor ones (40.4%) (p < 0.002). The mortality was significantly higher in CHild C group (25%), than in groups B (14.3%) and A (2.3%) (p < 0.05 and p < 0.002, respectively). We recommend to carry out early endoscopy in every cirrhotic patient suffering from gastrointestinal bleeding, by skilled performers who are able to recognize the gastric red signs, before making a decision about potentially dangerous therapeutic measures, such as surgery, balloon tamponade, etc.
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PMID:[Upper digestive hemorrhage in liver cirrhosis: clinical and endoscopic findings]. 134 Nov 18

Increased portal pressure is the product of both increased resistance to splanchnic flow through the liver and increased blood flow in the portal circuit. Although portal hypertension in children is less common than in adults, the important clinical end results are the same, ie, esophageal variceal hemorrhage, ascites, and hypersplenism. The etiology of portal hypertension in children is very different from adults in whom cirrhosis (most commonly secondary to alcohol) is the predominant cause. In children, extrahepatic obstruction due to portal vein thrombosis is the most common cause. However, as children survive longer with biliary atresia, cystic fibrosis, and other liver diseases, the incidence of intrahepatic obstruction causing portal hypertension is increasing. The treatment has also undergone a dramatic evolution over the last decade with the near extinction of portosystemic shunt procedures and their replacement with endoscopic treatment of esophageal varices and liver transplantation.
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PMID:Portal hypertension. 134 80

The influence of octreotide and somatostatin on liver metabolic activity were studied in 16 patients with cirrhosis that was positive for hepatitis B surface antigen (HBsAg). In patients receiving a 50 micrograms bolus and a 50 micrograms/hr infusion of octreotide, the hepatic blood flow, hepatic clearance, and the maximum velocity/metabolic elimination rate constant (Vmax/km) were significantly reduced after octreotide infusion compared with basal values. Similarly, the hepatic blood flow, hepatic clearance, and Vmax/km were significantly decreased in patients receiving a 250 micrograms bolus and a 250 micrograms/hr infusion of somatostatin. The extraction ratio and the systemic hemodynamic values, including cardiac index, heart rate, mean arterial pressure, and systemic vascular resistance, showed no significant changes in patients receiving either octreotide or somatostatin. These findings suggest that, as with somatostatin, octreotide reduced hepatic blood flow and impaired liver metabolic activity in patients with HBsAg-positive cirrhosis. These effects may have important clinical implications in the management of bleeding esophageal varices in patients with cirrhosis.
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PMID:Octreotide decreased liver metabolic activity in patients with hepatitis B surface antigen-positive cirrhosis. 135 73

Portal hypertension is characterised by alterations in the splanchnic and systemic circulation resulting in the development of portosystemic collateral channels, the most important of which are found in the lower oesophagus and stomach. The major clinical complication of gastro-oesophageal varices is bleeding and over the last decade there has been considerable interest in the pharmacological management of this complication. The factors currently implicated in the development of gastro-oesophageal varices in patients with cirrhosis include a) increased portal vascular resistance, b) splanchnic and systemic vasodilatation and c) changes in the lower oesophageal venous anatomy [palisade and perforating venous zones]. In a patient with gastrointestinal bleeding, endoscopic examination of the upper gastrointestinal tract will confirm the diagnosis of portal hypertension by confirming the presence of gastro-oesophageal varices. Cirrhosis is the most common aetiological factor for gastro-oesophageal varices, but imaging techniques, including Doppler ultrasound, computerised tomography and venous phase angiography, may be required to exclude extrahepatic portal venous obstruction from the differential diagnosis. Although the pathogenesis of variceal rupture remains unclear, several risk factors for variceal haemorrhage have been identified, including a) increased size, b) high intravariceal-portal pressure, c) increased varix wall tension characterised by the presence of red spots observed at endoscopy (particularly in large varices since wall tension is related to variceal size), and d) poor liver function. Although oesophagitis may be observed at endoscopy, an erosive mechanism is no longer considered to be of pathogenic significance. A high portal pressure in the immediate postbleeding period is now recognised as predictive of rebleeding. Periodic elevations in intravariceal pressure, associated with the release of enhanced endogenous vasoactive compounds, or beta-adrenergic-mediated stress-related increases in portal pressure, may contribute to the rupture mechanism. Consequently, portal hypertension is now being more widely considered as a multiorgan disorder associated with changes in blood flow within both systemic and splanchnic vascular beds. This article reviews the factors currently implicated in the development of portal hypertension and the approach to diagnosis. The pathogenesis of variceal bleeding will also be considered.
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PMID:Mechanisms and consequences of portal hypertension. 138 66

