摘要:

AbstractThirteen patients with cirrhosis and tense ascites (six with and seven without peripheral edema) underwent 4‐ to 15‐liter paracentesis without intravenous “colloid” replacement. Cardiac output increased from 6.6 ± 0.7 liters per min at baseline to 8.2 ± 0.7 liters per min (p<0.003) 1 hr after large‐volume paracentesis completion and fell to 7.5 ± 0.69 liters per min (p<0.05 vs. baseline, p<0.02 vs. 1 hr) 24 hr after large‐volume paracentesis completion. There was no change in mean arterial pressure or mean pulmonary artery pressure. Central venous pressure fell from 9.1 ± 0.8 mm Hg at baseline to 8.6 ± 1.4 mm Hg 1 hr post‐large‐volume paracentesis to 6.8 ± 1.0 mm Hg (p<0.005 vs. baseline, p<0.02 vs. 1 hr value) at 24 hr, and pulmonary capillary wedge pressure fell from 13.1 ± 0.9 to 11.1 ± 1.3 mm Hg 1 hr after large‐volume paracentesis and to 9.89 ± 1.2 (p<0.01 vs. baseline, p<0.03 vs. 1 hr after large‐volume paracentesis) at 24 hr. Heart rate fell from 90 ± 3.0 to 85 ± 2.9 beats per min (p<0.01) 1 hr after large‐volume paracentesis completion, but increased to 89 ± 2.5 beats per min (p<0.02 vs. 1 hr after large‐volume paracentesis) at 24 hr. Blood urea nitrogen fell from 13.3 ± 1.8 to 11.7 ± 1.6 mg per dl (p<0.004) 1 hr after large‐volume paracentesis, but was unchanged at 24 and 48 hr after large‐volume paracentesis. Serum creatinine did not change during the study, but creatinine clearance fell from 77 ± 12.0 ml per min at baseline to 67 ± 7.0 ml per min (p<0.05 vs. baseline) 24 hr after large‐volume paracentesis and to 60 ± 7.5 ml per min (p<0.05 vs. baseline) 48 hr after large‐volume paracentesis. Serum sodium concentration at baseline was 135 ± 1.2 mEq per liter; 1 hr after large‐volume paracentesis decreased to 133 ± 1.5 mEq per liter (p<0.03); and at 48 hr was 132 ± 2.1 mEq per liter (p<0.03). Serum aldosterone fell from 59.3 ± 17.0 to 41 ± 12 ng per dl 1 hr after large‐volume paracentesis (p<0.05), but increased to 59 ± 17.0 mg per dl (p<0.05 vs. 1 hr after large‐volume paracentesis) at 24 hr. Plasma renin activity did not change at 1 hr, but increased from baseline 21.8 ± 5.9 to 35.9 ± 12.0 ng per ml per hr 24 hr after large‐volume paracentesis (p<0.07 vs. 1 hr and baseline value). There was no change in plasma atrial natriuretic factor levels from baseline to 1 hr post‐large‐volume paracentesis, but it did fall from baseline (176 ± 22 pg per ml) to 24 hr after large‐volume paracentesis (156 ± 20 pg per ml, p<0.05). Estimated hepatic blood flow (assessed by galactose clearance) did not change during the study. Nonedematous patients had greater drop in central venous pressure at 24 hr after large‐volume paracentesis (5 ± 1.7 vs. 8 ± 1.3 mm Hg, p<0.05) than those with edema and also had an increase in heart rate (82 ± 3.1 to 84 ± 3.4 beats per min) compared to a fall (97 ± 2.7 to 93 ± 2.0 beats per min) at 24 hr in those with edema (p<0.03). We conclude that large‐volume paracentesis has no immediate adverse cardiovascular effect, but does produce a p

