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PubMed1982

Platelet adhesiveness to glass beads in liver disease.

Patients with liver disease have abnormal platelet function. We have investigated the retention of platelets to glass beads in fulminant hepatic failure, cirrhosis and normal controls. Glass bead retention was significantly increased in fulminant hepatic failure (91.5 +/- 4.8%, n = 10) compared with controls (80.2 +/- 8.5%, n = 10) whereas it was significantly reduced in cirrhosis (46.2 +/- 26.8%, n = 10). The increased platelet adhesiveness might predispose to the formation of platelet aggregates in the blood observed during charcoal haemoperfusion in patients with fulminant hepatic failure.

Acetaminophen↗

PubMed1990

Ovine white-liver disease (OWLD). Trace elements in liver.

Trace elements in liver were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), in cobalt/vitamin B12 supplemented lambs on the same pastures as well as clinically healthy, but sometimes subclinical B12 deficient lambs on other pastures (H). Liver Co was marginal to deficient in both OWLD lambs (S lambs) and H lambs. Supplementation with B12 or Co elevated liver Co. Liver copper was significantly lower in OWLD lambs than in the H lambs, and Co/B12 supplementation on pasture generally had no significant effect on the contents. Dosing lambs on OWLD pastures with copper oxide needles (SCuO), however, resulted in high/toxic liver Cu. Dosing with Co, Se and Cu glass boluses resulted in adequate liver Cu, except for 1 lamb with toxic amounts indicating dissolution and absorption of the bolus. OWLD lambs had significantly lower liver molybdenum than H lambs, and Co/B12 supplementation elevated values, while CuO treatment depressed them. Liver zinc, manganese and selenium are also reported.

Animals↗

PubMed1987

Kinetics of drug action in disease states. XIX. Effect of experimental liver disease on the neurotoxicity of theophylline in rats.

There are pronounced interindividual differences in the neurotoxicity of theophylline in humans as reflected by the wide range of plasma theophylline concentrations associated with the occurrence of life-threatening, generalized seizures in patients treated with this widely used bronchodilator. The variability indicates that there may be a number of as yet unrecognized risk factors for theophylline neurotoxicity. After the development of an animal model of theophylline-induced seizures, renal failure was identified as one such risk factor. This investigation was designed to determine if experimental liver disease will alter the neurotoxic effect of theophylline. Studies were performed on rats with extrahepatic cholestasis produced by bile duct ligation and with hepatic necrosis induced by carbon tetrachloride administration and on respective controls. Theophylline was infused i.v. at 1.03 mg/min until the onset of maximal seizures. Theophylline and theophylline metabolite concentrations at that time were determined in serum (unbound and total drug), brain and cerebrospinal fluid. Extrahepatic cholestasis was associated with small increases in unbound theophylline concentration in serum, theophylline concentration in brain and serum free fraction in serum at onset of seizures. The concentrations of theophylline metabolites were negligible. There were no apparent effects of extrahepatic cholestasis or hepatic necrosis on theophylline concentrations at onset of seizures in cerebrospinal fluid, the fluid that was shown in a preceding study to be the best indicator of the theophylline concentration at the site of the neurotoxic effect. It is concluded that experimental liver disease had no apparent effect on the neurotoxicity of theophylline under the conditions of this investigation.

Acute Kidney Injury↗

PubMed1993

Epidemiology of alcoholic liver disease.

Although mortality from alcoholic liver disease has declined in some Western countries in recent years, elsewhere it is increasing and overall it remains a major health problem. Deaths are predominantly seen in patients with alcoholic hepatitis or cirrhosis, and when they occur in patients with fatty liver are usually unrelated to liver disease. Progression to cirrhosis is correlated with the severity of fatty liver and particularly with the presence of alcoholic hepatitis. Mortality from cirrhosis is strongly correlated with per capita alcohol consumption. The decline in cirrhosis mortality rates seen recently is related in part to decreases in per capita consumption, but probably also to the growth of self-help organizations which facilitate abstinence from alcohol. Recent studies suggest there is not an invariable dose-response relationship between alcohol intake and the severity of liver disease and that alcohol has a permissive effect which allows other aetiological factors to operate. Factors that influence susceptibility to alcoholic liver disease include gender (women develop alcoholic cirrhosis more readily than men), concomitant hepatitis C infection and possibly hepatitis B infection. It is uncertain whether HLA status or immune mechanisms are implicated. The systematic use of screening tests for hazardous consumption combined with early intervention therapies offers a good prospect of reducing morbidity and mortality from alcoholic liver disease.

