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At least 199 records · Page 11Linked to original sources
PubMed2005

Neonatal hemochromatosis: fetal liver disease leading to liver failure in the fetus and newborn.

Acute liver failure in the newborn is relatively rare but often fatal. The broadest definition of acute liver failure is failure of the vital functions of the liver occurring within weeks or a few months of the onset of clinical liver disease. Therefore, by definition, any liver failure in the newborn can be construed to be acute liver failure. A second component of the general definition of acute liver failure is the lack of known preexisting liver disease. In the case of neonatal acute liver failure, preexisting disease would by definition be liver disease that affects the fetus. Almost nothing is known about fetal onset liver failure, and there is no literature addressing the subject. This review will address fetal liver disease that leads to liver failure in the fetus or newborn.

Female↗
PubMedDate not supplied

[Primary alcoholic cardiac disease and alcoholic liver disease. Anatomopathological study].

In order to find out if there is an association between alcoholic heart disease and alcoholic liver disease, and to discover the prevalence and characteristics of anatomical findings in the heart at alcoholic subjects, a prospective study was realized during the autopsies of patients younger than 60 years old, who had died with alcoholic liver disease not associated with an obvious heart disease. A second group of subjects containing similar characteristics of the first group, only without a past history of alcoholism nor liver disease, were used as controls. The comparison between the two groups in respect to: age, nutritional status, macroscopic and microscopic findings of the heart, frequency and degree of atherosclerosis revealed no statistical difference. In conclusion, we submit that the subjects who had died from liver disease also presented myocardial alterations, but that these did not differe from those observed in the control subjects.

Adult↗
PubMed2002

[Indications for liver transplantation in chronic liver diseases].

Surgical resection of the diseased liver together with the implantation of a new donor organ allows patients with chronic liver failure to survive longer as well as to achieve a better quality of life. In life-threatening acute and chronic hepatic failure liver transplantation represents the only causal and long-term therapeutic option. This is also true for several genetically defined liver diseases. Five-year survival approaches 70 % in most cases. Three of four patients regain a nearly normal life with complete reintegration into their professional work. Drawbacks of this therapeutic option relate to a life-long dependence on drugs and medical services as well as to the risks associated with the surgical procedure and the side-effects of a continuous drug-induced immunosuppression. Mortality and morbidity are considerably increased during the first three months after operation. These limitations and the dramatically low availability of donor organs necessitate the application of all conservative measures before a transplantation procedure should be performed. However, the surgical option should be evaluated early enough to allow for a good chance of success. Profound knowledge of prognosis and medical treatment of each individual liver disease is a prerequisite for correct indication and timing of liver transplantation.

Chronic Disease↗
PubMed2006

Cognitive impairment in people diagnosed with end-stage liver disease evaluated for liver transplantation.

Cognitive impairments are common in patients with end-stage liver disease (ESLD). The aim of the present study was to identify and characterize the neuropsychological deficits between groups of patients with a variety of causes of ESLD and to assess the impact of heavy alcohol use on cognitive functioning. Cognitive functioning in 300 consecutive outpatients presenting for liver transplantation evaluation was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). All patients underwent a psychiatric interview and a physical and laboratory assessment. The prevalence of neuropsychological impairment was highest among patients with liver disease secondary to alcohol. Poor performance on neuropsychological testing was correlated strongly with the severity of liver disease as measured by the model for end-stage liver disease (MELD). After controlling for the linear effects of MELD in subsequent analysis, a group difference emerged in patients with cholestatic liver disease showing less cognitive impairment when compared to all other groups. After controlling for the severity of liver disease, those patients with a history of alcohol abuse or dependence were found to perform more poorly on neuropsychological testing than those patients without such a history. Furthermore, the presence of these cognitive impairments predicted disability independent of the severity of the underlying liver disease.

Adolescent↗
PubMed1977

Heparinised clotting factor concentrates in patients with Christmas disease and liver disease.

Evidence has been sought of activation of the coagulation system in two groups of patients following the infusion of two heparinised clotting factor concentrates. No changes were detected in 13 patients with mild hepatic dysfunction. In six studies on patients with Christmas disease induced abnormalities occurred in only one. Activation of the coagulation mechanism did not occur in another individual who had received the same batch of material.

Blood Cell Count↗
PubMed2004

Recent advances in alcoholic liver disease. IV. Dysregulated cytokine metabolism in alcoholic liver disease.

Alcoholic liver disease (ALD) remains a leading cause of death from liver disease in the United States for which there is no FDA-approved therapy. Abnormal cytokine metabolism is a major feature of ALD. Elevated serum concentration levels of TNF-alpha and TNF-alpha-inducible cytokines/chemokines, such as IL-6, -8, and -18, have been reported in patients with alcoholic hepatitis and/or cirrhosis, and levels correlated with markers of the acute phase response, liver function, and clinical outcome. Studies in animal models support an etiologic role for cytokines in the liver injury of ALD. Cytokines, such as transforming growth factor-beta, play a critical role in the fibrosis of ALD. Multiple new strategies are under investigation to modulate cytokine metabolism as a form of therapy for ALD.

