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

This paper reports the preliminary results of a prospective randomized trial comparing endoscopic variceal sclerosis and distal splenorenal shunt (DSRS) in the management of patients with cirrhosis and variceal bleeding. Seventy-one patients have been entered; 36 have received sclerosis and 35 DSRS. Randomization of the study population was stratified on Child's A/B (56%) and Child's C (44%). Sixty-one per cent had alcoholic and 39% non-alcoholic cirrhosis. No patients have been lost to follow-up, which currently stands at a median of 26 months. Rebleeding occurred significantly (p less than 0.05) more frequently in patients in the sclerosis group (19 of 36: 53%) compared to DSRS (1 of 35: 3%), but only 11 of 36 (31%) were not controlled by further sclerosis and failed that therapy. Patients in whom sclerosis failed underwent surgery. Survival was significantly (p less than 0.01) improved in the sclerosis group (+ surgery in 31%), with an 84% 2-year survival compared to a 59% 2-year survival in the DSRS group. Portal perfusion was significantly (p less than 0.05) better maintained in the sclerosis (95%) compared to the DSRS (53%) group. Galactose elimination capacity improved significantly (p less than 0.05) in 21 patients successfully managed by sclerosis at 1 year and was significantly (p less than 0.01) better maintained in the sclerosis compared to DSRS group. The authors conclude that endoscopic sclerosis: has a higher rebleeding rate than DSRS, with one third of patients failing therapy from rebleeding; allows significant improvement in liver function when successful; and gives significantly improved survival in the management of variceal bleeding when backed up by surgical therapy for patients with uncontrolled rebleeding.
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PMID:Distal splenorenal shunt versus endoscopic sclerotherapy for long-term management of variceal bleeding. Preliminary report of a prospective, randomized trial. 348 41

From 1968 to 1984, 250 patients with cirrhosis and bleeding esophageal varices underwent portal disconnection of the esophagus using either Murphy's button (before 1974) or an esophageal device developed by one of the authors (after 1974). One hundred and thirty-four patients underwent operation on an elective basis and 116 underwent emergency procedures. With the use of Child's classification, 62 patients were class A, 125 were class B and 63, class C. The over-all operative mortality rate was 24.4 per cent but this varied with the hepatic functional status and whether or not the operation was done on an elective or emergency basis. The long term survival rates were 53 per cent at one year, 36 per cent at three years, 24 per cent at five years and 8 per cent at ten years. Ninety-six per cent of the patients were without proved recurrent esophageal bleeding at one year, 88 per cent at three years, 79 per cent at five years and 66 per cent at ten years. Portal disconnection of the esophagus using an anastomotic button is a simple and effective procedure which can benefit many patients with cirrhosis who undergo an operation for bleeding varices on an elective or emergency basis. It constitutes an efficacious prophylactic means for preventing recurrent bleeding from esophageal varices.
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PMID:Long term results after portal disconnection of the esophagus using an anastomotic button for bleeding esophageal varices in cirrhosis. 348 93

It is controversial whether the occurrence of ascites and gastrointestinal bleeding in cirrhosis is related to the severity of portal hypertension. Portal pressure was examined in 124 unselected patients with portal hypertension due to chronic liver disease to evaluate this issue. Portal pressure was less in patients without complications of chronic liver disease (11.7 +/- 3.0 mmHg, n = 16) as compared to patients who had bled from varices or erosive gastritis (16.6 +/- 3.4 mmHg, p less than 0.001, n = 49), who had ascites (16.2 +/- 3.0 mmHg, p less than 0.001, n = 78) or both (16.5 +/- 3.0 mmHg, p less than 0.001, n = 19). Portal pressure was similar in patients bleeding from varices and erosive gastritis (16.7 +/- 3.4 mmHg, n = 43; vs 16.2 +/- 4.0 mmHg, n = 6, respectively) and in patients with refractory and nonrefractory ascites (16.2 +/- 3.5, n = 21; vs 16.2 +/- 3.5 mmHg, n = 57). The lowest portal pressure recorded in a patient with variceal bleeding was 9.0 mmHg. The lowest portal pressure recorded in a patient with ascites was 8.0 mmHg. Esophageal varices (graded 0-4 at endoscopy) were larger in patients with a history of bleeding from esophageal varices as compared to patients without such a history (3.2 +/- 0.7 vs 2.0 +/- 0.9, p less than 0.001). Serum albumin concentration was greater in patients without ascites as compared to patients with ascites (33 +/- 5 vs 26 +/- 5 g/l p less than 0.001) but was similar in patients with refractory and nonrefractory ascites (25 +/- 7 vs 26 +/- 5 g/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Portal hypertension: a permissive factor only in the development of ascites and variceal bleeding. 349 Jun 15

