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PubMed1994

[The relationship between RBC ferritin content in chronic liver diseases and iron deposition in hepatocytes].

The erythrocyte (RBC) ferritin content was measured in patients with chronic liver diseases including alcoholic liver disease, liver cirrhosis (LC) and hepatocellular carcinoma (HCC), and normal subjects as controls. The relationship between RBC ferritin content and iron deposition in hepatocytes was studied. The mean RBC ferritin content (MV +/- 1SD) from normal subjects was 20.7 +/- 9.7 ag/cell in male, 11.1 +/- 5.5 ag/cell in female (ag = 10(-18)g). RBC ferritin content from chronic liver disease was higher than that of normal subjects, especially in liver cirrhosis. It elevated to 71.0 +/- 52.2 ag/cell in male, and 41.6 +/- 35.0 ag/cell in female. The iron deposition in hepatocyte was observed mostly in patients with RBC ferritin content over 20 ag/cell. The microheterogeneities of RBC ferritin from liver cirrhosis was examined by isoelectric focusing (IEF) and compared with that of normal subjects. RBC ferritin from normal subjects was detected at pI range from 5.1 to 5.7 in most cases, while it was detected at pI range from about 5.0 to 6.0 in the liver cirrhosis. More basic ferritin was detected in the latter and the peaks of pI was also more basic than that of normal controls. Since patients with liver cirrhosis examined had iron deposition in hepatocytes, it is conceivable that the occurrence of basic ferritin reflects iron overload in the liver. Taking these results together, it was concluded that the presence of iron deposition in hepatocytes and the degree of iron overload can be assumed from the determination of RBC ferritin content, a noninvasive procedure.

Chronic Disease↗
PubMed1990

Rifampin relieves pruritus in children with cholestatic liver disease.

Chronic cholestatic liver disease in children frequently results in severe intractable pruritus. Current forms of therapy, including cholestyramine, are usually ineffective. Therefore, a 6-wk, double-blind, crossover study was designed to test the ability of rifampin to relieve pruritus in children with chronic cholestasis. Rifampin proved effective in alleviating pruritus in all five children tested compared with a placebo-treated group. After the 6-wk study period, rifampin was continued for 6 mo, and its effectiveness was maintained. No complications resulted from rifampin use. This study and a similar study in older patients with primary biliary cirrhosis suggest that a highly effective form of therapy is available for treatment of severe pruritus in patients with chronic cholestasis. These patients must be carefully selected and frequently monitored.

Adolescent↗
PubMed1977

Hepatic scintigraphy in management of infants and children with liver disease.

Scintiscans of liver and spleen using technetium 99m sulphur colloid in 15 infants with extrahepatic biliary atresia and 11 infants with severe obstructive jaundice (7 with genetic deficiency of alpha 1-antitrypsin) showed similar hepatic size, pattern of isotope uptake, and splenic abnormality with no distinguishing features. In 37 older children with a variety of liver disorders, the scan was invaluable in showing filling defects in five instances. Selenomethionine was taken up not only by the two filling defects due to hepatoblastoma but also in a haemangioendothelioma. In the remaining patiens liver scanning confirmed hepatic abnormality and the necessity for more specific invasive diagnostic investigations.

Cholestasis↗
PubMed1999

Expression of hepatocyte growth factor (HGF) and HGF receptor (c-met) proteins in liver diseases: an immunohistochemical study.

BACKGROUND: Hepatocyte growth factor (HGF) is a potent mitogen for hepatocytes in vivo as well as in vitro. Serum levels of HGF vary in liver diseases, reflecting liver damage and dysfunction. However there are no studies reporting expression of HGF and HGF receptor (c-met protein) simultaneously in various liver diseases. METHODS: To clarify the clinical significance of HGF/c-met protein expression in liver diseases, liver tissues from 62 patients consisting of 7 with acute hepatitis (AH), 20 with chronic hepatitis (CH), 9 with liver cirrhosis (LC) and 26 with hepatocellular carcinoma (HCC) were immunohistochemically examined. RESULTS: Intense staining of HGF was observed in patients from AH, CH and LC, although no immunoreactivity was seen in HCC. The expression of c-met protein was higher in patients with HCC and AH than in those with CH (p < 0.05). A correlation of immunoreactivity between HGF and c-met protein was not observed expect in patients with LC (p < 0.01). The extent of c-met expression had no correlation with differentiation of HCC, tumour size, presence of portal invasion, or serum AFP levels. CONCLUSION: The results of the present study suggest that HGF plays an important role in human liver diseases, mostly in a manner independent of c-met protein expression.

