Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIVER DISEASE”

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 109 records · Page 6Linked to original sources
PubMed2003

CYP enzyme polymorphisms and susceptibility to HCV-related chronic liver disease and liver cancer.

Cancer risk can be influenced by the exposure to endogenous or environmental toxins. Polymorphic enzymes involved in the metabolic activation/detoxification of carcinogens may account for individual variations of risk. We studied the polymorphisms of five enzymes of the P450 superfamily, CYP1A1, CYP1A2, CYP2D6, CYP2E1 and CY3A4, as risk factors for liver disease progression and cancer in hepatitis C virus-infected patients. CYP genotyping was performed by polymerase chain reaction (PCR) restriction fragment length polymorphism or allele-specific PCR. Different stages of disease were considered, as follows: 90 asymptomatic carriers and 87 chronic hepatitis, 92 cirrhosis and 91 hepatocellular carcinoma (HCC) cases. Reference allele frequencies were obtained from 99 blood donors. Allele distributions among categories were compared using the chi(2) test. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to express relative risks. Independent associations were modeled by correspondence analysis and logistic regression. Frequencies of the CYP1A1 highly inducible alleles, MspI m2 and Val, were increased in liver disease patients compared with carriers; no specific association with HCC was found. The high-activity CYP2E1 c2 allele was underrepresented among HCC patients with respect to other HCV categories, including cirrhosis. CYP2D6 poor metabolizer (PM) genotypes were significantly more frequent in healthy subjects (7.1%) and carriers (11.1%) than in hepatitis/cirrhosis (4.6%) and HCC (1.2%) patients. This was confirmed by multivariable analysis. PM genotypes protected against progressive disease as ORs reduced proportionally to stage. The age at diagnosis for HCC was anticipated in non-PM individuals. No differences were seen for CYP1A2 and CYP3A4 genes. Polymorphic variants of CYP genes may contribute to the progression of liver disease and HCC risk in HCV-infected subjects.

Aged↗
PubMed1991

Histochemical properties of vascular and sinusoidal endothelial cells in liver diseases.

Liver biopsy specimens with or without liver diseases were examined immunohistochemically to determine the distribution of endothelial cell markers, factor VIII-related antigen (FVIII-RAg). Ulex europaeus agglutinin I (UEA-I) lectin and PAL-E. We also investigated the localization of laminin, a component of the basement membrane. In normal livers, FVIII-RAg, UEA-I and laminin were negative in sinusoidal endothelial cells, but positive in blood vascular endothelia of the portal area. The antigen detected by PAL-E was distributed in venous endothelial cells. PAL-E did not label endothelial cells of the artery. In the lobule, immunoreactivity with PAL-E was weakly detected only in some sinusoids of the periportal area. In chronic active hepatitis and liver cirrhosis, FVIII-RAg and UEA-I stained endothelial cells of neovasculatures in the enlarged portal areas of the fibrous septum surrounding pseudolobules. Some sinusoidal endothelial cells in cirrhotic livers were reactive to UEA-I and FVIII-RAg, whereas PAL-E-positive cells were found rarely in the pseudolobules. In carcinomatous sinusoidal endothelial cells, FVIII-RAg, UEA-I and PAL-E were strongly stained. Laminin underlay these carcinomatous sinusoids. These suggest capillarization of sinusoids in hepatocellular carcinoma. The histochemical approach using endothelial cell markers could be a practical tool in the diagnosis of hepatocellular carcinoma.

Antibodies, Monoclonal↗
PubMed2005

Liver transplantation for hepatitis C virus related liver disease.

Liver transplantation is a useful treatment for end stage liver disease of all aetiologies but recurrent disease presents an ongoing challenge, particularly for hepatitis C virus (HCV) where recurrence is almost universal. Immunosuppression is needed for all patients after transplantation and should be tailored to the individual patient, with particular problems being noted for those with HCV. The longer term effects of immunosuppression, particularly renal failure and the adverse effects of certain treatments on the liver graft, have become more important as survival improves and results are studied for longer periods after transplantation.

Antiviral Agents↗
PubMed1998

Adult liver transplantation for metabolic liver disease.

Liver replacement provides an effective method of replacing a failing liver, and corrects the underlying defect in many metabolic conditions. Results of liver transplantation for metabolic diseases have been encouraging, with the exception of hereditary hemochromatosis, in which infectious and for which cardiac complications appear to increase posttransplant mortality. An improved understanding of the underlying genetic and molecular defect will lead to advances in medical therapy and perhaps will decrease the need for liver replacement. The prospects of gene therapy are being pursued for many metabolic disorders, however until this research leads to direct clinical application, liver transplantation remains the only effective option for many patients with metabolic liver disease.