Portal pressure in distal oesophageal varices near the cardia was measured 71 times directly during endoscopy in 44 patients (average age: 52 years; 18 female and 26 male subjects) with confirmed diagnosis of liver cirrhosis and portal hypertension who had suffered from bleeding of oesophageal varices. No significant differences in portal pressure were seen on grouping the patients according to individual Child stages. However, a significant difference was found (P less than 0.01) on comparing the patients (n = 26) without recurrent bleeding (average follow-up period 10 months) with those who had an early (n = 5) and a late recurrent bleeding (n = 13). Although the number of cases was small a risk group for recurrent bleedings was defined at portal pressure values of 25 mm Hg and higher.
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PMID:[Endoscopic pressure measurement in distal esophageal varices. A prospective study]. 349 55

Surgical bile flow restoration in extrahepatic biliary atresia (EHBA) does not prevent the development of ongoing hepatic fibrosis and cirrhosis. Portal connective matrix was studied on liver biopsies obtained from seven children submitted to portoenterostomy. Electron microscopy and immunohistochemical techniques (using specific antibodies directed against collagen isotypes and associated glycoproteins) were performed. The study of extracellular and cellular components of connective matrix demonstrated the existence of two distinct areas according to their situation with regard to ductular proliferation: loose connective matrix--mainly composed of fibronectin, type III collagen, type IV collagen and laminin--associated with microvessels and myofibroblasts proliferation characterized periportal zones adjacent to bile ductules; in areas distant from ductular proliferation, connective matrix appeared dense, composed of type I and type III collagen associated with fibroblasts. The connective matrix pattern observed in periductular areas can be compared to that described in cicatricial and hypertrophic processes where the myofibroblastic cell population is known to play an important role in fibrosis development. Although the connective matrix activation process remains unclear in EHBA, it may be suggested that activation of a connective tissue cellular clone might be responsible for this portal fibromatosis.
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PMID:Human extrahepatic biliary atresia: portal connective tissue activation related to ductular proliferation. 353 4

Portal fibrosis is considered to be pivotal in the pathogenesis of portal hypertension associated with extrahepatic biliary obstruction. The histological features, however, include diffuse hepatocyte hyperplasia as well as portal fibrosis, but not cirrhosis, and it is possible that the contribution of hepatocyte hyperplasia in the initiation of portal hypertension is equally important. If so, we hypothesised that patients with biliary obstruction and a coincident condition such as liver atrophy, or hepatic resection, with the potential of accelerating the hepatocyte proliferation caused by biliary obstruction itself, might be expected to develop portal hypertension earlier than patients with biliary obstruction alone. To examine this concept we studied 10 patients with postcholecystectomy bile duct stricture, portal hypertension and liver atrophy, or hepatic resection (group I) and compared them with nine patients with postcholecystectomy stricture and portal hypertension, but no atrophy or resection (group II). Portal hypertension was diagnosed a mean 28 months (range 18-48 months) after cholecystectomy in group I compared with 62 months (range 36-100 months) for patients in group II (p less than 0.005 Mann-Whitney test). Thus hepatocyte hyperplasia may be an important part of the mechanism underlying the development of portal hypertension in chronic biliary disease.
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PMID:Role of liver atrophy, hepatic resection and hepatocyte hyperplasia in the development of portal hypertension in biliary disease. 366 54