Adult↗
PubMedDate not supplied

[Glutathione in the treatment of chronic fatty liver diseases].

In chronic steatosic liver disease, alcohol or non-alcohol related or HBV, HCV, HDV associated, a reduction in hepatic glutathione and, consequently, in the detoxifying effects of hepatocytes is observed. Intravenous administration of high dose glutathione in patients with chronic steatosic liver disease has shown that glutathione significantly improves the rate of some hepatic tests (bilirubin, GOT, GPT, GT) even several months after treatment interruption. Further confirmation of the efficacy of GSH treatment is provided by the reduction of malondialdehyde, a marker of hepatic cell damage. The optimal results obtained in patients receiving 1800 mg/die/i.v. advocate the use of this high dosage.

Adult↗
PubMed2003

[Infective endocarditis in patients with chronic liver disease: clinical and prognostic assessment].

INTRODUCTION AND OBJECTIVES: Chronic liver disease increases the susceptibility to bacterial infections and infective endocarditis. Our aim was to determine the clinical and microbiological features and the prognosis in patients with chronic liver disease who also had infective endocarditis. PATIENTS AND METHOD: One hundred and seventy-four consecutive inpatients at our institution were recruited and followed. Thirty of them had chronic liver disease. Clinical, microbiological and echocardiographic variables were analyzed and, in some cases, histological variables were also recorded. RESULTS: Patients with chronic liver disease were younger (36 11 vs 54 18 years; p < 0.01) and had a larger proportion of intravenous drug users (73 vs 16%; p < 0.01), HIV infection (47 vs 10%; p < 0.01), right valve involvement and spleen enlargement, but heart failure appeared less often (7 vs 34%; p = 0.003). Thirty percent of the patients with and 51% of patients without chronic liver disease underwent surgery for infective endocarditis. Total mortality among patients with and without chronic liver disease was 40% and 31%, respectively. After adjustment for age and for the incidence of congestive heart failure, chronic liver disease doubled mid-term mortality with a RR = 2.45 (p = 0.015). CONCLUSIONS: Chronic liver disease has a significant impact on the prognosis in patients with infective endocarditis, and these patients should therefore be considered a high risk group.

Adult↗
PubMed1979

Electron microscopy of hepatitis B virus components in chronic active liver disease.

Eighteen liver biopsy specimens from patients with hepatitis B surface antigen (HBsAg) positive chronic aggressive hepatitis were studied by electron microscopy. All cases were selected on the basis of positive liver cell membrane fluorescence for HBsAg on immunohistochemical investigation. Striking changes in the morphology of the liver cell membrane were observed in nearly all cases. Furthermore, a dual aspect of hepatitis B core antigen (HBcAg) is described. HBcAg particles may occur as either 'naked' or 'cloudy' particles surrounded by semi electron dense material. The nature of the 'cloud' remains to be identified.

Chronic Disease↗
PubMedDate not supplied

Sites of conditional essential fatty acid deficiency in end stage liver disease.

BACKGROUND: End stage liver disease (ESLD) is a devastating illness. Its protean manifestations involve many different aspects of disturbed hepatic function. One consequence of ESLD is a decrease in plasma levels of very long chain polyunsaturated fatty acids (VL-PUFAs), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA), the former important for eicosanoid metabolism and the latter for retinal and brain membrane structure. The purpose of this study was to define the VL-PUFA changes in liver disease by comparing plasma and tissue levels of VL-PUFAs in controls to patients with ESLD. METHODS: Fatty acid profiles from plasma, red blood cell (RBC) membranes, muscle, liver, and fat tissue from ESLD patients undergoing liver transplants were measured and compared with control patients undergoing elective liver resection. RESULTS: Fatty acid profiles from plasma and RBC membranes showed significant decreases in AA and DHA levels in patients with ESLD compared with controls. However, there were no significant differences in tissue fatty acid composition between ESLD patients and controls. CONCLUSIONS: ESLD affects the liver's ability to maintain circulating levels of AA and DHA, and thereby presumably RBC membrane levels. However, solid tissues appear not to be affected by ESLD. Although the mechanism for these changes remains to be defined, it is consistent with hepatic impairment of elongation and desaturation to produce VL-PUFA for transport. The present results also suggest that dietary interventions to include preformed VL-PUFA rather than their precursors, linoleic and alpha linolenic acid, would be needed to normalize plasma VL-PUFA levels in patients with ESLD.