A distal splenorenal (Warren) shunt was performed on a 39-year-old female with bleeding esophageal varices secondary to portal hypertension and cirrhosis. On the twelfth postoperative day, however, she rebled, and angiography revealed that the shunt was occluded. Using a percutaneous approach, successful balloon angioplasty and recanalization was performed. The patient did well and was discharged without further bleeding. Percutaneous transluminal angioplasty (PTA) appears to be effective in dilating occluded splenorenal shunts, obviating a second surgical procedure in high-risk patients.
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PMID:Percutaneous transluminal angioplasty of an occluded distal splenorenal shunt. 138 95

A prospective evaluation was conducted of 94 unselected patients ("all comers") with biopsy-proven Child's class C cirrhosis (93% alcoholic) and endoscopically proven acutely bleeding esophageal varices who underwent emergency portacaval shunt (EPCS) (85% side-to-side, 15% end-to-side) within 8 hours of initial contact (mean, 6.1 hours) during the past 12 years. Follow-up has been 100% and includes all patients for at least 1 year, and 61 patients (65%) for 5 to 12 years. Incidence of serious risk factors on initial contact was: ascites, 97%; jaundice, 86%; portal-systemic encephalopathy including past history, 71%; severe muscle wasting, 96%; alcohol ingestion within 7 days, 66%; delirium tremens, 16%; serum albumin, less than or equal to 2.5 g/dL 76%; indocyanine green dye retention greater than or equal to 50% in 45 minutes, 66%; serum glutamic-oxaloacetic transaminase greater than or equal to 100 units/L, 60%; hyperdynamic cardiac output greater than or equal to 6 L/minute, 98%. Mean Child's point score was 13.7 out of a maximum of 15. EPCS reduced mean corrected free portal pressure from 286 to 23 mm saline, and permanently controlled variceal bleeding in every patient. Of the 94 patients, 74 (80%) left the hospital alive and 68 (72%) survived 1 year. Five-year actuarial survival rate is 64%. Hepatic failure was the main cause of death during initial hospitalization as well as during follow-up, when it was related to continued alcoholism. Portal-systemic encephalopathy, which was present on initial contact in 55% of patients, occurred at some time during follow-up in 18.7%, but was recurrent and required dietary protein restriction in only 9%, all of whom had resumed alcoholism. The low incidence of portal-systemic encephalopathy was attributable to the lifelong program of follow-up with regular dietary counseling and continued emphasis on both protein restriction to 60 g/day and abstinence from alcohol. Abstinence was sustained in 69%, liver function improved in 82%, general health was judged excellent or good in 73%, and Child's risk class converted to class B in 73% and class A in 21%. Excluding retirees because of age, 42% were gainfully employed or engaged in full-time housekeeping. Long-term shunt patency was documented in 100% of survivors by yearly angiography or Doppler ultrasonography. It is concluded that EPCS within 8 hours of initial contact permanently controls variceal hemorrhage and results in prolonged survival and a life of acceptable quality in many alcoholic cirrhotic patients in Child's class C.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Is portal-systemic shunt worthwhile in Child's class C cirrhosis? Long-term results of emergency shunt in 94 patients with bleeding varices. 141 75


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