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PubMed1982

Enzymatic sulphation of bile salts in man. Bile salt sulphotransferase activity in percutaneous liver biopsy specimens from patients with liver disease.

Bile salt sulphation in liver disease was investigated by measuring the bile salt sulphotransferase level in percutaneous liver biopsy specimens from 27 patients. The same magnitude of mean specific enzyme activity was found in patients with cholestatic and non-cholestatic liver disease. No significant difference of the mean bile salt sulphotransferase activity was found when patients with and without reduced liver function as evidence from the intravenous galactose tolerance test were compared. The present results indicate that induction of liver bile salt sulphotransferase does not occur to a significant extend in clinical conditions with cholestasis.

Alanine Transaminase↗

PubMed1998

Alpha 1-antitrypsin phenotype of children with liver diseases in Thailand.

Alpha1-antitrypsin deficiency (PiZZ) constitutes not only the most common hereditary cause of liver diseases, but also of the most prevalent metabolic diseases in need of liver transplantation. It is a codominantly inherited disorder which predisposes to chronic liver disease, usually beginning in early infancy. The purpose of the present study has been to investigate alpha 1-antitrypsin phenotype in pediatric patients with various liver diseases. Phenotypic identification of alpha 1-antitrypsin variants has been carried out in 69 children with various liver diseases and 100 healthy controls using isoelectric focusing on polyacrylamide gel slabs. PIMM represents the most common phenotype detected in both groups (92% in the group with liver diseases and 88% in normal controls). We could detect PiZZ in only one healthy child but in none of those with liver diseases. Consequently alpha 1-antitrypsin deficiency does not appear to be a common cause for liver disease among children in Thailand. Further studies are necessary to elucidate the frequency of various alpha 1-antitrypsin variants and the clinical relevance with respect to liver diseases in Thailand.

Child↗

PubMed2003

Screening test data analysis for liver disease prediction model using growth curve.

This study was done based on screening test data accumulated from 1994 to 2001 for studying of risk factor related with liver disease and prediction model of liver disease. In the existing study related with liver, the main current is studying on liver cancer, not on liver disease, previous step into liver cancer. As a result of estimating prediction model through the risk factors of liver disease and the growth curve on the basis of data, it is shown that most of the risk factors about liver disease are also those about known well as liver cancer. In addition, to investigate liver disease prevalence from the viewpoint of the future, this study presumed risk factor through the various growth curve analysis and examined logistic regression, decision tree and neural network from those estimators. In the case of neural network using growth curve estimator of Xi(5)=alphai+betaiT+epsiloniT, accuracy of liver disease was 72.55% and sensitivity was 78.62%. On the other hand, in the case of liver disease prediction model using recent screening test data estimator, accuracy was 72.09% and sensitivity was 71.72%. Those are lower than liver disease prediction model of growth curve analysis. In the various liver disease prediction models assumed by growth curve and many distinction models, when growth curve estimator was used, sensitivity value was improved.

Humans↗

PubMed1987

Procollagen type I production by hepatocytes: a marker of progressive liver disease?

The presence of collagen-producing cells and its relation to disease activity were determined in cryostat liver tissue sections from subjects with active cirrhosis (n = 15), inactive cirrhosis (n = 5), chronic persistent hepatitis (n = 8), or normal histology (n = 3) by means of an immunofluorescence technique using a monoclonal antibody to the carboxy-terminal domain of procollagen type I (anti-Pc). In all patients with active cirrhosis hepatocytes showed a strong intracellular staining with anti-Pc; in 4 of them bileducts also showed a membrane-like reaction. By contrast, tissue sections from chronic inactive liver disease and normal liver were essentially negative. These findings suggest that in chronic liver disease hepatocytes and sometimes biliary epithelium produce collagen and that production is related to disease activity. The detection of active production of procollagen type I by hepatocytes could become a useful marker of progressive liver disease.

Adult↗

PubMed1995

Intrahepatic mast cells in chronic liver diseases.