Arachidonic Acid↗
PubMed2000

Identification of a locus for autosomal dominant polycystic liver disease, on chromosome 19p13.2-13.1.

Polycystic liver disease (PCLD) is characterized by the growth of fluid-filled cysts of biliary epithelial origin in the liver. Although the disease is often asymptomatic, it can, when severe, lead to complications requiring surgical therapy. PCLD is most often associated with autosomal dominant polycystic kidney disease (ADPKD); however, families with an isolated polycystic liver phenotype without kidney involvement have been described. The clinical presentation and histological features of polycystic liver disease in the presence or absence of ADPKD are indistinguishable, raising the possibility that the pathogenetic mechanisms in the diseases are interrelated. We ascertained two large families with polycystic liver disease without kidney cysts and performed a genomewide scan for genetic linkage. A causative gene, PCLD, was mapped to chromosome 19p13.2-13.1, with a maximum LOD score of 10.3. Haplotype analysis refined the PCLD interval to 12.5 cM flanked by D19S586/D19S583 and D19S593/D19S579. The discovery of genetic linkage will facilitate diagnosis and study of this underdiagnosed disease entity. Identification of PCLD will be instrumental to an understanding of the pathogenesis of cyst formation in the liver in isolated PCLD and in ADPKD.

Adult↗
PubMed1989

Plasma leucine enkephalin is increased in liver disease.

Plasma methionine enkephalin is increased in liver disease and may contribute to some of the clinical manifestations of hepatic failure. To determine if another 'small' opioid peptide is increased in the plasma of patients with liver disease, leucine enkephalin was measured by radioimmunoassay. Its plasma concentration was raised approximately five-fold in patients with acute liver disease (median 1490 pmol/l, range 830-2420) and three-fold in patients with cirrhosis with ascites (960 pmol/l, 470-2900), compared with disease controls (325 pmol/l, 180-740) and healthy controls (305 pmol/l, 180-560). The increase in plasma leucine enkephalin was proportional to the degree of liver damage, as judged in the patients with acute liver disease by its correlation with the prothrombin time (r = 0.691, p less than 0.01) and alanine aminotransferase (r = 0.502, p less than 0.05), and in the patients with cirrhosis by its negative correlation with the plasma albumin (r = -0.743, p less than 0.001). It is unclear whether the raised plasma leucine enkephalin in liver disease is a consequence of diminished hepatic inactivation, increased secretion from sympathetic nerves and adrenal glands, or both.

Acute Disease↗
PubMed1985

Histochemical characteristics of fat-storing cells in alcoholic liver disease: a study by the gold chloride method using needle biopsy specimens of the liver.

To evaluate the relationship between fat-storing cells and fibrosis of the liver in alcoholic liver disease, the characteristics of fat-storing cells were studied by light microscopy with a modification of Kupffer's gold chloride method. Liver biopsy specimens were obtained at laparoscopy with a Trucut needle from 59 patients with alcoholic liver disease, 10 with no hepatic fibrosis, 18 with mild fibrosis, 18 with moderate fibrosis, and 13 with liver cirrhosis. These specimens were divided into three classes (weak, moderate, and strong) with respect to the response of fat-storing cells to the gold chloride reaction, which indicates the amount of vitamin A contained in fat-storing cells. It was found that in alcoholic liver disease the gold chloride reaction became weaker as hepatic fibrosis progressed (P less than 0.001). By contrast, no significant association was observed between the gold chloride reaction and the degree of hepatic fibrosis in 74 specimens from patients with nonalcoholic liver disease. These results show that in alcoholic liver disease hepatic fibrosis is characterized histochemically by the reduced response of fat-storing cells to the gold chloride reaction. The role of the change in fat-storing cells in alcoholic liver disease remains to be elucidated.

Biopsy, Needle↗
PubMed1994

Alcohol-related liver disease: treatment controversies.