ISSN:0270-9139    

DOI:10.1002/hep.1840070302

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractOne hundred and twelve consecutive Child Class A and B cirrhotic patients were included in a prospective controlled trial aimed at investigating the efficacy and safety of endoscopic sclerotherapy vs. distal splenorenal shunt in the elective treatment of hemorrhage from esophagogastric varices. Fifty‐seven patients were randomly allocated to splenorenal shunt and 55 to endoscopic sclerotherapy. Since only 4 of the 55 patients assigned to endoscopic sclerotherapy had to be excluded after randomization and before treatment as compared to 14 of the 57 patients assigned to splenorenal shunt, it is suggested that the applicability of endoscopic sclerotherapy is greater than that of splenorenal shunt. One patient in each group died within 30 days of the procedure and two in the endoscopic sclerotherapy group were lost to follow‐up just after discharge. Variceal rebleeding during follow‐up occurred in 37.5% (18/48) of patients in the endoscopic sclerotherapy group and in 14.3% of those in the splenorenal shunt group (6/42) (p<0.02), whereas hepatic encephalopathy was more frequent in patients submitted to splenorenal shunt (10/42, 24%) than in those treated by endoscopic sclerotherapy (4/48, 8%) (p<0.05). The therapeutic modality was the only variable with independent predictive value for rebleeding during follow‐up, whereas for hepatic encephalopathy, the therapeutic modality, and the presence of encephalopathy related to the bleeding episode each showed independent predictive value. Early and long‐term mortality, did not differ between the two therapeutic groups, being the 2‐year survival was 71% for splenorenal shunt and 68% for endoscopic sclerotherapy. It is concluded that endoscopic sclerotherapy is a good alternative to splenorenal shunt in the elective treatment of esophageal variceal bleeding, especially in patients prone to develop hepatic enc

ISSN:0270-9139    

DOI:10.1002/hep.1840070303

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractHeavy diffuse bleeding from congested gastric mucosa (congestive gastropathy) was treated by propranolol (dose = 24 to 480 mg per day) in 14 consecutive patients with portal hypertension. Thirteen patients (93%) stopped bleeding within 3 days. Gastric mucosal cherry red spots (a sign of severe gastropathy) were unchanged in 5 patients, became less obvious in 4 and appearances returned to normal in 5. Propranolol was discontinued electively in seven patients after 2 to 6 months; four of these patients rebled from the same lesion and stopped bleeding when propranolol was recommenced. No patient has rebled from congestive gastropathy while receiving propranolol during follow‐up of 12 to 42 (median = 23) months.A further 24 patients with nonbleeding congestive gastropathy received 160 mg long‐acting propranolol per day in a double‐blind placebo controlled cross‐over trial. Twenty‐two patients completed the study; in nine patients, endoscopic grading of congestive gastropathy improved after propranolol compared to three after placebo (p<0.05). Although the mechanism of action is not understood, propranolol appears to have a clinically significant role in the management of nonvariceal gastric bleeding in portal hyp

ISSN:0270-9139    

DOI:10.1002/hep.1840070304

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractWe examined the hemodynamic changes induced by transient splenic arterial occlusion using a balloon catheter to investigate the hemodynamic effect of transcatheter splenic arterial embolization—a procedure that has been used since its introduction in 1973 as therapy for hypersplenism and more recently for portal hypertension. The blood flow volume was measured in 20 patients with liver disease using an ultrasonic duplex system (Toshiba SAL50A/SDL‐01A). The portal venous pressure was also measured via a 3F catheter using a transducer. The catheter was placed in position by substituting it for a 25‐gauge needle that had been inserted into the portal vein under ultrasonic guidance percutaneously and transhepatically.Splenic arterial occlusion caused a drop in splenic venous blood flow from 708 ± 487 to 241 ± 155 ml per min, in portal venous blood flow from 993 ± 439 to 807 ± 419 ml per min and in portal venous pressure from 17.4 ± 7.2 to 14.4 ± 6.1 mm Hg. The latter two reductions were less than expected from the decrease in the splenic venous blood flow volume. This phenomenon was caused by an increase in the mesenteric venous blood flow from 475 ± 126 to 630 ± 270 mm per min.This increase may be due to a compensatory mechanism under the control of a regulatory loop in the liver or portal vein, and there seems to be a relationship between splenic and intestinal circulation in portal hypertension that maintains hepati

