Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Liver Dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed1981

Multiple systems organ failure: VII. Reduction in plasma branched-chain amino acids--correlations with liver failure and amino acid infusion.

Lower fractional concentrations of branched-chain amino acids were found in trauma-septic patients who did not survive than in those who survived (p values less than or equal to 0.046 to 0.001). A liver dysfunction scale was constructed on the basis of the levels of plasma bilirubin, albumin, SGOT, prothrombin time, and neurologic encephalopathy. Increased liver dysfunction was associated with reduced plasma fractional branched-chain amino acids for all branched-chain amino acids in both the surviving and nonsurviving patients except for valine in the nonsurviving group. This decrease was statistically significant (p less than or equal to 0.041 to 0.001) for leucine and isoleucine in the nonsurvivors and for valine in the survivors. The infusion of amino acids was associated with a decrease in the fractional concentrations in the nonsurvivors for leucine while the fractional concentrations of isoleucine in the nonsurvivors and isoleucine and valine in the survivors rose. The statistically significant changes (p less than 0.018 to 0.001) were for leucine in the nonsurvivors and isoleucine and valine in the survivors. When the liver dysfunction and amino acid infusion related changes are taken in;to account there were no significant differences in the fractional branched-chain concentrations between survivors and nonsurvivors. Liver dysfunction and low fractional branched-chain amino acids were linked in magnitude in a way that is consistent with the low branched-chain amino acids producing the liver dysfunction.

Amino Acids↗
PubMed2006

Liver biopsy interpretation for causes of late liver allograft dysfunction.

Evaluation of needle biopsies and extensive clinicopathological correlation play an important role in the determination of liver allograft dysfunction occurring more than 1 year after transplantation. Interpretation of these biopsies can be quite difficult because of the high incidence of recurrent diseases that show histopathological, clinical, and serological features that overlap with each other and with rejection. Also, more than one insult can contribute to allograft injury. In an attempt to enable centers to compare and pool results, improve therapy, and better understand pathophysiological disease mechanisms, the Banff Working Group on Liver Allograft Pathology herein proposes a set of consensus criteria for the most common and problematic causes of late liver allograft dysfunction, including late-onset acute and chronic rejection, recurrent and new-onset viral and autoimmune hepatitis, biliary strictures, and recurrent primary biliary cirrhosis and primary sclerosing cholangitis. A discussion of differential diagnosis is also presented.

Biopsy, Needle↗
PubMed2006

Molecular adsorbent recirculating system in patients with early allograft dysfunction after liver transplantation: a pilot study.

Early allograft dysfunction (EAD) after orthotopic liver transplantation (OLT) causes marked morbidity and mortality. We conducted a prospective pilot study to assess the safety and efficacy of molecular adsorbent recirculating system (MARS) in treatment of EAD after OLT. Twelve consecutive adult liver allograft recipients with a median age of 48 years, 9 of whom were male, were prospectively included and supported with MARS. EAD was defined as the presence of at least 2 of the following: serum bilirubin >10 mg/dL, prothrombin time <40%, aspartate aminotransferase or alanine transferase >1,000 U/L, and plasma disappearance rate of indocyanine green (PDR(ICG)) <10% per minute within 72 hours after reperfusion. One-year patient and graft survival was 66%. There was a significant decrease in serum bilirubin (P = 0.002), serum creatinine (P = 0.006), and aspartate aminotransferase (P = 0.005) and a significant increase in PDR(ICG) (P = 0.007) after MARS treatment. Prothrombin time, albumin level, and platelet count remained stable. Sustained improvement of renal and neurological function and of mean arterial pressure were observed. No MARS-related adverse effects occurred. MARS treatment provides a safe approach to the treatment of EAD after OLT. On the basis of this pilot study, a multicenter randomized clinical trial that uses MARS treatment in EAD after OLT has been initiated.

Adsorption↗
PubMed2006

Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease.