Amyloidosis↗
PubMed1982

Immunohistochemical characterization of hepatic tissue lymphocyte subpopulations in liver disease.

Liver biopsies from 27 patients were studied by the indirect immunofluorescence and immunoperoxidase technique for relative distribution of B cells and T-cell subpopulations. T-cell subsets were defined for OKT4(+) (helper/inducer) and OKT8(+) (suppressor/cytotoxic) cells by using mouse hybridoma monoclonal antibodies. Patients with chronic active hepatitis and those with primary biliary cirrhosis showed marked relative increments in suppressor/cytotoxic OKT8(+) lymphocytes within hepatic lymphocytic infiltrates. Other patients with acute hepatitis or those with only reactive changes also showed a relative increment in OKT8(+) T lymphocytes within hepatic biopsy material. These findings suggest that tissue lymphocytic subpopulation increments in suppressor/cytotoxic T-cell subpopulations are commonly associated with hepatic lymphocytic infiltrates and may be related to disorders of immune regulation or expression in some of these disorders.

Adolescent↗
PubMed1995

Expression of cell adhesion molecules on liver-associated lymphocytes and their ligands on sinusoidal lining cells in patients with benign or malignant liver disease.

Liver sinusoids, in contrast with the capillaries of other tissues, contain large numbers of sequestered lymphocytes. These blood-borne cells preferentially home in the liver. The mechanism regulating the recruitment of these cells and molecular regulation of the recognition of endothelial cells is as yet unclear. The present study sought to evaluate the cell adhesion molecules on human liver-associated lymphocytes and their ligands on sinusoidal lining cells in 29 patients undergoing partial hepatectomy for liver tumors. Liver-associated lymphocytes and peripheral blood lymphocytes were analyzed by flow cytometry using monoclonal antibodies. Frozen sections of liver tissue were stained according to alkaline phosphatase anti-alkaline phosphatase method. Cytometric analysis showed that virtually all liver-associated lymphocytes expressed on their surface the cell adhesion molecules LFA-1 and VLA-4. This liver-associated lymphocyte population also presented a significantly higher percentage of Mac 1, ICAM-1, and LFA-3 and an increased surface expression of LFA-1, LFA-2, and NCAM in comparison with peripheral blood lymphocytes. It was likewise shown that sinusoidal cells express ICAM-1, ICAM-2, ICAM-3, VCAM-1 and LFA-3 ligands. Liver-associated lymphocytes thus strongly express a number of different adhesion molecules. The corresponding ligands were also detected on sinusoidal lining cells. LFA-1 and VLA-4 would seem to be important pathways of temporary lymphocyte-endothelial adhesion in liver sinusoids.

Adenoma↗
PubMed1990

[Assay of serum collagen markers in chronic liver diseases and liver cancer].

In order to identify the most useful marker to diagnose hepatic fibrosis, type III procollagen peptide (P-III-P), laminin P1, and prolyl-hydroxylase (PH) in sera obtained from patients with liver diseases were simultaneously measured and compared with histological features of chronic hepatitis and with tumor size estimated on abdominal CT scan. Further more, the diagnostic accuracy of these markers was evaluated by using discriminant analysis. P-III-P and laminin P1 were closely correlated with the activity of chronic hepatitis. These two markers most accurately discriminated between the compensated stage of liver cirrhosis and the decompensated stage, and between liver cirrhosis and hepatocellular carcinoma. Laminin P1 was found to most clearly distinguish chronic hepatitis from liver cirrhosis. P-III-P was significantly correlated with the size of hepatocellular carcinoma. However, PH failed to discriminate among liver diseases, and showed no significant correlation with a liver tumor size. And none of the markers examined were correlated with a degree of hepatic fibrosis. From these results, the analysis of both serum P-III-P and laminin P1 is a useful approach to evaluate hepatic collagen metabolism.

Adult↗
PubMed2003

First report of a psychosocial intervention for patients with alcohol-related liver disease undergoing liver transplantation.