The therapy of alcohol-related liver disease remains relatively unsatisfactory despite years of research designed to understand the pathogenesis of alcoholic liver injury and the processes involved in recovery from alcohol-related liver injury. Drugs such as the corticosteroids and colchicine appear to have a place in the management of some patients with alcohol-related liver disease but their use is not widespread in clinical practice. Liver transplantation has become an increasingly used therapy in patients with advanced liver disease but the enthusiasm of the early 1990s is now being replaced by a more cautious approach, particularly to those who have not abstained from alcohol for a significant period prior to transplant assessment. The brightest area in any discussion of treatment approaches to alcoholic liver disease is that of predicting the future. A number of agents designed to modify the inflammatory response and the endotoxaemia associated with significant alcoholic liver injury may be more beneficial than current drugs used for severe alcoholic hepatitis or cirrhosis. As in all discussions of alcohol-related liver disease and its management, it is important to highlight the need to exclude other forms of liver injury in patients who drink heavily as those diseases respond more to specific therapies than does alcoholic liver disease. The underlying therapy for all patients with alcoholic liver disease is abstinence from alcohol and the importance of encouraging patients to cease their damaging intake of alcohol can not be overemphasised.

Adrenal Cortex Hormones↗
PubMed2004

Does liver-disease aetiology have a role in cerebral blood-flow alterations in liver cirrhosis?

BACKGROUND: Studies using brain-imaging techniques have shown changes in regional blood flow (rCBF) in patients with liver cirrhosis. It remains unknown whether the aetiology of liver disease accounts for these changes. AIMS: To evaluate whether the aetiology of liver cirrhosis is associated with different patterns of rCBF. MATERIALS AND METHODS: A total of 50 patients with end-stage liver disease and no overt encephalopathy were studied. Thirteen age-matched subjects admitted to the neurology department for headache were used as controls. Exclusion criteria were focal brain lesions, severe brain atrophy and any abnormalities found on computed tomography scan suggesting other central nervous system diseases, alcohol intake or use of neuroactive drugs for at least 6 months. rCBF was assessed using single-positron-emission tomography (SPECT) with 99mTc-hexamethylpropylene amine oxime (99mTc-HM-PAO) as a tracer in all patients and controls. The Mann-Whitney U test was used for statistical analysis. RESULTS: The liver-disease aetiology was as follows: alcoholic (A) in 19 patients; viral (V) (hepatitis B virus, hepatitis D virus, hepatitis C virus) in 14 patients; alcoholic with concomitant viral (A + V) in five patients; and cholestatic (C) (primary biliary cirrhosis, primary sclerosing cholangitis) in 12 patients. SPECT showed significantly lower rCBF in cirrhotic patients than in controls for most cortical and subcortical regions and in alcoholic and viral patients than in cholestatic liver disease patients for some cortical regions. When patients were grouped according to previous alcohol abuse (including cases with a concomitant viral aetiology), rCBF was significantly lower in the frontal superior, medial and temporal inferior regions in the alcoholic group. CONCLUSIONS: Cerebral blood flow is significantly lower in patients with liver cirrhosis than in controls and, among cirrhotics, it is lower in alcoholic and viral cirrhosis than in cholestatic liver disease. In patients with previous alcohol abuse, cerebral blood flow was significantly more reduced in the frontal and temporal regions compared with patients without previous alcohol abuse.

Adult↗
PubMedDate not supplied

An overview of psychiatric issues in liver disease for the consultation-liaison psychiatrist.

Liver disease is a common cause of morbidity and mortality in the United States and elsewhere. Arising from infectious, hereditary, or toxin-induced sources, the detection of liver disease often requires a high index of suspicion. Clinical presentations are highly variable and are often accompanied by neuropsychiatric symptoms. This fact, along with an increased incidence of liver disease among patients with primary psychiatric disorders and the presence of varied drug use, complicates the tasks of providing care to patients with liver disease. To assist the consultation-liaison psychiatrist, the authors present the first of a two-part series focused on psychiatric issues in liver disease.

Brain↗
PubMed2004

Digestive and liver diseases statistics, 2004.

