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)

Between 1986 and 1989, orthotopic liver transplantations were performed in our unit for 17 patients with incurable alveolar echinococcosis. Ten patients had hilar involvement (group I), and seven patients had posterior localization (five of them had chronic Budd-Chiari syndrome) (group II). The delay between diagnosis and the orthotopic liver transplantation was more than 48 mo in group Ia (six patients), less than 24 mo in group Ib (four patients) and less than 48 mo in group II. Previous operations were more common in group Ia than in group Ib and II. Five patients have died-four in group I and one in group II. The actuarial survival rate at 15 mo was 75%. Early reoperations were frequent (69%), mainly caused by rebleeding. Bacterial and fungal infections occurred only in group Ia (four cases) and group II (three cases). In eight patients (palliative group), residual foci of infected nonhepatic tissue occurred after surgery. The titer of specific antibodies decreased during the first 3 mo in all the patients but one. In patients with radical liver transplantation, the complete disappearance of specific antibodies occurred within 2 yr in four cases. In the remaining five patients, specific antibodies remained detectable, but no evidence of recurrence has been obtained up to now. In the palliative group, a peak of specific IgM occurred at 3 mo; an increase of specific IgG was observed later. The growth of residual parasitic foci was relatively slow, and all these patients remained asymptomatic with a mean follow-up of 19 mo. We conclude that orthotopic liver transplantation is feasible in incurable alveolar echinococcosis and could be proposed without delay to patients with parasitic Budd-Chiari syndrome or complicated secondary biliary cirrhosis. In the other cases, the best time to perform an orthotopic liver transplantation is more difficult to determine. Nevertheless, in the perspective of an orthotopic liver transplantation, the management of these patients has to change, and repetitive laparotomies for palliative surgical procedures have to be replaced by interventional radiology.
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PMID:Orthotopic liver transplantation for incurable alveolar echinococcosis of the liver: report of 17 cases. 205 Mar 23

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.
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PMID:[Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites]. 205 24

In twenty-seven patients with venography-documented Budd-Chiari syndrome (BCS), underlying diseases included polycythemia vera (nine patients), membranous occlusion of the inferior vena cava (three), and cirrhosis (two). In only nine patients did the syndrome occur in the absence of any predisposing factor. All patients with a membranous web were relatively young (mean age 29 years) and were born in Morocco. With regard to prognosis, three groups could be delineated. Eight patients formed a rapidly progressive group, with mean survival from first symptom of only 4.3 weeks, and were characterized mainly by their relatively advanced age and minimal enlargement of the spleen.
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PMID:Budd-Chiari syndrome in Israel: predisposing factors, prognosis, and early identification of high-risk patients. 206 48

A 72-year-old female who had suffered from lower extremity edema and liver cirrhosis due to Budd-Chiari syndrome with massive thrombus in IVC was treated by PTA and placement of self-expandable metallic stent. Thrombolysis therapy after PTA was very effective. Five months later, she had no clinical symptom due to IVC stenosis.
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PMID:[Clinical experience of percutaneous transluminal angioplasty and expandable metallic stent placement for Budd-Chiari syndrome with massive thrombus in the inferior vena cava; report of a case]. 214 55

Occlusion or obstruction of hepatic venous outflow results in the Budd-Chiari syndrome. The disorder should be suspected in any patient who suddenly develops massive ascites, and the diagnosis can be confirmed quickly and accurately by hepatic venography. In the absence of surgical intervention, survival is rare. Inferior venacavography and percutaneous liver biopsy can be performed safely in these patients, and both procedures provide useful information for the selection of appropriate surgical therapy. Most cases of the Budd-Chiari syndrome are amenable to mesocaval or mesoatrial shunting. Those patients with documented cirrhosis or fulminant hepatic failure are best managed by orthotopic liver transplantation.
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PMID:Diagnosis and management of the Budd-Chiari syndrome. 836 52

Simultaneous determination of ascitic fluid and serum adenosine deaminase (ADA) activity was evaluated as a diagnostic aid in peritoneal tuberculosis. The ascites was due to peritoneal tuberculosis (group 1), cirrhosis of the liver (group 2), cirrhosis of the liver with spontaneous bacterial peritonitis (group 3), peritoneal malignancy (group 4), Budd-Chiari Syndrome (group 5) and miscellaneous conditions (group 6). Serum from patients of pulmonary tuberculosis and healthy volunteers was analysed for enzyme activity. In patients with peritoneal tuberculosis the ascitic fluid and serum ADA activity was significantly higher than for the other groups (P less than 0.001). Levels above 36 u/l in ascitic fluid and above 54 u/l in the serum suggest tuberculosis. The ascitic fluid/serum ADA ratio was also higher in patients with peritoneal tuberculosis than with other causes of ascites (P less than 0.01). A ratio of more than 0.984 was suggestive of tuberculosis.
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PMID:Adenosine deaminase (ADA) in peritoneal tuberculosis: diagnostic value in ascitic fluid and serum. 221 61