Oxidative stress and hepatic mitochondria play a role in the pathogenesis of nonalcoholic fatty liver disease. The aim of the present study was to evaluate the role of hepatic mitochondrial dysfunction and oxidative stress in the pathogenesis of the disease. Fatty liver was induced in Wistar rats with a choline-deficient diet (CD; N = 7) or a high-fat diet enriched with PUFAs-omega-3 (H; N = 7) for 4 weeks. The control group (N = 7) was fed a standard diet. Liver mitochondrial oxidation and phosphorylation were measured polarographically and oxidative stress was estimated on the basis of malondialdehyde and glutathione concentrations. Moderate macrovacuolar liver steatosis was observed in the CD group and mild liver steatosis was observed in the periportal area in the H group. There was an increase in the oxygen consumption rate by liver mitochondria in respiratory state 4 (S4) and a decrease in respiratory control rate (RCR) in the CD group (S4: 32.70 +/- 3.35; RCR: 2.55 +/- 0.15 ng atoms of O2 min-1 mg protein-1) when compared to the H and control groups (S4: 23.09 +/- 1.53, 17.04 +/- 2.03, RCR: 3.15 +/- 0.15, 3.68 +/- 0.15 ng atoms of O2 min-1 mg protein-1, respectively), P < 0.05. Hepatic lipoperoxide concentrations were significantly increased and the concentration of reduced glutathione was significantly reduced in the CD group. A choline-deficient diet causes moderate steatosis with disruption of liver mitochondrial function and increased oxidative stress. These data suggest that lipid peroxidation products can impair the flow of electrons along the respiratory chain, causing overreduction of respiratory chain components and enhanced mitochondrial reactive oxygen species. These findings are important in the pathogenesis of nonalcoholic fatty liver disease.

Animals↗
PubMed1984

Hyperglucagonemia in hepatic cirrhosis: its relation to hepatocellular dysfunction and normalization on recovery.

Plasma glucagon, insulin and glucose concentrations, and liver function tests were determined after an overnight fast in 24 normal subjects and 50 male cirrhotic patients. In cirrhotic patients with normal liver profiles, plasma glucagon remained within normal limits, irrespective of the presence of portasystemic anastomoses either pathological or surgical. Hyperglucagonemia was documented in presence of advanced liver dysfunction alone. Significant correlations were established between plasma glucagon and several liver function tests, i.e., serum bilirubin, albumin/globulin ratio, and prothrombin time. Moreover, hyperglucagonemia normalized on recovery from clinical manifestations and improvement in liver profile. Plasma insulin was raised primarily in the presence of a significant portasystemic shunting and maximum levels were observed in patients manifesting advanced liver dysfunction as well. However, no correlation was evident between plasma insulin and any of the liver function tests. Fasting plasma glucose was not altered in cirrhotic patients. Therefore, it is concluded that in hepatic cirrhosis, glucagon secretion by pancreatic alpha-cell may be dependent on the severity of the hepatocellular damage whereas portasystemic shunting may be responsible for hyperinsulinemia which may be further exaggerated in presence of advanced liver dysfunction.

Adult↗
PubMed2005

Cognitive performance and liver function among recently abstinent alcohol abusers.

It has frequently been suggested that some of the enduring subtle cognitive impairments seen in sober alcohol-dependent persons may be a result of subclinical liver dysfunction. Cognitive performance and liver function among 85 recently abstinent alcohol-dependent persons were assessed by means of a neuropsychological examination and the GGT test of liver function. Unlike some previous studies, no relationships were found between the two areas of functioning. It is argued that lack of statistical power did not account for the failure to find an association between the two domains. The proposition that residual cognitive impairment in abstinent alcoholic persons is (partly) mediated by earlier liver dysfunction rests on slight empirical foundations and remains speculative.

Alcoholism↗
PubMed1999

Primary biliary cirrhosis associated with membranous glomerulonephritis.

A 33-year-old woman was admitted to our department for evaluation of liver dysfunction and proteinuria. A liver biopsy specimen showed ductular proliferation and moderate portal fibrosis indicating stage II primary biliary cirrhosis. A renal biopsy specimen showed mild to moderate mesangial cell proliferation without crescent formation or interstitial nephritis. Immunofluorescent staining revealed deposition of immunoglobulin G (IgG), third component of complement (C3), and Clq on glomerular basement membranes. The findings indicated stage I membranous glomerulonephritis. Administration of ursodesoxycholic acid together with prednisolone, azathioprine, and dipyridamole decreased proteinuria and improved cholestatic liver dysfunction.

Adult↗
PubMed2001

Troglitazone and liver function abnormalities: lessons from a prescription event monitoring study and spontaneous reporting.