Animals↗
PubMed1992

Variations in the glycoforms of serum alpha 1-antichymotrypsin in liver diseases and after liver transplantation.

1. Using crossed immunoaffinity electrophoresis with free concanavalin A in the first dimension, we studied the microheterogeneity of alpha 1-antichymotrypsin due to various glycoforms in sera from patients with various liver diseases and after liver transplantation. 2. Studies by isoelectric focusing and immunoblotting and by crossed immunoelectrophoresis without concanavalin A in the first dimension allowed us to show that there is no dramatic variation in electrophoretic heterogeneity of alpha 1-antichymotrypsin in the serum of patients with liver diseases or after liver transplantation when compared with that of normal subjects. Therefore the heterogeneity observed in crossed immunoaffinity electrophoresis is due to various interactions with concanavalin A. 3. The results were expressed as the ratio of concanavalin A non-reactive glycoforms plus concanavalin A weakly reactive glycoforms to concanavalin A reactive glycoforms, called R alpha 1-ACT. R alpha 1-ACT was significantly higher in patients with cirrhosis (n = 53) when compared with normal subjects (n = 30). The median R alpha 1-ACT was 1 (range 0.72-1.25) in normal subjects. It was 1.6 (range 1.18-3.02), 1.45 (range 0.65-4.12) and 2.24 (range 1.03-19) in cirrhosis of Child's grade A, B and C, respectively. There was a dramatic decrease in glycoforms with mostly biantennary glycans in some patients with Child's grade C cirrhosis. Serum levels of alpha 1-antichymotrypsin were lower than normal only in some patients with Child's grade C cirrhosis. 4. Among the patients with acute viral hepatitis studied (n = 17), five were studied longitudinally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Morpho-functional study of the kidney in patients with kidney disease and liver disease with magnetic resonance].

INTRODUCTION: We studied renal function and perfusion after the i.v. injection of Gd-DTPA-BMA, a nonionic paramagnetic contrast agent, to assess renal morphology and function in normal subjects, in renal insufficiency patients and in patients with hepatic failure and normal renal function. The latter were chosen because some patients with advanced hepatic failure may suffer from the hepatorenal syndrome, characterized by severe vasoconstriction in the renal cortical vessels. We investigated if dynamic MRI can detect early renal perfusion abnormalities in the patients who will eventually develop this syndrome. MATERIAL AND METHODS: Thirty MR examinations were carried out on 30 subjects after the i.v. injection of Gd-DTPA-BMA. Our series consisted of: 10 normal subjects; 10 renal insufficiency patients; 10 patients with hepatic failure and normal renal function. MR examinations were performed on a Philips ACS II scanner operating at 1.5 T. Two sequences were carried out in all cases: T1-weighted SE and T1-weighted TGE sequences after the bolus injection of .1 mmol/kg contrast agent. Renal longitudinal diameter and parenchymal thickness were measured in all cases and signal intensity time curves were always made. The signal intensity of the cortex, corticomedullary junction, medulla and pyelocaliceal system of each kidney was measured using a region of interest (ROI). The signal intensity curves were made considering quantitative parameters, including the area below the curve (ASC), the peak (P) and the time to peak (T-P). RESULTS: Longitudinal diameter and parenchymal thickness values were significantly lower in renal insufficiency patients than in normal subjects. Four phases were demonstrated after i.v. contrast agent injection in normal subjects, namely A) the cortical phase, B) the corticomedullary junction phase, C) the medullary phase, D) the pyelocaliceal phase. No signal intensity decrease in the medullary and pyelocaliceal curves was observed in renal insufficiency patients. Signal intensity curves values were lower in hepatic failure patients than in those with normal renal function. Hepatic failure patients could be divided into two groups: 5 patients had low P and ASC values and 4 had normal P and ASC values. The patients with lower P and ASC values developed the hepatorenal syndrome within a few months of the MR examination. DISCUSSION: Signal intensity decreased in the pyelocaliceal system phase in normal subjects because of the high paramagnetic contrast agent concentration. The lack of signal intensity decrease in renal insufficiency patients was caused by the reduced capability of concentrating Gd-DTPA-BMA. Lower signal intensity values in hepatic failure patients may be considered an early sign of the hepatorenal syndrome.

Adult↗
PubMed1992

Pregnancies complicated by liver disease and liver dysfunction.

Although liver dysfunction is infrequently seen in pregnancy, it can result in severe maternal and fetal compromise. An unrecognized case of acute fatty liver may result in both maternal and fetal death. Failure to screen for hepatitis B can result in a newborn who will be a hepatitis carrier for life. Because of such consequences, the obstetrician must remain vigilant for signs of liver dysfunction and must understand the pathophysiology of these disorders.

Cholestasis, Intrahepatic↗
PubMed1981

On the kinetics of glycocholate uptake and excretion by the normal and diseased liver in man.

