Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From January 1978 to August 1987, 21 patients received a peritoneovenous shunt using the Le Veen valve (LVV). The indications criteria were the long-term diuretic therapy failure (mean time = 24.4 months) or resistence to medical therapy during hospital internment. The 21 patients underwent 36 surgeries, being 4 valve position review and 11 changes of LVV. The mean age was 51.6 years. Fifteen patients had alcoholic cirrhosis, 3 postnecrotic cirrhosis, one Budd-Chiari syndrome, one mansoni Schistosomiasis, and one malignant ascites. Ten were Child B and 9 Child C patients. Eight patients with history of previous esophageal varices bleeding (EVB) underwent endoscopic sclerotherapy (EE) before LVV implantation. Seven patients died in the early postoperative period (3 Child B and 4 Child C patients). Three patients died due to EVB and the others as consequence of hepatic failure (one), cardiac insufficiency (one), sepsis (one), and bronchopneumonia (one). The mean follow-up was 19.9 months (1-61). Early LVV occlusion occurred in 4 patients and late valve occlusion in others 4 patients. The LVV changes were done at ambulatorial preceeding. Ten patients (47.6%) died in late follow-up and in these cases death was related to the main disease course. It is concluded that: 1) LVV is a useful therapy in patients with intractable ascites, since it is not the terminal manifestations of disease; 2) early mortality is related to liver function and late mortality to main disease course; 3) ascitic patients with EVB should undergo endoscopic sclerotherapy before LVV implantation.
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PMID:[Use of the Leveen shunt in the treatment of clinically intractable ascites]. 325 81

The effect of oral testosterone treatment (200 mg tid) on liver morphology was examined in a double-blind, placebo controlled study including men with alcoholic cirrhosis (n = 126). Liver biopsies obtained before randomization showed micronodular cirrhosis in 119 patients (94%), alcoholic hepatitis in 64 (51%), and fatty liver in 104 (83%). These and other morphological findings did not differ significantly in the patients randomized to testosterone (n = 76) and to placebo (n = 50) (skewed randomization 3:2). Follow-up liver specimens (biopsies or autopsies) obtained after a median treatment duration of 30 months demonstrated a significant (p less than 0.01) increase in the prevalence of macronodular cirrhosis (from 6 to 51%) and a significant (p less than 0.01) decrease in the prevalence of alcoholic hepatitis (to 21%) and of fatty liver (to 52%). Testosterone treatment did not significantly influence the prevalence of these changes. Further, testosterone treatment had no significant effect on the prevalence of other morphological changes, including vascular and malignant changes. However, in the testosterone-treated group one patient developed diffuse sinusoidal dilation and one patient showed Budd-Chiari's syndrome. The degree of fatty liver and of alcoholic hepatitis in follow-up liver specimens were significantly (p less than 0.002) higher among patients who consumed ethanol during follow-up than in patients who abstained (76 versus 22% and 30 versus 6%). In conclusion, this study does not establish any indication or any contraindication in terms of hepatic histopathology with the possible exception of hepatic venous thrombosis for the use of oral testosterone treatment in men with alcoholic cirrhosis.
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PMID:No effect of long-term oral testosterone treatment on liver morphology in men with alcoholic cirrhosis. 330 Feb 74

We performed a prospective study on 375 patients with liver disease, 60% female, for whom orthotopic liver transplantation (OLT) was considered during 1977-1985. Fifty-four per cent had cirrhosis, 8.5% congenital/hereditary disorders, 25% malignant tumour, 6% benign tumour, 2% Budd-Chiari syndrome, 1.5% acute hepatic failure, 3% other diagnoses, and 10% were under 15 years of age. As of July 1st, 1985, 99 patients (47 chronic active/inactive cirrhosis (CAC/CIC), 28 primary biliary cirrhosis (PBC), five hepatocellular carcinoma (HCC), 19 other diagnoses) were accepted for OLT (median age 40 years, 10% under age 15). By that date, 45 patients (median age 42), had had an OLT (20 CAC/CIC, 15 PBC, three biliary atresia, two HCC, five other diagnoses). Fifty-four per cent (201 patients) were rejected for transplantation. The primary reasons for rejection were: no indication (11%), age (5%), other surgical procedures possible (3%), severe liver failure (14%), extrahepatic spread of liver tumour (11%), cardiovascular or pulmonary problems (2%), severe hepatic bone disease (1%), and miscellaneous (7%). Thirty per cent of the patients with CAC/CIC, 38% with PBC, 88% with HCC and 71% with biliary atresia were rejected. In the CAC/CIC, PBC and biliary atresia patients severe liver failure was the most frequent reason for rejection (62%, 50% and 60%, respectively). In HCC, extrahepatic tumour spread was the most frequent reason (72%) for rejection. In this category only two patients (7%) ultimately underwent liver transplantation.
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PMID:Selection criteria and decisions in 375 patients with liver disease, considered for liver transplantation during 1977-1985. 330 82