Performing transplantations in patients with alcoholic liver disease raises great concerns for both clinicians and lay people, not least because of the fear that relapse back to drinking after the procedure may lead to poor outcomes. Therefore it is important to develop and evaluate new strategies for assessing and supporting such patients. A program of psychosocial intervention was developed to assist patients undergoing transplantation for alcoholic liver disease in coping with their alcohol problems. We describe a feasibility study of its implementation in a group of 20 such patients. This report shows that it is feasible to deliver a time-limited psychological intervention to patients undergoing assessment for liver transplantation. The intervention was readily integrated into the usual transplantation process and was acceptable to both patients and staff. Further research is required to clarify its impact on longer-term outcome measures.

Adult↗
PubMed2005

Long-term follow-up of patients with alcoholic liver disease after liver transplantation in Sweden: impact of structured management on recidivism.

OBJECTIVE: No systematic evaluation has been performed previously in the Scandinavian countries on patients transplanted for alcoholic liver disease (ALD). Data are limited on the impact of structured management of the alcohol problem on the risk of recidivism following transplantation in ALD. MATERIAL AND METHODS: A total of 103 ALD patients were compared with a control group of patients with non-alcoholic liver disease (NALD). The recidivism rates for ALD patients transplanted between 1988 and 1997 as well as after 1998 (institution of structured management) were compared. RESULTS: The median follow-up was 31 (6-60) months in the ALD group and 37 (12-63) months in the control group (NS). The overall survival rates at 1- and 5 years were, respectively, 81% and 69% for the ALD group and 87% and 83% for the non-alcoholic group. The proportion of patients with Child-Pugh C (75%) was higher in ALD patients than in NALD patients (44%) (p<0.01). Thirty-two (33%) ALD patients resumed taking some alcohol after transplantation; 17 patients (18%) were heavy drinkers. A multivariate analysis showed that: sex, age, marital and employment status, benzodiazepine use and a history of illicit drug abuse did not predict the risk of alcohol relapse post-Tx. Nineteen out of 40 (48%) patients transplanted before the start of structured management had resumed alcohol but 13 (22%) out of 58 after this intervention (p=0.002). CONCLUSIONS: ALD is a good indication for liver transplantation, with similar results in the ALD patients. Structured management of the alcohol problem before and after transplantation is important in minimizing the risk of recidivism.

Adult↗
PubMed2002

Antikeratin antibodies in sera of patients with connective tissue disease and liver disease.

Sera from 93 patients with connective tissue disease, 36 rheumatoid arthritis, 41 systemic lupus erythematosus, 12 polymyositis/dermatomyositis and 4 systemic sclerosis and sera from 12 patients with liver disease, along with sera of 10 healthy subjects, were tested for antikeratin antibodies using enzyme-linked immunosorbent assay in which the wells were coated with human epidermal keratin. Values above the mean+SD of the 10 healthy subjects were found in 8.3% of rheumatoid arthritis, 29.3% of systemic lupus erythematosus, 33.3% of polymyositis/dermatomyositis, 50% of systemic sclerosis, 16.7% of liver disease patients, and 20% of healthy subjects. The results indicated a character of naturally occurring antibody of antikeratin antibodies in human sera.

Antibodies↗
PubMed2006

Cardiac surgery in children with end-stage liver disease awaiting liver transplantation.

BACKGROUND: Cardiac repair for congenital heart disease in children awaiting liver transplantation presents unique therapeutic challenges and dilemmas. We tested the hypothesis that operations in these children requiring cardiopulmonary bypass (CPB) were not associated with prohibitive morbidity and mortality. METHODS: Over the last 10 years (1994-2004), five infants were identified in our database with end-stage liver disease and awaiting liver transplantation that required cardiac surgery. Primary end point for the study was mortality. Secondary end points included morbidity and time to liver transplantation. The new pediatric end-stage liver disease (PELD) model was used to score liver disease severity. RESULTS: Three boys and two girls with mean age of 8.6 months (range, 1.5-21 months) and mean PELD of 18.0 (range, 10-29) required CPB for repair. The only early mortality in the series occurred after cardiac arrest during creation of a central shunt. The child expired two days later despite extracorporeal membrane oxygenation support. The patient had important myocardial hypertrophy. All other patients survived and underwent successful liver transplantation. CONCLUSIONS: Children with significant congenital heart disease awaiting liver transplantation can undergo safe cardiac repair with judicious perioperative support thereby reducing the risks of subsequent liver transplantation.

Comorbidity↗
PubMed1976

The occurrence of orcein-positive hepatocellular material in various liver diseases.