Serum concentrations of glycocholate and plasma disappearance curves of i.v. injected 14C-glycocholate were measured in 6 controls and 12 patients with liver disease. On the basis of these data, hepatic uptake and biliary excretion of serum glycocholate were calculated using a previously described 3-compartmental model. The results demonstrate that the hepatic uptake increases in correlation with the serum concentrations even if the biliary excretion decreases. As a consequence of reflux of glycocholate into the serum, increases also, indicating an increased bidirectional flux of bile acids in patients with elevated serum concentrations. These findings a) confirm that hepatic uptake and biliary excretion of glycocholate are independent transport mechanisms in man, b) indicate that hepatic uptake the more effective transport mechanism in the diseased liver, and c) suggest that liver uptake and reflux are different transport mechanisms. The possible pathophysiological importance of these findings is discussed.

Biological Transport, Active↗
PubMed2006

Increased serum resistin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance.

CONTEXT: The recently discovered hormone resistin is linked to the development of insulin resistance, but direct evidence of resistin levels in humans with nonalcoholic fatty liver disease (NAFLD) is lacking. METHODS: We conducted this study to assess the relationship between serum resistin and NAFLD. We measured serum resistin and biochemical, hormonal, and histological correlates in 28 NAFLD patients, 33 controls, and 30 obese patients [body mass index (BMI), >30 kg/m2] without NAFLD. RESULTS: Resistin and adiponectin expression were measured in sc adipose tissue by quantitative RT-PCR. Resistin was higher in NAFLD patients compared with controls (5.87 +/- 0.49 vs. 4.30 +/- 0.20 ng/ml; P = 0.002) and obese patients (4.37 +/- 0.27 ng/ml; P = 0.002). Increased resistin mRNA was also found in the adipose tissue of NAFLD patients compared with controls and obese subjects. CONCLUSIONS: Both NAFLD and obese patients had lower adiponectin levels, whereas leptin was increased only in the obese group. No correlation was found between resistin and high-sensitivity C-reactive protein, BMI, homeostasis model assessment, insulin, glucose, transaminases, and lipid values. A positive correlation was found between resistin and histological inflammatory score. These data report increased resistin in NAFLD patients that is related to the histological severity of the disease, but do not support a link between resistin and insulin resistance or BMI in these patients.

Adiponectin↗
PubMed2001

Immunotherapy directed against alpha-fetoprotein results in autoimmune liver disease during liver regeneration in mice.

BACKGROUND & AIMS: Priming immune responses against alpha-fetoprotein (AFP) highly expressed in the majority of hepatocellular carcinomas results in significant antitumoral T-cell responses. Liver regeneration in humans and mice, however, is also associated with increased AFP expression. Therefore, we evaluated the risk of AFP-directed immunotherapeutic approaches to induce autoimmunity against the regenerating liver. METHODS: Mice were immunized with DNA encoding mouse AFP. For induction of liver regeneration, partial hepatectomy was performed and mice were monitored by serial histopathologic examinations and measurements of serum ALT activities (U/L), and by determination of the kinetics of AFP-specific T-cell responses. RESULTS: Livers of AFP immune mice without partial hepatectomy were characterized by minor lymphocytic infiltrations without transaminase elevations. By contrast, a significant hepatocyte damage was observed in regenerating liver that correlated well with the number of AFP-specific CD8(+) T cells, the activity of liver regeneration, and the level of AFP synthesis. Autoimmune liver damage was mediated by CD4(+) T cell-dependent CD8(+) cytotoxic T lymphocytes. CONCLUSIONS: These results show that priming of T-cell responses against shared tumor-specific self antigens may be accompanied by induction of autoimmunity dependent on the level of expression of the self antigen and have important implications for the development of antitumoral vaccines targeted against antigens that are not strictly tumor-specific.

Animals↗
PubMed2002

Endotoxin and its binding proteins in chronic liver disease: the effect of transjugular intrahepatic portosystemic shunting.

BACKGROUND: Gut-derived endotoxin is insufficiently cleared by the diseased liver, and thus, is elevated in plasma of patients with chronic liver disease (CLD). Endotoxin action might be modified by binding to soluble CD14 (sCD14) and lipopolysaccharide-binding protein (LBP), both of which have not yet been sufficiently studied in CLD. METHODS: Endotoxin, sCD14 and LBP have been determined in peripheral blood of 72 patients and 39 control subjects, and in portal and hepatic venous blood of 12 patients during transjugular intrahepatic portosystemic shunt (TIPS) implantation. RESULTS: Peripheral endotoxin (average 3-fold increased compared to controls), LBP, and sCD14 plasma levels were elevated in chronic liver disease irrespective of Child stage m, preserve/absence of cirrhosis or aetiology. LBP, and sCD14. Furthermore, endotoxin levels in the portal vein (38.1 +/- 6.1 pg/ml) were only slightly elevated compared to the hepatic vein (29.2 +/- 4.4 pg/ml), and peripheral endotoxin levels did not increase after TIPS. CONCLUSIONS: Decreased hepatocellular function rather than hepatic blood shunting might be responsible for endotoxemia. The elevation in LBP and sCD14 levels may be a consequence of endotoxemia.

Acute-Phase Proteins↗