OBJECTIVES: To investigate whether there were any cases of liver function abnormalities possibly associated with troglitazone use in general practice in England. DESIGN: A prescription-event monitoring (PEM) study was undertaken between October 1997 and December 1997. SETTING: Data from prescriptions were obtained electronically for the troglitazone cohort in the immediate postmarketing period. STUDY PARTICIPANTS: Event data were obtained for a total of 1344 patients. RESULTS: Troglitazone was effective in 394 (75%) of the 529 patients for whom an opinion was given. The most frequent reasons for stopping treatment related to drug tolerability were malaise/lassitude (16 reports), abnormal liver function tests (II reports) and nausea/vomiting (9 reports). The major cause of stopping troglitazone was because the drug was withdrawn from the market (1101 reports). 30 patients with liver dysfunction were identified from the cohort. In 9 of these patients there were alternative explanations for the liver dysfunction and hence these patients were not followed up further. 21 patients were followed up, for whom 19 questionnaires were returned. In 5 patients their liver dysfunction was assessed as possibly related to troglitazone, in 6 patients the liver dysfunction was unlikely to be attributed to troglitazone, while in 7 patients it was difficult to assess the causality because of limited information and confounding factors. The remaining patient was not included as this individual did not fit the inclusion criteria of the study. CONCLUSION: Although the cohort is small (the drug was available for only 3 months in the UK), 5 patients with abnormal liver function, considered possibly related to troglitazone were detected in this PEM study. It is possible for PEM to contribute to the elucidation of safety signals in the UK.

Adult↗
PubMed1988

[Long-term TPN for short bowel syndrome].

One hundred and sixty three children who received total parenteral nutrition (TPN), including 7 cases of short bowel syndrome, were studied to evaluate the role of TPN in the management of infants with extremely short bowel. Three of the seven were died of sepsis related with central venous catheter (CV catheter) during the period of malabsorption when TPN was necessary. Two children of other diseases were died of catheter sepsis, 5 out of 163 in total, making the mortality late of TPN 3%. Incidence of CV catheter related complications was significantly less frequent in Broviac catheter when compared with conventional Silastic catheter (p less than 0.01). Another significant complication of TPN in cases of short bowel syndrome was hepatic dysfunction. Cholestatic liver dysfunction seemed to be cleared when enteral feeding was started even with TPN going on. Oral feeding should be started in the early postoperative period with concomitant TPN covering the fluid loss. A case of copper deficiency with high output jejunostomy and a case of urolithiasis with hyperoxaluria complicated with short bowel were reported.

Catheterization↗
PubMed2000

[Transcatheter arterial embolization for advanced hepatocellular carcinoma--indications and limitations].

Many patients with advanced hepatocellular carcinoma (HCC) in stage IV have no surgical indications. Transcatheter methods such as transcatheter arterial embolization (TAE) and hepatic arterial infusion chemotherapy play a main role of the treatment for advanced HCC. Conventional TAE (from proper hepatic artery) is performed for patients without liver dysfunction. Patients with severe liver dysfunction could not in the past be treated with TAE, but lately it has become possible to treat them with the method of segmental TAE or subsegmental TAE due to the development of a microcatheter and advances in equipment. Although technical progress is remarkable, there are no fixed guidelines for advanced HCC. Suitable methods for individuals need to be discussed.

Antibiotics, Antineoplastic↗
PubMed2001

Papillary adenocarcinoma of the subvesical duct.

This is, to our knowledge, the first report of papillary adenocarcinoma originating in the subvesical bile duct. A 77-year-old man was referred to our hospital for further evaluation of liver dysfunction. Serum liver function test results on admission included: aspartate aminotransferase, 99 IU/l; alanine aminotransferase, 149 IU/l; lactate dehydrogenase, 438 IU/l; alkaline phosphatase, 992 IU/l; leucine aminopeptidase, 320 IU/l; and gamma-glutamyl transpeptidase, 593 IU/l. Serum carbohydrate antigen (CA) 19-9 value was high (80 U/ml). Abdominal ultrasonogram, computed tomographic scan, and percutaneous transhepatic cholangiogram demonstrated a mass in the common hepatic duct, and dilatation of the intrahepatic bile ducts. A laparotomy was performed on May 14, 1997. The tumor originated in the dilated subvesical duct that joined the common hepatic duct, and projected into the common hepatic duct. The patient underwent cholecystectomy, resection of the subvesical duct and the common hepatic duct, dissection of regional pericholedochal lymph nodes, and Roux-en-Y hepaticojejunostomy. The resected tumor presented macroscopically as a papillary mass measuring 4.0 x 2.0 cm. The pathological diagnosis was papillary adenocarcinoma. The immunostaining positivity rates for MIB-1 and p53 protein were 49.6% and 33.8%, respectively.