We studied the effects of endoscopic sclerotherapy with transhepatic variceal obliteration on portal hemodynamics in 20 patients with cirrhosis (six with a spontaneous splenorenal shunt and 14 without it). Portal venous flow 1 month after combined therapy (measured by pulsed Doppler flowmeter) was significantly increased compared with that before therapy (n = 20, 843 +/- 339 vs. 669 +/- 253 ml/min, p less than 0.001). Portal vein catheterization and portal venous flow measurement were repeated 18 months after therapy in eight patients without a splenorenal shunt before therapy and in two patients with a splenorenal shunt before therapy. Two of the former developed a splenorenal shunt. In these 10 patients, portal venous flow before, one month, and 18 months after therapy was 617 +/- 219, 784 +/- 227, and 720 +/- 224 ml/min, respectively, and in 8 of 10 patients the portal venous flow at 18 months remained similar to the values at one month. Portal vein pressures were not significantly elevated 18 months after therapy (35.4 +/- 6.4 vs. 33.6 +/- 5.1 cm H2O) and the mean portal vein pressure change was 2.75 cm H2O (range -6 to +7.5 cm H2O). To summarize, portal venous flow was significantly increased one month after combined sclerotherapy in cirrhotics, the portal venous flow at 18 months remained similar to the values at 1 month in most patients, and the change in portal vein pressure after therapy was small.
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PMID:The effects of endoscopic sclerotherapy combined with transhepatic variceal obliteration on portal hemodynamics. 367 92

Ground-glass hepatocytes resembling those seen in HBsAg carriers on hematoxylin and eosin and on trichrome stained sections, but giving a negative reaction to orcein and a positive one to PAS, were found in liver biopsy specimens from nine asymptomatic former alcoholics who were on treatment with cyanamide, in one of four who had been treated with cyanamide several months before the liver biopsy procedure, in none of 15 treated with disulfiram, and in one of eight who had apparently not received aversive drugs. Portal and periportal inflammatory changes and fibrosis were more frequently observed in biopsy specimens containing PAS-positive ground-glass hepatocytes than in those without, but cirrhosis was found with a similar frequency. It is concluded that periportal PAS-positive ground-glass hepatocytes are a histological marker of cyanamide treatment.
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PMID:Cyanamide hepatotoxicity. Incidence and clinico-pathological features. 368 93

Portal-systemic shunting is an important circulatory abnormality in patients with cirrhosis. This study explores the potential of the natural polyol D-sorbitol as test compound for non-invasive assessment of shunting. Ten normal subjects, 10 patients with cirrhosis and 12 cirrhotics with surgical portacaval shunts were studied after oral and intravenous administration of a 2 g dose of sorbitol. As measured by the H2 breath test, removal from the intestinal lumen was complete in both groups. Bioavailability of sorbitol, calculated as ratio of the areas under the plasma concentration/time curve after p.o. and i.v. administration, was zero in normal subjects, 0.29 +/- 0.15 in cirrhotic patients, and 0.38 +/- 0.11 in patients with portacaval shunts. Calculation of bioavailability on the basis of urinary outputs of sorbitol gave similar results. It is concluded that the bioavailability of sorbitol reflects portal-systemic shunting, although the relatively low figures suggest some degree of sorbitol metabolism by enterocytes.
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PMID:Non-invasive evaluation of portal-systemic shunting in man by D-sorbitol bioavailability. 369 59

The effect of the calcium channel blocking agent, verapamil, on microcirculatory patterns and hepatic function was investigated in the perfused liver of cirrhotic rats. Compared with controls, cirrhotic livers had higher vascular resistance, increased intrahepatic shunting, and smaller extravascular albumin space and larger extravascular sucrose space, as determined by a multiple-indicator dilution technique. Hepatic function, estimated by determining propranolol and antipyrine extraction, was markedly reduced in cirrhotic livers. Portal pressure was then reduced 25% either pharmacologically by verapamil or hydrodynamically by lowering inflow. Verapamil decreased vascular resistance by 22%. This was associated with a 38% reduction in intrahepatic shunting and a 62% increase in extravascular albumin space. Hydrodynamically lowering pressure had no or adverse effects. The verapamil-induced improvement in microcirculatory characteristics was associated with a significant improvement in oxygen consumption (+21%) and antipyrine clearance (+20%). We conclude that the microvascular distortions of liver cirrhosis in the rat are partially reversible by vasodilators like verapamil.
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PMID:Verapamil favorably influences hepatic microvascular exchange and function in rats with cirrhosis of the liver. 373


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