Twenty-six patients with the Budd-Chiari syndrome were treated surgically at the Johns Hopkins Hospital. Twenty-one of the patients were female and five were male, with a median age at diagnosis of 37 years. Nine patients had polycythemia vera, 6 were receiving estrogen therapy, 5 had a previous hepatitis A or B infection, and 4 had cirrhosis. There was one case each of hepatic malignancy, paroxysmal nocturnal hemoglobinuria, and idiopathic thrombocytopenic purpura. In five cases no etiologic factors or associated disorders were identified. Ascites was the most common presenting feature in this group of patients. Hepatic function at the time of diagnosis, as measured by standard serum chemistries, was only minimally abnormal. The diagnosis of the Budd-Chiari syndrome was confirmed in all 26 patients by hepatic vein catheterization. Inferior vena cavography was also performed and revealed caval occlusion in 4 patients, significant caval obstruction in 13 patients, and a normal vena cava in 9 patients. Interpretation of the vena cavogram was helpful in selecting the appropriate surgical procedure for each patient. Twenty-three of the twenty-six patients underwent percutaneous liver biopsy before operation, with no morbidity or mortality. Four patients had well-established cirrhosis noted on biopsy. Thirty mesenteric-systemic venous shunts were performed on the 26 patients. In 11 patients a mesocaval shunt was performed and in one instance conversion to a mesoatrial shunt was required as a second procedure. In 15 patients a mesoatrial shunt was performed as the initial procedure. Graft thrombosis occurring in 2 of these 15 patients prompted one revision in 1 patient and 2 revisions in the second patient. After mesenteric-systemic venous shunt, eight of the patients (31%) died before discharge from the hospital. The remaining 18 patients in this series were discharged from the hospital alive and well with patent shunts. Patients were followed for a median of 43 months (range, 9 months to 13 years). Five late deaths occurred between 5 and 84 months after the operation. Three- and five-year actuarial survival rates were 65% and 59%, respectively.
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PMID:Current management of the Budd-Chiari syndrome. 200 20

Five of six patients with angiographically proved Budd-Chiari syndrome (hepatic venous outflow obstruction) showed multiple specific MRI abnormalities: striking reduction in caliber or complete absence of the hepatic veins, "comma-shaped" intrahepatic collateral vessels, and/or marked constriction of the intrahepatic inferior vena cava. The sixth patient had angiographically proven sinusoidal hepatic venous obstruction and patent central hepatic veins; MRI showed ascites but revealed no specific features of the Budd-Chiari syndrome. Patients with end-stage cirrhosis also showed compressed, distorted hepatic veins; however, these cirrhotic livers were distinguished by their small size, nodular surface, and extrahepatic collateral varices. In patients without cirrhosis or the Budd-Chiari syndrome, normal hepatic, portal, and inferior caval veins were routinely seen when technically adequate MRI examinations were obtained (94 of 100 cases). Four of the six patients with Budd-Chiari syndrome had been treated surgically. In three, MRI identified patent portocaval shunts. In the fourth, angiographically confirmed shunt stenosis was demonstrated by MRI.
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PMID:MRI of the Budd-Chiari syndrome. 242 7

To evaluate the diagnostic value of radionuclide inferior veno-cavagraphy (RIVC) for Budd-Chiari Syndrome, RIVC using Tc99m was performed on 106 patients with massive ascites. A positive RIVC result was defined as having at least two of the three following criteria: (1) a delay of more than 4 seconds in visualizing the heart; (2) sharply truncated inferior vena cava with marked hang-up of isotope activity; and (3) extensive collateral circulation. Of the 106 patients, 18 were RIVC positive and were later confirmed by operation or contrast venography to have Budd-Chiari Syndrome with IVC obstruction. Of the remaining 88 RIVC negative patients, 3 were shown by operation, computerized tomography and cardiac echo, respectively, to be Budd-Chiari Syndrome with IVC obstruction. Thus, the diagnostic sensitivity and specificity of RIVC for this syndrome was 85.7% and 100% respectively. If RIVC is combined with hepatic scintigraphy, it will help to elucidate the anatomic and functional change of IVC, as well as, liver parenchymal disease, such as liver cirrhosis, hepatic tumor or hepatic vein obstruction. RIVC is a simple safe, accurate, noninvasive and reproducible procedure. This study confirms the high diagnostic specificity and sensitivity of RIVC. We therefore recommend RIVC as the first-line study for IVC patency. Contrast venography may be used as a confirmatory study in preparation for surgical intervention.
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PMID:[The diagnostic value of radionuclide inferior veno-cavagraphy in Budd-Chiari syndrome]. 259 48

Orthotopic liver transplantation (OLT) has become standard therapy for patients with acute hepatic necrosis and end-stage liver disease. This study measured change in hepatic function (galactose elimination capacity [GEC]), liver blood flow (low dose galactose clearance: flow), hepatic volume (CT scan; volume) and morphology after OLT. The aim was to measure the physiologic response after OLT and compare this response with that after selective shunt (SS) and sclerotherapy (ES) to determine which patients should receive specific therapy. Between January 1987 and November 1988, 37 patients underwent OLT. Operative mortality was 18%, which was similar to that of SS in Child's C cirrhotics. GEC and volume were less in transplant patients than in cirrhotics treated with SS or ES. GEC, flow, and volume normalized after OLT; GEC was preserved after ES and SS, but volume decreased. Three preoperative patterns were observed that can aid in selection of OLT candidates. Patients with chronic cirrhosis (chronic active hepatitis; cryptogenic) need OLT when GEC is less than or equal to 225 mg/min and volume is less than or equal to 50% normal. Patients with Budd-Chiari Syndrome require OLT if cirrhosis has evolved. Patients with sclerosing cholangitis and primary biliary cirrhosis qualify for transplants when complications of the portal hypertensive syndrome develop. The studies can also direct therapy for ES failures. Selective shunt is indicated in those patients with stable disease whose GEC is greater than or equal to 300 mg/min and liver volume is greater than 75% normal; OLT is indicated for cirrhotics with GEC that is less than 225 mg/min and liver volume that is less than 50% predicted normal.
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PMID:Change in hepatic function, hemodynamics, and morphology after liver transplant. Physiological effect of therapy. 265 Jun 42


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