Adenocarcinoma, Papillary↗
PubMed2005

Management of Budd-Chiari syndrome.

Thrombotic occlusion of the hepatic veins leads to liver dysfunction and liver failure requiring liver transplantation in advanced cases. The cause for the occlusion of the hepatic veins is not completely understood. However, several underlying conditions such as polycytemia, factor V Leiden mutation, and protein C and S deficiency are found in these patients. We here report our single-center experience with 18 consecutive patients with Budd-Chiari Syndrome (BCS) who were treated at our institution between August 1992 and June 2003. Twelve patients underwent liver transplantation, three patients received stents into the hepatic veins or vena cava, another patient was treated with TIPSS (transjugular intrahepatic postosystemic stent shunt), and one patient underwent surgical mesocaval shunting. Three patients, among those the patient with TIPSS, were put on anticoagulant therapy and are scheduled for liver transplantation. We outline the indication for an approach tailored to the stage of the disease and the adaption of the procedures with the deterioration of clinical conditions. Surgical aspects and postoperative management with a focus on liver transplantation are outlined. We conclude from our observations that the management of BCS requires an approach that exhausts conservative approaches until clinical conditions deteriorate with respect to portal hypertension or liver function. Conservative management, i.e., interventional and supportive medical therapy, has been used up to 8 years in our series, until the time for liver transplantation is reached. Liver transplantation for BCS had more complications than transplantation for other liver diseases in our series. Therefore, we propose to keep liver function stable using interventional techniques to maintain venous outflow. If venous outflow cannot be interventionally restored and liver function deteriorates or cirrhosis develops during this time course, liver transplantation is the therapy of choice.

Adult↗
PubMed2004

Mechanical cardiac support system for patients with postcardiotomy cardiogenic shock: analysis of risk factors for survival.

OBJECTIVE: Mechanical cardiac support system (MCSS) has been used for adult patients in postcardiotomy cardiogenic shock and has been shown to provide excellent oxygenation and hemodynamic support. However, MCSS has a number of disadvantages that include high incidence rate of complications (e.g. stroke, bleeding) and limited duration of sufficient support. The objective of this study is to identify perioperative and postoperative factors for survival in patients having MCSS. METHODS: From January 1991 to April 2001, MCSS has been applied to 22 adult patients in postcardiotomy cardiogenic shock. These patients' charts were retrospectively reviewed. RESULTS: Of 22 patients, 9 patients (41%) were successfully weaned, and 6 (27%) were hospital survivors. The duration of assist ranged from 21 to 211 hours (median 66 hours). In 7 (78%) out of 9 patients who could be weaned from MCSS, MCSS were required for less than 3 days. Major complications were reexploration for bleeding (18%), leg ischemia (45%), renal dysfunction (77%), liver dysfunction (59%), infection (31.8%), hypoxia due to lung dysfunction (36%) and cerebral dysfunction (41%). pH, base excess, HCO3-, urine output, transfused platelets at first 24 hours of MCSS and preoperative body surface area were significant predictors for survival. CONCLUSION: The indices of insufficient hemodynamic support such as progression of acidosis or poor urine output are significant predictors for early death. Early conversion from MCSS to long-term assist device, such as left ventricular assist device, should be considered when these factors are associated with poor cardiac recovery.

Acidosis↗
PubMed1992

Treatment of small hepatocellular carcinomas.

There is growing interest in screening to detect symptomless hepatocellular carcinoma (HCC), which should be easier to treat than symptomatic tumours. Combined alpha-fetoprotein and ultrasound monitoring can detect HCCs of 1 cm, and Lipiodol retention can be detected in tumours smaller than 1 cm. A number of treatment options are available. Surgical resection may be curative in selected patients with a single small tumour, but the cirrhotic patient is left with a diseased liver and the risk of tumour recurrence or death from underlying liver dysfunction. Orthotopic liver transplantation is a rational treatment for patients with decompensating cirrhosis and a small HCC, but it is expensive and necessitates immunosuppression. A variety of targeted or local therapies, either individually or in combination, can be used to treat HCC. These include percutaneous alcohol injection into an HCC, which may be an alternative to surgical resection. Tumour necrosis can be seen after targeted Lipiodol chemotherapy or radiotherapy. Transcatheter arterial embolisation selectively embolises the feeding artery, and can be combined with Lipiodol chemotherapy. Small tumours are thus amenable to treatment, even in patients who cannot have surgery. Screening and treatment for symptomless HCC seems justified, unless controlled trials teach us differently.