Liver biopsy results and clinical records from 13 patients with sickle cell anemia were reviewed to assess the relative importance of local ischemia or of factors unrelated to sickling as a cause of their liver disease. Two of the biopsy specimens were normal and one showed cirrhosis. Nine patients had received multiple blood transfusions and nine had cholelithiasis, of whom two also had choledocholithiasis. Seven had both risk factors. Five had lobular cholestasis and four had acute or chronic hepatitis. One biopsy specimen showed changes of the Budd-Chiari syndrome. Another showed clear portal tract changes of large bile duct obstruction but no mechanical blockage of the biliary system; this suggests the thickened bile as postulated by Muirhead. Otherwise the changes observed were those to be expected in a heavily transfused population with a high prevalence of gallstones.
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PMID:Histopathologic features of liver biopsy specimens in sickle cell disease. 334 26

Hemodynamic profiles were obtained for patients with portal hypertension secondary to the Budd-Chiari syndrome who underwent mesoatrial shunting procedures. In contrast to the well-known hyperdynamic, low-resistance state of chronic cirrhosis, patients with the Budd-Chiari syndrome had normal cardiac index and systemic vascular resistance values before anesthesia and surgery. Opening the mesoatrial shunt produced a 46% (p less than 0.01) increase in cardiac index and a 38% (p less than 0.01) decrease in overall systemic vascular resistance. Right atrial pressure and pulmonary capillary wedge pressures were sharply increased--by 5.3 mm Hg and 4.7 mm Hg, respectively (p less than 0.01). A mathematical model was developed to assess the cause of the observed changes in systemic vascular resistance. The model suggests that the hemodynamic changes seen with shunt opening are unlikely to be the result of shunt effects alone and that dilatation of peripheral vascular beds is probable. Thus shunting converts the normal systemic vascular resistance and cardiac index of patients with the Budd-Chiari syndrome to the high-output, low-resistance state seen in patients with chronic cirrhosis. Although the physiology is complex, we conclude that the data are consistent with release, by the shunting process, of a systemic vasodilator.
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PMID:Mesoatrial shunt hemodynamics. 338 74

Reports of thrombosis rates as high as 40 percent with the mesocaval H shunt led us to review our results with the mesocaval C shunt in 33 consecutive patients. Their ages ranged from 23 to 69 years (mean 50 +/- 12 years). There were 21 male and 12 female patients. The causes of portal hypertension included alcoholic cirrhosis in 13 patients, primary biliary cirrhosis in 6 patients, postnecrotic cirrhosis in 6 patients, cryptogenic cirrhosis in 3 patients, the Budd-Chiari syndrome in 4 patients, and portal vein thrombosis in 1 patient. Twelve patients were in Child's class A, 8 were in Child's class B, and 13 were in Child's class C. Operative mortality was 24 percent (8 of 33 patients) but occurred only in class C patients under nonelective conditions. Shunt patency was determined by one or more of the following: autopsy, angiography, and a lack of recurrent varices or hemorrhage. Autopsies were performed in 12 patients from 1 week to 72 months after operation. All 12 C shunts were widely patent. Angiography was performed in 13 patients from 1 to 38 months postoperatively. All 13 C shunts were patent; however, 2 eventually stenosed and attempts at ballon angioplasty were only moderately successful. Follow-up to time of death or to date was possible in 24 of 25 survivors, and ranged from 3 to 123 months. Evidence of recurrent varices, variceal hemorrhage, or both developed in only two patients (2 of 24, 8 percent), both of whom had stenosed shunts.
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PMID:Long-term patency of the mesocaval C shunt. 348 13