ISSN:0270-9139    

DOI:10.1002/hep.1840070305

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractIn a previous randomized trial, we demonstrated that propranolol prevented recurrent gastrointestinal bleeding in patients with cirrhosis. We have undertaken the present study in a new group of patients to ascertain the factors associated with rebleeding. Among 232 patients with cirrhosis admitted for gastrointestinal bleeding, 127 were included. They received propranolol orally at a dose reducing the heart rate by 25%. The median follow‐up period was 682 days. The following factors were studied: cause of cirrhosis; severity of cirrhosis; hepatocellular carcinoma recognized after inclusion; compliance; persistent decrease in heart rate; dose of propranolol; alcohol abstinence; previous history of hemorrhage; time interval from hemorrhage to onset of propranolol administration, and source of bleeding. The percentage of patients free of rebleeding was 71% at 1 year and 57% at 2 years. Only five factors were significantly and independently associated with rebleeding: occurrence of hepatocellular carcinoma; lack of compliance; lack of persistent decrease in heart rate; lack of abstinence, and previous history of bleeding. In conclusion, this study confirms the results of our previous trial and suggests that certain factors play a role in the mechanism of rebleeding in patients receiving propranolo

ISSN:0270-9139    

DOI:10.1002/hep.1840070306

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractThe role of changes in blood‐brain barrier permeability in the pathogenesis of hepatic encephalopathy remains uncertain. To test the hypothesis that brain microvessel permeability is nonselectively increased in hepatic encephalopathy we measured the blood‐brain barrier permeability‐surface area product in rats with acute liver failure induced by intraperitoneal injection of galactosamine. The permeability‐surface area products to the diffusion‐limited tracers, sucrose and methylaminoisobutyric acid, were determined as a measure of blood‐brain barrier permeability. Animals were examined 24, 36 and 42 hr after injection, at times when they were stuporous, but not comatose. No significant elevations of the permeability‐surface area products for either compound were detected in clinically affected experimental animals when compared to controls. Our results indicate there is no generalized increase in brain vascular permeability during hepatic insufficiency in precom

ISSN:0270-9139    

DOI:10.1002/hep.1840070307

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractThe aim of this study was to determine the prognostic significance of functional changes in the liver during progression of cirrhosis. Liver function was quantitated weekly by the aminopyrine breath test (measuring microsomal function) and the galactose breath test (measuring cytosolic function) in rats made cirrhotic by bile duct ligation (n = 14) and in sham‐surgery controls (n = 9). Nine rats died spontaneously of cirrhosis. Both the aminopyrine breath test and galactose breath test were sensitive (89%) predictors of death within 1 week, but the galactose breath test was more specific (83%). Morphometric measurements of livers from surviving cirrhotic animals and controls (n = 5 each) showed that mean hepatocyte mass was maintained in the cirrhotic livers [cirrhosis (17.0 ± 2.0) vs. controls (13.9 ± 0.9 gm)]. The galactose breath test was also maintained, whereas the aminopyrine breath test was significantly decreased in the surviving cirrhotics. The galactose breath test, but not the aminopyrine breath test, correlated with hepatocyte mass (r = 0.67). The aminopyrine breath test correlated with microsomal aminopyrineN‐demethylase activity (r = 0.78). Serial use of quantitative liver tests allows prediction of time of death from cirrhosis in this