BACKGROUND & AIMS: Digestive and liver diseases are associated with substantial morbidity and mortality in the United States. Statistics about the incidence, prevalence, mortality, and resource utilization of digestive and liver diseases in the United States may be cumbersome to obtain because they are scattered in multiple sources. These data may be useful for policy makers, grant applicants, and authors. METHODS: Data on the most common gastrointestinal and liver diseases were collected from large publicly available national databases. Information was collected on inpatient and outpatient gastrointestinal complaints and diagnoses, gastrointestinal cancers, and deaths from common liver diseases. RESULTS: The leading gastrointestinal complaint prompting an outpatient visit is abdominal pain, with 12.2 million annual visits, followed by diarrhea, nausea, and vomiting. Abdominal pain is the leading outpatient gastrointestinal diagnosis, accounting for 5.2 million visits annually, followed by gastroesophageal reflux disease, with 4.5 million visits. Gallstone disease is the most common inpatient diagnosis, with 262,411 hospitalizations and a median inpatient charge of USD$11,584. Colorectal cancer is the most common gastrointestinal cause of death and is the most common gastrointestinal cancer, with an incidence of 54 per 100,000. Among gastrointestinal cancers, primary liver cancer had the highest increase in incidence from 1992 to 2000. CONCLUSIONS: Gastrointestinal and liver diseases are associated with significant outpatient and inpatient healthcare utilization. Following trends in utilization is important for determining allocation of resources for health care and research.

Biliary Tract Diseases↗
PubMed1986

Immune thrombocytopenia and response to splenectomy in chronic liver disease.

Six patients had chronic liver diseases of diverse origin, persistent unexplained thrombocytopenia, and no palpable splenic enlargement. Platelet-associated IgG levels were increased in all cases. Two patients underwent splenectomy; the spleens weighed 375 and 230 g. Each patient had prompt, complete, and sustained platelet count normalization. Two other patients treated briefly with prednisone had no response. These observations indicate that a minimally enlarged spleen may be responsible for thrombocytopenia in chronic liver disease and suggest that immune mechanisms may contribute to thrombocytopenia in this setting.

Adult↗
PubMed1991

Hepatic aldehyde dehydrogenase (E.C. 1.2.1.3.) isoenzymes and malondialdehyde levels in alcoholic liver disease.

To clarify the controversially discussed behaviour of hepatic ALDH isozymes in different liver diseases, 98 liver biopsy specimens were investigated as to their total ALDH and their isozyme activity. Simultaneously the malondialdehyde (MDA) content was measured in both biopsy samples and serum. The results show a significant decrease of the "low Km" isozyme E-2 activity depending on the severity of the liver disease. The tendency for the E-2 activity to decrease was greater in alcoholic than in nonalcoholic liver diseases. Although in all our diagnosis groups elevated MDA concentrations could be measured in both serum and liver tissue, a direct specific inhibitory effect on the E-2 activity could not be confirmed. The change from the low Km pathway to the high Km pathway of aldehyde detoxification, however, may contribute to the progress in alcoholic liver disease.

Aldehyde Dehydrogenase↗
PubMed2002

Blood antioxidant levels in patients with alcoholic liver disease correlate with the degree of liver impairment and are not specific to alcoholic liver injury itself.

BACKGROUND: Enhanced production of reactive oxygen species may play a pathogenic role in alcoholic liver injury. AIMS: To investigate whether various antioxidant parameters in blood are affected in different stages of alcoholic liver disease and how specific the changes are relative to non-alcoholic cirrhosis. METHODS: Patients with alcohol abuse without cirrhosis (n=14), with alcoholic cirrhosis [Child-Pugh scores A (n=9), B (n=5) and C (n=18)] and with non-alcoholic cirrhosis [Child-Pugh score C (n=6)] and healthy controls (n=13) were studied. Levels of reduced glutathione and glutathione peroxidase activity in blood, erythrocytic superoxide dismutase activity and carotenoids, alpha-tocopherol and malondialdehyde in plasma were measured. RESULTS: Levels of reduced glutathione were significantly decreased in Child-Pugh score C cirrhotics, alcoholic or not in origin, whereas oxidized glutathione and glutathione peroxidase activity were not affected. Superoxide dismutase activity and alpha-tocopherol levels were not significantly different in the various groups. Carotenoid levels were significantly lower in alcoholic cirrhotics (Child-Pugh score C) vs. controls. Malondialdehyde levels were elevated only in cirrhotics Child-Pugh score C, alcoholic or non-alcoholic. CONCLUSIONS: Levels of reduced glutathione and malondialdehyde reflect the degree of liver impairment, more than the relation with alcohol intake. Decreases in several antioxidant levels are not specific to alcoholic liver injury.

Adult↗