Liver specimens from 103 patients with various hepatic diseases and from 297 consecutive liver biopsies examined routinely were stained with orcein after oxidation of the tissue sections with potassium permanganate. Orcein-positive dark brown cytoplasmic material could be demonstrated in 27 cases with long-standing cholestasis. These patients had either primary biliary cirrhosis, the cholestatic liver disease of ulcerative colitis or chronic active hepatitis, advanced alcoholic cirrhosis or secondary biliary cirrhosis due to extrahepatic biliary obstruction. Orcein-positive material could not be demonstrated in congenital disorders of bilirubin metabolism or in hemochromatosis. Similarly, it could not be found in acute, toxic, alcoholic or chronic persistent hepatitis.

Adult↗
PubMed2025

Newly identified single-nucleotide polymorphism associated with the transition from nonalcoholic fatty liver disease to liver fibrosis: results from a nested case-control study in the UK biobank.

BACKGROUND: Genetic factors may have a significant influence on the likelihood of liver fibrosis in individuals with nonalcoholic fatty liver disease (NAFLD). The present study was conducted to explore how single-nucleotide polymorphism (SNP) impacts the development of fibrosis in those suffering from NAFLD. MATERIALS AND METHODS: Utilizing the UK Biobank dataset, we conducted a nested case-control analysis among NAFLD participants, defining the case group as those with liver fibrosis and cirrhosis during follow-up. For our in vitro investigations, we employed the LX-2 human hepatic stellate cell line. Our procedures included cultivating these cells, employing SAMM50-rs2073080 plasmid techniques to enhance the expression of recently discovered SNPs, and conducting biochemical assays. To quantify gene expression, we used real-time PCR with fluorescence detection. RESULTS: The study analyzed data from 5467 participants (1094 cases and 4373 controls). Genome-wide association analysis identified nine significant loci, including the novel rs2073080 variant, strongly associated with NAFLD-associated hepatic fibrosis. In vitro TGF-&#x3b2; modeling revealed significant upregulation of &#x3b1;-SMA and COL1A1, confirming model effectiveness. Oxidative stress markers like elevated malondialdehyde (MDA) and reduced catalase (CAT) and superoxide dismutase (SOD) levels indicated liver damage in the TGF-&#x3b2; group. SAMM50-rs2073080 was upregulated in the NAFLD-associated fibrosis model. In vitro experiments on LX-2 cells showed that SAMM50-rs2073080 overexpression led to increased fibrosis, as indicated by higher cellular MDA levels and lower CAT and SOD levels, compared to the vector group. CONCLUSION: Our research highlights a significant association of SAMM50-rs2073080 with the progression of NAFLD to hepatic fibrosis, and the in vitro experiments further corroborated these findings.

Humans↗
PubMed1996

Pharmacokinetics and pharmacodynamics of cisatracurium in patients with end-stage liver disease undergoing liver transplantation.

We determined the pharmacokinetics and pharmacodynamics of cisatracurium, one of the 10 isomers of atracurium, in 14 patients with end-stage liver disease undergoing liver transplantation and in 11 control patients with normal hepatic and renal function undergoing elective surgery. Blood samples were collected for 8 h after i.v. bolus administration of cisatracurium 0.1 mg kg-1 (2 x ED95). Plasma concentrations of cisatracurium and its metabolites were determined using an HPLC method with fluorescence detection. Pharmacokinetic variables were determined using non-compartmental methods. Neuromuscular block was assessed by measuring the electromyographic evoked response of the adductor pollicis muscle to train-of-four stimulation of the ulnar nerve using a Puritan-Bennett Datex (Helsinki, Finland) monitor. Pharmacodynamic modelling was completed using semi-parametric effect-compartment analysis. Volume of distribution at steady state was 195 (SD 38) ml kg-1 in liver transplant patients and 161 (23) ml kg-1 in control patients (P < 0.05), plasma clearance was 6.6 (1.1) ml kg-1 min-1 in liver transplant patients and 5.7 (0.8) ml kg-1 min-1 in control patients (P < 0.05), but elimination half-lives were similar: 24.4 (2.9) min in liver transplant patients vs 23.5 (3.5) min in control patients (ns). The time to maximum block was 2.4 (0.8) min in liver transplant patients compared with 3.3 (1.0) min in control patients (P < 0.05), but the clinical effective duration of action (time to 25% recovery) was similar: 53.5 (11.9) min in liver transplant patients compared with 46.9 (6.9) min in control patients (ns). The recovery index (25-75% recovery) was also similar in both groups: 15.4 (4.2) min in liver transplant patients and 12.8 (1.9) min in control patients (ns). After cisatracurium, peak laudanosine concentrations were 16 (5) and 21 (5) ng ml-1 in liver transplant and control patients, respectively. In summary, minor differences in the pharmacokinetics and pharmacodynamics of cisatracurium in liver transplant and control patients were not associated with any clinically significant differences in recovery profiles after a single dose of cisatracurium.