Mast cells are known to be present in human liver but their distribution and density in normal livers and in chronic liver diseases have not previously been examined. In this study, we quantified mast cell numbers and examined their distribution in percutaneous biopsy specimens from normal livers (n = 8) and in two chronic progressive liver diseases: primary biliary cirrhosis (PBC) (n = 40) and alcoholic liver disease (n = 33). We compared differences in mast cell density between these two forms of chronic liver disease because it had been suggested that mast cells may play a role in the development of liver fibrosis, particularly in patients with chronic cholestatic liver disease who frequently have increased plasma histamine levels. Mast cells were identified by immunohistochemistry using a specific monoclonal antibody (AA1) raised against mast cell tryptase after an initial study showed this to be more sensitive for the detection of mast cells than the conventional histochemical stain, toluidine blue. Our results showed that small numbers of mast cells (3.9 +/- 3.3/mm2) are present within the portal tracts and sinusoids of normal livers. In progressive chronic liver disease, increased numbers of mast cells were present, which correlated with the increasing amounts of liver fibrosis present. We found significantly more mast cells in the PBC group compared with the alcoholic group for a given amount of fibrosis. Our findings suggest that mast cells and their mediators may play a role in liver fibrogenesis.

Biopsy↗

PubMed2005

Immune phenotype and serum leptin in children with obesity-related liver disease.

CONTEXT: Little is known about pathogenesis of obesity-related liver disease in childhood. Data on the relationship among leptin, immunological parameters, and liver disease in obese children are lacking. OBJECTIVE: Thus, the objective of this study was to evaluate immune phenotype and leptin serum levels in obese children with and without obesity-related liver disease. DESIGN: The study was performed in two groups of consecutive obese children: the first formed by children with obesity-related liver disease, diagnosed in the presence of chronic hypertransaminasemia, liver steatosis at ultrasound, and absence of known etiologies; the second composed of children with isolated obesity. In all patients serum leptin, immunoglobulins, peripheral T, B, and natural killer (NK) cells were evaluated. RESULTS: Twenty-three children in the first group and 16 children in the second were considered eligible. Serum leptin was increased in both groups but without any significant difference. No significant correlation was found between leptin and aminotransferases, lipid serum levels, and all tested lymphocyte subpopulations. Patients with obesity-related liver disease showed significantly higher peripheral NK and B cell counts and IgA levels than children with isolated obesity. Furthermore, no correlation was found between severity of liver disease and lymphocyte subpopulations. CONCLUSION: In our study, leptin did not correlate with hepatic steatosis, aminotransferases, and serum lipids. Children with obesity-related liver disease showed significantly higher peripheral NK and B cells and IgA levels. Additional studies are required to define the pathogenetic role of these immunological findings.

Adolescent↗

PubMed2002

Propylthiouracil for alcoholic liver disease.

BACKGROUND: Alcohol is the most common cause of liver disease in the Western world today. Randomised clinical trials have addressed the question whether propylthiouracil has any efficacy in patients with alcoholic liver disease. OBJECTIVES: The objectives were to assess the efficacy of propylthiouracil on mortality, clinical symptoms and complications, liver biochemistry, and liver histology in patients with alcoholic liver disease. Adverse events were also analysed. SEARCH STRATEGY: The Cochrane Hepato-Biliary Group Controlled Trials Register (searched July 2001), The Cochrane Controlled Trials Register (Cochrane Library Issue 3, 2001), MEDLINE (January 1966 to July 2001), EMBASE (January 1985 to July 2001) were searched. These electronic searches were combined with full text searches. Manufacturers and researchers in the field were also contacted. SELECTION CRITERIA: Randomised clinical trials studying patients with alcoholic steatosis, alcoholic fibrosis, alcoholic hepatitis, and/or alcoholic cirrhosis were included. Interventions encompassed propylthiouracil at any dose versus placebo or no intervention. The trials could be double-blind, single-blind, or unblinded. The trials could be unpublished or published as an article, an abstract, or a letter and no language limitations were applied. DATA COLLECTION AND ANALYSIS: All analyses were performed according to the intention-to-treat method. The statistical package (RevMan and MetaView) provided by the Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated by components of quality and the Jadad-scale. MAIN RESULTS: Combining the results of six randomised clinical trials including 710 patients demonstrated no significant effects of propylthiouracil versus placebo on mortality (Peto odds ratio (OR) 0.91, 95% confidence interval (CI) 0.59 to 1.40), liver related mortality (OR 0.78, 95% CI 0.45 to 1.33), complications of the liver disease (OR 1.14, 95% CI 0.58 to 2.24), or liver histology. Propylthiouracil was associated with a non significant trend towards an increased risk of non-serious adverse events (OR 1.49, 95% CI 0.74 to 2.99) and with the seldom occurrence of serious adverse events (leukopenia). REVIEWER'S CONCLUSIONS: This systematic review could not demonstrate any significant efficacy of propylthiouracil on any clinically important outcomes (mortality, liver related mortality, liver complications, and liver histology) of patients with alcoholic liver disease and propylthiouracil was associated with adverse events. Accordingly, there is no evidence for using propylthiouracil for alcoholic liver disease outside randomised clinical trials.

