Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Passive liver congestion secondary to increased hepatic venous pressure may accompany congestive heart failure. Abnormal patterns of hepatic parenchymal contrast medium enhancement in 25 patients with advanced congestive heart failure who were studied with computed tomography (CT) include a lobulated, patchy, inhomogeneous pattern in all 25 patients, an irregular perivascular enhancement in 14, and a global delay in parenchymal enhancement in nine. CT examinations showed cardiomegaly in the 20 patients with cardiac failure and pericardial effusion or thickening in the five patients with pericardial disease. Also noted were distention of the inferior vena cava (IVC) in 24 patients, hepatomegaly in 23, early reflux of contrast medium into the IVC in 21 and hepatic veins in 16, and hepatic perivascular lymph-edema in six. The abnormal patterns are thought to be due to slowing of hepatic blood flow. Confusion with Budd-Chiari syndrome and other forms of multifocal hepatic disease is avoidable with clinical and radiologic correlation.
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PMID:Inhomogeneous enhancement of liver parenchyma secondary to passive congestion: contrast-enhanced CT. 291 31

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

Double-phase (dual-phase) spiral computed tomography (CT) represents a technologic advance that allows two evaluations of hepatic blood flow during a single 19-29-second breath hold: once during the hepatic arterial phase (HAP) and again during the portal venous phase (PVP). Perfusion disorders of the hepatic parenchyma are more readily observed at double-phase spiral CT. The various hepatic perfusion disorders are related to (a) portal venous inflow obstruction, (b) hepatic venous outflow obstruction (e.g., Budd-Chiari syndrome, cardiac failure, mediastinal fibrosis), (c) mediastinal or thoracic venous inlet obstruction, (d) focal liver lesions, (e) inflammatory processes, (f) normal anatomic variants in the hepatic blood supply, (g) altered hemodynamics after the placement of a transjugular intrahepatic portosystemic shunt, and (h) uncertain causes. In general, the area of involvement appears hyperattenuating on HAP images and of normal or near-normal attenuation on PVP images. Familiarity with the spiral CT appearances of different types of perfusion disorders allows the radiologist to separate clinically insignificant flow phenomena from perfusion disorders caused by underlying parenchymal or vascular disease.
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PMID:Evaluation of hepatic perfusion disorders with double-phase spiral CT. 908 76

An 18-month-old dog was examined because of ascites of 1 month's duration. Typical causes of ascites, including hepatic failure, heart failure, and protein-losing enteropathy, were ruled out. The dog's history included being hit by a car 6 months earlier, and the caudal vena cava had an S shape on thoracic radiographs. In addition, the abdominal fluid had a high protein concentration and low cellular content. These findings were all consistent with a diagnosis of postsinusoidal hypertension secondary to obstruction of hepatic venous outflow (Budd-Chiari-like syndrome). During exploratory thoracotomy, the pericardium appeared to have been torn from the heart and was partially wrapped around the caudal vena cava, causing a constriction. The pericardium was removed and the dog recovered without any further complications. Blunt trauma has been previously reported to cause kinking of the caudal vena cava and Budd-Chiari-like syndrome in dogs; but in these dogs, clinical signs of ascites developed a few days to several weeks after the traumatic incident. It appears that, depending on the cause of the hepatic venous outflow obstruction, onset of Budd-Chiari-like syndrome may be delayed for months.
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PMID:Surgical correction of late-onset Budd-Chiari-like syndrome in a dog. 953 Apr 22

The use of helical CT, infusing pump and non-ionic contrast media has enabled the evaluation of different hepatic circulatory phases during contrast injection. Starting the acquisition of scans 20 to 30 seconds after the injection at a rate of 3 to 4 ml/sec the arterial enhancing of the liver is depicted. THROMBOSIS OR COMPRESSION OF THE PORTAL VEIN: Hypervascular triangle-shaped was with peripheral base can be seen, secondary to the increased arterial flow to compensate for the diminished portal flow. ARTERIOPORTAL SHUNTS: This condition can be caused by tumors such hepatocellular adenocarcinomas and hemangiomas, trauma, interventional procedures, cirrhosis, AVMs and surgery. INFLAMMATORY LESIONS: Hypervascular areas can be seen during the arterial phase in abscesses or cholecystitis, returning to their normal condition in the arterial phase. ANATOMIC VARIANTS: Third veins coming from the periphery (capsular veins, accessory cystic vein and an aberrant gastric vein) supply enhanced blood earlier than the portal circulation. OTHER CAUSES: In liver cirrhosis diffuse hyperattenuated areas can be seen during the arterial circulation. In right-sided heart failure, pericardial disease and Budd-Chiari Syndrome, "mosaic areas" can also be noted. In other patients these perfusion disorders were considered unknown. TUMORS: The well-differentiated hepatocellular carcinoma is a lesion with a predominant arterial blood supply, thus appearing in general hyperdense in this phase. Hemangiomas may appear as highly hyperdense lesions in the arterial phase and can be misinterpreted as HCC if smaller than 2 cm. (30% of cases). Focal nodular hyperplasia is a benign lesion (vascular malformation associated with focal nodules of hepatocellular hyperplasia) with increased arterial blood supply. Hepatic adenomas show an important hypervascularity during the arterial phase and, if large, they may present a small central scar and or capsule. Low or high-grade dysplastic nodules can sometimes be seen as hypervascular areas during the arterial phase. Although most metastasis are depicted as hypodense lesions sometimes they can show arterial hypervascularity such as carcinoid and pancreatic islet cell metastasis.
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PMID:[Liver hyperdensity during arterial phase on CT exams]. 1147 23