ISSN:0270-9139    

DOI:10.1002/hep.1840070308

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractTo determine whether the aminopyrine breath test can be used to document the presence of cirrhosis in patients with cholestatic liver disease, 19 patients (13 primary biliary cirrhosis, 4 sclerosing cholangitis and 2 chronic extrahepatic bile duct obstruction) underwent clinical and biochemical evaluations, liver biopsies and an aminopyrine breath test. Results were compared with those in 10 patients with biopsy‐proven chronic active hepatitis with bridging and/or cirrhosis and in 22 healthy subjects. The aminopyrine breath test results in the 10 cholestatic patients with cirrhosis were not significantly different from the results in precirrhotic cholestatic patients (mean ± S.D., 11.2 ± 5.0 vs. 11.6 ± 2.8 %dose per 2 hr, p<0.05) or healthy subjects (11.5 ± 2.9 %dose per 2 hr). In contrast, the results in the patients with chronic hepatitis were markedly depressed (3.2 ± 1.9 %dose per 2 hr, p<0.05). The aminopyrine breath test results did not correlate with results of conventional liver function tests in the cholestatic patients. These results demonstrate that the aminopyrine breath test is not clinically useful in identifying the presence of cirrhosis in patients with cholestatic liver disease, and provide further evidence that decreased microsomal enzyme function is a late feature of cholestatic liver d

ISSN:0270-9139    

DOI:10.1002/hep.1840070309

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractHuman sera, containing anti‐liver‐kidney microsome antibody as demonstrated by indirect immunofluorescence, were obtained from a subgroup of young patients with autoimmune chronic hepatitis. The anti‐liver‐kidney microsome antibody‐positive sera were used to study the localization of the liver‐kidney microsome antigen in hepatocytes. Immunoblot analysis of microsomal subfractions, lysosomal membranes, plasma membranes, mitochondria and purified ribosomes obtained from rat liver demonstrated that this antibody recognizes a protein of 50 kD present only in endoplasmic reticulum membranes. Immunogold labeling of ultrathin frozen sections and immunoperoxidase staining of 11 to 15 μm cryostat sections were used to detect the liver‐kidney microsome antigen in rat liver tissue. The anti‐liver‐kidney microsome antibody binds to antigenic domains on the cytoplasmic face of smooth and rough endoplasmic reticulum membranes of hepatocytes. No labeling was observed of the Golgi apparatus, peroxi‐somes, mitochondria, lysosomes, nuclei or plasma membranes. Not only was the antigen recognized by the anti‐liver‐kidney microsome antibody specific for endoplasmic reticulum membranes, but it was also specific for the endoplasmic reticulum of hepatocytes only, since no labeling was observed in any organelle of Kupffer or endothelial cells. Therefore, the anti‐liver‐kidney microsome antibody can be considered as a marker for endoplasmic

ISSN:0270-9139    

DOI:10.1002/hep.1840070310

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY

摘要:

AbstractThe acute vanishing bile duct syndrome can be defined as an irreversible, rejection‐related condition that affects hepatic allografts within 100 days after orthotopic liver transplantation and whose presence requires retransplantation. We have observed the acute vanishing bile duct syndrome in 5 of 48 consecutive patients (approximately 10%) who underwent orthotopic liver transplantation. In 4 cases, the condition progressed relentlessly within approximately 7 to 11 weeks after orthotopic liver transplantation from mild rejection to severe rejection to acute vanishing bile duct syndrome. A fifth patient had severe rejection in the first week and required retransplantation after 17 days because of thrombotic venoocclusive disease complicating the acute vanishing bile duct syndrome. Clinically, signs of impending acute vanishing bile duct syndrome included abrupt onset of fever and jaundice and marked elevation of serum bilirubin and alkaline phosphatase levels which persisted despite antirejection treatment. Biopsy specimens revealed destructive cholangitis (rejection cholangitis), ductopenia, and, if retransplantation was delayed, presence of noninflammatory, “burnt‐out” portal tracts without bile ducts. We recommend to base the diagnosis of acute vanishing bile duct syndrome on documentation of severe ductopenia in at least 20 portal tracts which may require several consecutive needle biopsies. Rejection arteriopathy which was found in 3 of our 5 cases might have been another important diagnostic clue but could not be recognized prior to retransplantation. The pathogenesis of acute vanishing bile duct syndrome is not clear; until the condition had manifested itself, we found no qualitative differences between acute reversible and irreversible rejection. After retransplantation, severe rejection has recurred in the four patients who could be evaluated in this regard; one of these patients already needed a second retransplantation for vanishing bile duct s

ISSN:0270-9139    

DOI:10.1002/hep.1840070311

出版商:W.B. Saunders    

年代:1987

数据来源: WILEY