Antimetabolites↗

PubMed1996

Neutrophil activation in chronic liver disease.

OBJECTIVE: To assess the relationship between neutrophil activation and indices of disease severity in patients with chronic liver disease. METHODS: Plasma neutrophil elastase was measured by radioimmunoassay as a marker of neutrophil activation, and disease severity assessed by standard clinical, biochemical, haematological and histological techniques. PATIENTS: Eighty-eight patients with chronic liver disease were studied, Thirty-nine had alcohol-induced liver disease (ALD), 18 autoimmune chronic hepatitis, 13 cryptogenic cirrhosis, seven primary biliary cirrhosis, six primary sclerosing cholangitis, three haemochromatosis and two secondary biliary cirrhosis. Seventy-three patients were cirrhotic and 15 were non-cirrhotic, confirmed by biopsy. RESULTS: Levels of neutrophil elastase were raised in Childs C cirrhotic patients with ALD compared with Childs A or B patients with ALD (P < 0.01), Childs A or B patients with non-ALD (P < 0.01), and Childs C patients with non-ALD (P = 0.02). In patients with ALD, neutrophil elastase correlated with prothrombin time (r = 0.679, P = 0.001), bilirubin (r = 0.587, P < 0.001), Child-Pugh score (r = 0.546, P < 0.001) and inversely with serum albumin (r = -0.511, P < 0.001). In patients with non-ALD, there were no correlations with the measurements of with transaminase levels. CONCLUSION: Neutrophil activation, as measured by plasma neutrophil elastase, is a marker of disease severity in patients with alcohol-induced chronic liver damage, but not in those with other causes of liver disease.

Autoimmune Diseases↗

PubMed1981

[Therapy of aminoacid and protein metabolism disturbances in liver disease (author's transl)].

1. The role of the liver in synthesis and metabolism of proteins, in the metabolism of certain aminoacids, and in urea synthesis is described. 2. In the liver disease protein synthesis may be reduced. The activity of lysosomal proteases is enhanced during acute hepatitis and in cirrhosis. Diseases of the liver may be associated with various derangements in the metabolic pathways of particular aminoacids. Synthesis of urea is decreased in chronic liver disease. 3. Nutrition for patients with chronic liver disease needs to include sufficient calories and has to be well balanced. Parenteral nutrition and diet in patients with edema and ascites deserves special attention. Dietary treatment of patients with cirrhosis of the liver and impending or already existing hepatic encephalopathy is outlined.

Amino Acids↗

PubMed1998

Immunological liver diseases in children.

Autoimmune liver diseases comprise a number of disorders in which inflammatory damage to the liver is believed to derive from an autoimmune attack. These include autoimmune hepatitis (AIH), characterised by positive smooth muscle and/or nuclear (SMA/ANA) or liver kidney microsomal type 1 (LKM1) antibodies, autoimmune sclerosing cholangitis (ASC), usually SMA/ANA positive, and AIH after liver transplantation, which is positive for SMA, ANA, or atypical LKM. These disorders often present with symptoms indistinguishable from prolonged acute hepatitis. Less commonly the onset is insidious, with nonspecific symptoms, or with complications of portal hypertension. For AIH and ASC, experimental evidence suggests that usually in individuals genetically predisposed to autoimmunity, a liver self antigenic peptide is recognized by T lymphocytes which promote a cascade of autoaggressive processes. For AIH after liver transplantation, the pathogenic mechanisms remain to be elucidated. All types of autoimmune liver disorders appear to respond favourably to early treatment with prednisolone with or without azathioprine. For patients presenting with fulminant hepatic failure or with already advanced cirrhosis, immunosuppression is rarely effective and the only mode of treatment is liver transplantation. The role of other immunosuppressant or immunomodulatory drugs, like cyclosporin A, tacrolimus or ursodeoxycholic acid, in the treatment of autoimmune liver disorders remains to be defined.