Eighteen liver transplant recipients were followed up for 10 years after a trial of immunosuppression withdrawal. Three groups were identified according to the early outcome of complete (group A, n = 5), partial (group B, n = 9), and unsuccessful (group C, n = 4) withdrawal of immunosuppression. The indications for liver transplantation (LT) (August 1983-December 1988) were as follows: primary biliary cirrhosis (n = 3), primary sclerosing cholangitis (n = 3), Budd-Chiari syndrome (n = 3), acute liver failure (n = 3), hepatitis C virus (HCV) cirrhosis (n = 1), HCV and autoimmune hepatitis (n = 1), HCV and alcohol-related cirrhosis (n = 1), HCV and hepatocellular carcinoma (HCC) (n = 1), cystic fibrosis (n = 1), and liver metastases from testicular teratoma (n = 1). Immunosuppression was based on cyclosporine. All patients experienced 1 or more complications of prolonged immunosuppression (median, 7 years; range, 5-11). Thirteen patients (72%) are alive at a median interval of 17 years (range, 16-21) after LT. Of the 5 patients in group A, 2 currently have normal graft function with no rejection episodes, and 3 have restarted immunosuppression following late low-grade acute rejection (n = 1), retransplantation for chronic rejection (n = 1), and kidney transplantation (n = 1). Of the 9 patients in group B, 5 died. The deaths were due to ruptured arterial pseudoaneurysm following retransplantation, HCC recurrence, cardiac failure, renal failure, and posttransplant lymphoma at 5, 7, 7, 14, and 17 years after LT, respectively. All 4 patients in group C are alive on a full immunosuppressive regimen. Long-term follow-up of 18 LT recipients withdrawn from immunosuppression has shown that at a median of 17 years 10% of patients remain off all immunosuppression.
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PMID:Long-term outcome of immunosuppression withdrawal after liver transplantation. 1591 39

A 24-year-old-man had right-sided heart failure of 3 months' duration. A Doppler echocardiogram revealed atrium and right ventricular enlargement, obliteration of the right ventricular apex, and a mass with an echolucent center measuring 20x21 mm in the right ventricular outlet. He died of pulmonary embolism. At autopsy, a huge organized thrombus obliterating the right ventricular apex passing through the tricuspid valve to the right atrium and then extending to the inferior vena cava up to the suprahepatic veins was seen. Histologically, an intense fibrotic thickening of the endomyocardium extending into the myocardium was observed. Cardiac thrombosis associated with endomyocardial fibrosis should be added to the list of causes of Budd-Chiari syndrome.
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PMID:Endomyocardial fibrosis as a cause of Budd-Chiari syndrome and fatal pulmonary embolism. 1923 Jul 15

A 13-year-old, spayed female golden retriever was referred for further evaluation of ascites, characterized as a modified transudate, detected after an episode of acute collapse. Prior to referral, the dog was treated for suspected right-sided heart failure and developed ventricular tachycardia. On referral, echocardiography ruled out cardiac causes for the effusion, and following stabilization the dog was taken to surgery for abdominal exploration. Surgery revealed entrapment of the left lateral liver lobe within the falciform ligament. Surgical removal of the entrapped liver lobe and falciform fat resulted in resolution of the Budd-Chiari-like syndrome. No abdominal effusion was seen on follow-up ultrasound examination. This is the first reported case of Budd-Chiari-like syndrome caused by liver lobe entrapment within falciform fat that was successfully corrected with surgery.
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PMID:Budd-Chiari-like syndrome in a dog due to liver lobe entrapment within the falciform ligament. 1972 50

Liver transplantation (LT) is an effective treatment option in patients with Budd-Chiari syndrome and end-stage liver disease. However, the procedure may lead to a sudden increase in cardiac preload, which in turn may cause heart failure. Although assays of B-type natriuretic peptide (BNP) are increasingly used in diagnosis, management, and prediction of heart failure, the role of BNP after LT has not been well defined. Herein, we describe the case of a 56-year-old woman with Budd-Chiari syndrome who underwent LT and in whom heart failure was successfully managed using serial monitoring of BNP concentrations. The BNP concentration increased to 1735 pg/mL on postoperative day 4, and decreased to 180 pg/mL on postoperative day 19, at which time inotropic agents were discontinued.
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PMID:Serial monitoring of B-type natriuretic Peptide in management of heart failure after liver transplantation in a patient with Budd-Chiari syndrome: case report. 2083 89


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