Adult↗
PubMed2006

[Stabilisation of abstinence by means of psychoeducation for patients with alcoholic liver disease awaiting liver transplantation].

BACKGROUND: A manualised six-month psychoeducational intervention was conducted in patients with alcoholic liver disease and abstinence problems who were waiting for a transplantation. OBJECTIVES: In a naturalistic design it was investigated whether the intervention could improve patients' alcohol abstinence. METHODS: Between January 2002 and November 2003, 72 patients were enrolled in the therapeutic intervention, 48 of whom participated in group therapy. Health-related quality of life (SF-12), anxiety and depression (HADS-D), symptom strain (BSI) and social support (F-SOZU) were measured. Alcohol abstinence was examined in each group session by measuring the alcohol concentration in breath. RESULTS: At the beginning and end of the group therapy patients showed subsyndromal measures of anxiety and depression and minor symptoms of psychopathology. Physical quality of life was reduced (t = -8.694; df = 44; p < .001). Mental quality of life was in the range of the normative sample and was correlated with depression (r = -0.400; p = .009). Patients perceived high social support (t = 8.213; df = 45; p < .001). During the course of therapy four patients had relapses but the remaining patients stayed abstinent. Physical quality of life improved (t = -2.275; df = 27; p = .031), mental quality of life and symptom strain remained stable. CONCLUSIONS: The therapy presented here facilitated a stabilisation of mental well-being in patients with alcoholic liver disease who were waiting for organ transplantation. The relapse rate measured by alcohol concentration in breath remained low.

Adult↗
PubMed1983

Incidence of hepatitis B virus infection in alcoholic liver disease, HBsAg negative chronic active liver disease and primary liver cell cancer in Britain.

A study has been undertaken to determine the incidence of serum markers of hepatitis B virus (HBV) infection in British caucasian patients with biopsy-proven alcoholic liver disease (n = 56), HBsAg negative chronic active liver disease (CALD) (n = 47) and primary liver cell cancer (PLCC) (n = 27), compared to a hospital control population without liver disease (n = 112). No increased incidence of any serum marker of HBV infection was found in alcoholic liver disease or in 'lupoid' CALD (antinuclear factor positive 1:40 and/or smooth muscle antibody positive greater than 1:40). In contrast, the incidence of antibody to HB surface and core antigens was significantly increased (p less than 0.05) in patients with cryptogenic CALD. The incidence of hepatitis B surface antigen and antibodies to HB core and 'e' antigens was significantly increased (p less than 0.005) in PLCC.

Female↗
PubMed1978

Carcinoembryonic antigen in normal and diseased liver tissue.

Many reports have demonstrated an elevation of circulating carcinoembryonic antigen (CEA) in the majority of patients with alcoholic liver disease and, less frequently, in patients with nonalcoholic liver disease. Several explanations for this finding have been proposed, eg, increased production or release of CEA by the damaged liver, decreased hepatic metabolism, or diminished excretion of CEA of extrahepatic origin. In an attempt to clarify the mechanism of CEA elevation in liver disease, we have compared the CEA plasma level as measured by radioimmunoassay with CEA demonstrable in liver tissue by the indirect fluorescent antibody technique in 7 patients without significant changes in the liver biopsy specimen, 23 patients with alcoholic liver disease, and 16 patients with miscellaneous liver diseases such as acute or chronic nonalcoholic hepatitis or extrahepatic biliary obstruction. The mean CEA plasma level in patients with alcoholic liver disease was significantly higher than in patients with nonalcoholic liver disease (8.8 +/- 9.5 vs 2.7 +/- 2.5 ng/ml; P less than 0.02). In normal liver tissue, CEA was observed in the apical cytoplasm and along the luminal surface of bile duct epithelial cells, suggesting that under normal conditions CEA accumulates in and is excreted by bile ducts. In patients with alcoholic hepatitis and/or cirrhosis there was marked bile ductular proliferation and prominent cytoplasmic CEA-specific staining and both were associated with elevated CEA plasma levels in more than 80% of cases. In the group of miscellaneous liver diseases, bile ductule counts and CEA-specific staining did not correlate with CEA plasma levels. These observations suggest that proliferating bile ductules contribute to elevated plasma CEA in alcoholic patients.

Carcinoembryonic Antigen↗