Child↗

PubMed1994

Serum ferritin and transferrin saturation in patients with chronic alcoholic and non-alcoholic liver diseases.

OBJECTIVES: To compare serum ferritin concentration and transferrin saturation in patients with alcoholic and non-alcoholic chronic liver diseases. DESIGN: Consecutive patients with liver diseases. SETTING: The department of internal medicine in a teaching hospital. SUBJECTS: Three hundred and twelve patients with different liver diseases consecutively admitted between 1987 and 1992. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Fasting serum iron, transferrin and ferritin. RESULTS: Serum ferritin was increased above 200 micrograms L-1 in all 18 patients with haemochromatosis (range 310-6500 micrograms L-1), in 64 of 111 alcoholics (58%) and in 30 of 137 (22%) with chronic non-alcoholic liver diseases (P < 0.01). Twelve of 111 alcoholics (11%) had serum ferritin above 1000 micrograms L-1 compared with one of 137 (0.7%) with chronic non-alcoholic liver diseases. In 13 alcoholics who abstained after admission, serum ferritin decreased from 1483 micrograms L1 +/- 1134 to 388 micrograms L-1 +/- 237 (P < 0.001) after 1 1/2 to 6 weeks. The transferrin saturation was increased above 62% in 13 of 18 patients (72%) with haemochromatosis, in 16 of 105 alcoholics (15.2%) and in three of 132 (2.3%) with chronic non-alcoholic liver disease (P < 0.01). CONCLUSION: Serum ferritin is more frequently elevated in abusing patients with alcoholic liver disease than in patients with other chronic liver diseases such as autoimmune liver diseases and hepatitis C. Because serum ferritin decreases rapidly during abstinence, the measurement of ferritin for the detection of haemochromatosis in patients abusing alcohol should be postponed until the patients are abstaining. Most of the patients with increased serum ferritin have normal transferrin saturation values which can be used to separate them from haemochromatosis.

Adult↗

PubMed2006

Growing importance of liver disease in HIV-infected persons.

Liver disease is a growing problem in HIV-infected persons. In those who are able to take antiretroviral therapy, the forms of liver disease have changed and their relative importance has increased. This review focuses on liver disease in HIV-infected persons, caused by hepatitis C virus, hepatitis B virus, or treatment of HIV infection.

Anti-Retroviral Agents↗

PubMed1980

Low high-density lipoprotein and reduced antipyrine metabolism in members of a family with polycystic liver disease.

A family with polycystic liver disease was investigated in order to evaluate the role of the liver in determining the serum high-density lipoprotein (HDL) level and its relationship to the rate of antipyrine elimination from plasma. The four subjects with polycystic liver disease had low serum HDL cholesterol, total cholesterol, and apoprotein A-II levels as compared with others in the family. There was an inverse relationship between HDL cholesterol and apoproteins and the antipyrine half-life in plasma. The results demonstrate that serum HDL levels and the antipyrine metabolism, both reflectors of hepatic function, might be altered in parallel in subjects with polycystic liver. The findings presumably reflect the effects of cysts on liver parenchyma and changes in the hepatic blood flow.

Adult↗

PubMed2004

Epidemiology of alcoholic liver disease.

Alcohol is one of the main causes of end-stage liver disease worldwide, and alcoholic liver disease is the second most common reason for liver transplantation in the United States. Beginning in the 1970s, there was a gradual decline in alcoholic cirrhosis-related mortality in many countries. However, in the past few years, alcoholic liver disease mortality rates in several countries have stabilized or started to increase. There are significant ethnic and gender differences in alcoholic cirrhosis-related mortality rates. Furthermore, alcohol use increases the risk for liver disease in those infected with hepatitis C. A better understanding of the epidemiology of alcoholic liver disease will allow for improved diagnosis and management of this common problem.

Adult↗

PubMedDate not supplied

Ultrasonography of diffuse liver disease. A review.