Antineoplastic Agents↗
PubMed2004

"Off-license" use of recombinant activated factor VII.

Recombinant factor VIIa (rFVIIa) has been widely used in the treatment of bleeding episodes in haemophiliac patients with inhibitors. In haemostatic circles it has also been assessed in reversing oral anticoagulant therapy. Over the last few years, it has been used "off-label" in patients with uncontrolled bleeding due to haemostatic abnormalities due to trauma and/or massive blood loss, thrombocytopenia, platelet dysfunction or liver dysfunction. This review examines the proposed mechanism of action of rFVIIa in the context of current concepts of haemostasis and its pharmacological properties. The "off-license" use of rFVIIa is reviewed. The latter are reported mainly as case reports, case series. There is an overwhelming need for randomized controlled trials to assess rFVIIa's efficacy, dosing and safety in current "off-license" use.

Blood Coagulation Disorders↗
PubMed2002

Diagnostic issues in liver transplantation pathology.

Liver biopsy is used to determine the pathogenesis of liver dysfunction after liver transplantation. One or more causative factors may be identified on biopsy. The pathologist must be familiar with the histopathology of acute rejection to differentiate it from other potential complications, including biliary obstruction, intercurrent cytomegalovirus hepatitis, or recurrent disease. Consensus documents from the Banff international panel provide useful guidelines for the appropriate grading of acute and chronic rejection.

Acute Disease↗
PubMed2004

Pericarditis associated with Epstein-Barr virus reactivation in a patient following allogeneic peripheral blood stem cell transplantation from an HLA genotypic 1-locus mismatched sibling donor.

A 31-year-old woman with acute myeloblastic leukemia (AML) underwent allogeneic peripheral blood stem cell transplant (PBSCT). On day +274 following transplantation, the patient had severe chest pain, high-grade fever, and general fatigue. Electrocardiographic examination revealed ST segment elevation, and echocardiographic examination revealed an obvious pericardial. The diagnosis of pericarditis was made. We could not exclude the possibility of a combination of chronic GVHD involving the liver, because biochemistry examination revealed altered liver dysfunction, but liver biopsy was not performed. The patient underwent empirical treatment for bacterial or viral infection, and was given prednisolone for chronic GVHD. Retrospective serologic examination revealed that EBV reactivation had occurred at this time. This is the first reported case of pericarditis associated with EBV reactivation after allogeneic-stem cell transplantation (allo-SCT).

Adult↗
PubMed1996

Recurrence of nonalcoholic steatohepatitis following liver transplantation.

Patients with nonalcoholic steatohepatitis (NASH) may develop progressive liver dysfunction necessitating liver transplantation (OLT). We report the incidence of recurrent disease and outcome in patients undergoing OLT for NASH. Patients transplanted for NASH were identified according to pretransplant and explant liver histology. Patients with significant alcohol consumption were excluded. Medical records were reviewed to extract pre- and posttransplant data, including sequential body weight, biochemistry, and graft histology. Of 622 liver explants, eight patients had features consistent with NASH. All patients were female with a median age of 58. Seven patients were diagnosed with NASH preoperatively, including three who had undergone jejunoileal bypass. One patient was diagnosed as cryptogenic cirrhosis. At a median of 15 months following OLT, all of the eight patients were alive with no graft failure. Six patients developed persistent fatty infiltration in their graft, three of whom had accompanying hepatocellular degeneration, consistent with a diagnosis of recurrent NASH. In two patients, transition from mild steatosis to steatohepatitis and early fibrosis was observed over one to two years. The patients who did not develop recurrent steatosis had significant weight loss following transplantation, although the length of follow-up was relatively short. Patients undergoing OLT for NASH may develop recurrent steatosis shortly after transplantation, with possible progression to steatohepatitis and fibrosis. Although longer follow-up is necessary to determine the eventual prognosis related to the recurrent fat and fibrosis in the graft, patients with endstage liver disease due to NASH should be considered good candidates for OLT.

Adult↗