Five cases with primary Budd-Chiari syndrome due to membranous obstruction of the hepatic segment of the inferior vena cava were examined by CT. In all cases, CT demonstrated caudate lobe enlargement, reticular low density within the liver parenchyma, splenomegaly, and collaterals via the ascending lumbar veins and azygous system. Pathological study revealed liver cirrhosis or fibrosis in all cases. In two cases, calcification was shown in the region of the hepatic segment of the inferior vena cava. Our results suggested that the CT appearance of primary Budd-Chiari syndrome was rather characteristic and useful in diagnosis, although membranous obliteration could not be shown directly on CT.
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PMID:CT diagnosis of primary Budd-Chiari syndrome--membranous obstruction of the inferior vena cava. 356 87

Emergency endoscopic sclerotherapy (EEST) during continued moderate to severe bleeding was carried out using a flexible endoscope and absolute alcohol as a sclerosant in 38 patients with variceal bleeding. Portal hypertension was due to cirrhosis in 27, noncirrhotic portal fibrosis in eight, extrahepatic obstruction in two, and Budd-Chiari Syndrome in one patient. A technically adequate EEST could be carried out in 36 (95%) patients, with successful control of variceal bleeding in 35 (92%). Thirty-one episodes of rebleeding occurred in 12 (31.6%) patients. Twenty-nine (93.5%) of these episodes could be controlled with repeated EEST, giving an overall success of 87%. The new approach of repeating sclerotherapy on every rebleeding episode up to a maximum of three course within 24 hours, use of a wide bore injector, and certain other technical innovations were found safe and effective. The mean (+/- SD) amount of alcohol injected per patient was 9.23 +/- 3.3 ml and the mean (+/- SD) number of injections needed per patient were 6.0 +/- 3.07. Complications were minor, transient, and similar to conventional sclerotherapy. There were three deaths, two due to massive rebleeding and one due to hepatic encephalopathy. It can be concluded that EEST is technically feasible during active variceal bleeding and is an effective and relatively safe procedure. It can serve as the first line treatment in this group of patients.
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PMID:Repeated endoscopic sclerotherapy for active variceal bleeding. 387 33

Since 1980 an operation which reestablishes the blood outflow from occluded hepatic veins was performed in 7 patients with Budd-Chiari syndrome by one of us (A. Senning). Using extracorporeal circulation a dorsocranial cylindrical resection of the liver including the confluence of the occluded hepatic veins was performed by transcaval approach. The incised right atrium was sutured around the resected liver area. There was one intraoperative death. In 6 patients with a mean postoperative follow-up of 19.2 months (4-42 months), the patency of hepatoatrial anastomosis was documented by angiography or Doppler-2d-echocardiography. Four patients are free of symptoms and signs of Budd-Chiari syndrome. In one of two patients with associated cirrhosis compression of inferior vena cava reoccurred and in another patient esophageal varices persist. We conclude, that the hepatoatrial anastomosis is an effective treatment of Budd-Chiari syndrome.
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PMID:Treatment of Budd-Chiari syndrome by dorsocranial liver resection and direct hepatoatrial anastomosis. 395 Mar 59

An attempt has been made to investigate drug elimination in patients with liver disease. Antipyrine was chosen as a model drug. The patients were divided into three groups depending upon clinical, biochemical, radiologic and histologic findings; (1) mild (Idiopathic portal hypertension, extrahepatic portal vein obstruction and Gilbert's syndrome); (2) moderate (Budd-Chiari syndrome and amoebic liver abscess); (3) severe (acute hepatitis, chronic active hepatitis and cirrhosis). A prolongation in antipyrine half-life (t1/2) was observed in 108 patients with liver disease (24.59 +/- 1.72 h) as compared to 12 controls (11.63 +/- 0.86 h). Similarly, metabolic clearance rate was decreased in all liver disorders. Among liver function tests, antipyrine t1/2 showed a significant correlation with serum albumin and prothrombin time index. After phenobarbitone administration, antipyrine clearance studied in 37 patients showed a significant decrease in t1/2 and an increase in MCR. Antipyrine t1/2 in 26 patients after recovery was comparable to those of controls.
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PMID:Impairment of drug elimination in patients with liver disease. 398 89


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