Radiographically, the liver may appear normal even if severely diseased. Ultrasonography can be an important adjunct in the evaluation of diffuse parenchymal hepatic disease. Diffuse liver disease appears ultrasonographically as a change in liver echogenicity from normal when compared with the renal cortex or spleen. Diffuse liver disease can be characterized as either hyperechoic due to fatty change, steroid hepatopathy, and cirrhosis or hypoechoic due to congestion, suppurative hepatitis, and lymphoma. Ultrasonographic diagnosis of diffuse liver disease should be substantiated by biopsy and histopathologic evaluation.

Animals↗

PubMed2006

[Insulin resistance in non-alcoholic fatty liver disease].

Insulin resistance is the pathophysiological hallmark of various kinds of clinical diseases, including non- alcoholic fatty liver disease. Insulin resistance is the common characteristic of metabolic syndrome and its related features. Insulin resistance is a systemic disease that affects the nervous system, muscles, pancreas, kidney, heart and immune system, in addition to the liver. A complex interaction between genes and environment factors enhances insulin resistance and the phenotypic expression of NAFLD (non- alcoholic fatty liver disease) in individual patients. Advanced fibrotic liver disease is associated with many features of metabolic syndrome, and the risk of progressive liver disease should not be underestimated for the individuals suffering with metabolic disorders. Abnormalities of insulin signaling can cause the state of insulin resistance, but there is no clear cut scientific evidence that distorted insulin signaling is the primary pathophysiological defect. Increased adipose tissue mass can cause peripheral tissue insulin resistance via the changes of the adipocytokine secretory patterns. We discuss in this article the sequences of the insulin signaling cascades and the possible molecular targets of insulin resistance, the humoral "cross talk" between the distorted secretory patterns of the adipocytokines, and the peripheral tissue insulin resistance along with the pathophysiology of NAFLD.

Adipose Tissue↗

PubMed1987

Lecithin: cholesterol acyltransferase in liver disease.

Lecithin: cholesterol acyltransferase (LCAT) activity in patients with liver disease has been found to be either normal or lower than normal, but no information on LCAT mass in these patients is available. In this study, LCAT mass concentration together with LCAT activity and cholesterol esterification rate were measured in the plasma of 19 patients with cholestatic liver disease and 21 patients with non-cholestatic liver disease. The LCAT mass in plasma correlated positively with serum albumin (r = 0.69, p less than 0.001) and pre-albumin (r = 0.77, p less than 0.001) and negatively with serum bilirubin (r = -0.42, p less than 0.01) and bile salts (r = -0.43, p less than 0.01), thus reflecting the severity of liver disease and liver protein synthesizing capacity. In plasma, LCAT mass concentration also correlated well with LCAT activity (r = 0.88, p less than 0.001) and cholesterol esterification rate (r = 0.73, p less than 0.001), thereby indicating that the decrease of LCAT activity and cholesterol esterification rate in liver disease is primarily a function of decreased LCAT mass.

Cholestasis↗

PubMed2005

Histological progression of non-alcoholic fatty liver disease in Chinese patients.

BACKGROUND: Non-alcoholic fatty liver disease is an important cause of chronic hepatitis and cryptogenic cirrhosis. The natural history of non-alcoholic fatty liver disease is not well understood especially in Asian populations. AIM: To investigate the histological progression in Chinese patients with biopsy-proven non-alcoholic fatty liver disease. METHODS: Chinese patients who had liver biopsy at least 3 years ago and confirmed to have non-alcoholic fatty liver disease were invited for a second liver biopsy. Clinical and laboratory parameters related to their liver function and metabolic syndrome were recorded and analysed. Liver biopsies were scored for the degree of steatosis, necroinflammation and fibrosis. Correlation coefficients were calculated to assess the association between changes in histological scores and metabolic parameters. RESULTS: Seventeen patients who had been followed up for a median period of 6.1 (range: 3.8-8.0) years underwent a second liver biopsy. Nine (53%) patients had progressive disease with worsening of fibrosis score. No statistically significant correlation was found between the changes in histological scores and metabolic parameters. Seven patients developed hypertension or diabetes mellitus during the period of follow-up. CONCLUSIONS: Non-alcoholic fatty liver disease is a progressive disease in Chinese patients as in their Caucasian counterparts. Diagnosis of non-alcoholic fatty liver disease may predate development of new components of metabolic syndrome.

Adult↗