Carcinoma, Hepatocellular↗

PubMed1985

Laboratory evaluation of liver disease.

With respect to liver disease, the primary function of the laboratory is to identify its presence. Tests are not available that permit a specific diagnosis and an accurate prognosis. Several tests should be present in a minimum data base that can help identify hepatobiliary disease. They are ALT, SAP, total serum bilirubin, urine bilirubin, cholesterol, albumin, BUN, glucose, red cell morphology, and urine sediment. It is sometimes possible to tentatively identify whether a disease is primarily hepatocellular or biliary from the pattern of changes that occur in these tests. In addition, an estimate of the severity is sometimes possible when abnormal values are extreme. The keys are to avoid overinterpretation, use serial evaluations, and rely on a liver biopsy when definitive answers are needed. If liver disease is suspected but there are only marginal changes in the routine tests, the more sensitive tests of function, BSP retention and ammonia tolerance, are warranted. In the future, as more knowledge is gained about the responses of ARG, GGT, and ICG retention to naturally occurring diseases, these tests may join or replace some of those currently used. Also, as the ability to accurately and economically measure the various bile acids improves, a sensitive, yet noninvasive, method to detect and define modest changes in hepatobiliary function may result.

Ammonia↗

PubMed2006

[The relationship between serum adiponectin level and serum alanine aminotransferase elevation in Korean male with nonalcoholic fatty liver disease].

BACKGROUND/AIMS: Nonalcoholic fatty liver disease (NAFLD) comprises a large part of chronic liver diseases. Recently it was reported that adipokines are closely associated with the common risk factors for NAFLD, such as obesity, diabetes, dyslipidemia, and insulin resistance. We aimed to evaluate the changes in serum adiponectin, resistin and leptin concentrations related to alanine aminotransferase (ALT) elevations in Korean men with NAFLD. METHODS: We studies 38 men who were diagnosed with fatty liver by abdominal ultrasonography. None had a history of excessive alcohol consumption, autoimmune hepatitis, inherited or metabolic liver disease or viral hepatitis. The subjects were divided into two groups. One group had normal levels of ALT (n=28) and the other had increased ALT (n=10). We compared anthropometrical parameters, biochemical items and serum adipokine levels between these two groups. RESULTS: Serum adiponectin levels were lower in the increased ALT group than in the normal ALT group (3.89 +/- 1.77 vs 7.01 +/- 2.54 microgram/dL, P=0.001). But there were no significant differences in serum leptin and resistin levels between two groups (4.02 +/- 2.04 vs 3.26 +/- 1.41 ng/mL, p=0.245, 80.14 +/- 14.8 vs 80.5 +/- 11.34 ng/mL, P=0.937, respectively). Multiple linear regression analyses demonstrated that the serum adiponectin level is inversely correlated with serum ALT level and that the serum aspartate aminotransferase (AST) level is positively correlated with the serum ALT level. CONCLUSIONS: Our study shows that hypoadiponectinemia is associated with an ALT elevation in patients with NAFLD. Adiponectin may play an indirect role in the development of NAFLD.

Adiponectin↗

PubMed2005

13C-galactose breath test and 13C-aminopyrine breath test for the study of liver function in chronic liver disease.

BACKGROUND AND AIMS: Liver biopsy examination is the gold standard to diagnose the presence of cirrhosis. The aim of this study was to evaluate the accuracy of both 13 C-aminopyrine breath test ( 13 C-ABT) and 13 C-galactose breath test ( 13 C-GBT) in the noninvasive assessment of the presence of cirrhosis in patients with chronic liver disease. METHODS: We evaluated 61 patients with chronic liver disease of diverse etiologies (21 compensated cirrhosis). All patients underwent 13 C-GBT and 13 C-ABT, and the results were expressed as a percentage of the administered dose of 13 C recovered per hour (%dose/h) and as the cumulative percentage of administered dose of 13 C recovered over time (%dose cumulative). Results were analyzed according to absence vs presence of cirrhosis. RESULTS: On average, 13 C-GBT %dose/h and %dose cumulative were decreased significantly in patients with compensated cirrhosis, and the same finding was observed for 13 C-ABT results from 30 to 120 minutes. 13 C-GBT %dose/h at 120 minutes had 71.4% sensitivity, 85.0% specificity, and 83.7% accuracy, whereas 13 C-ABT %dose cumulative at 30 minutes had 85.7% sensitivity, 67.5% specificity, and 77.1% accuracy for distinguishing between the 2 subgroups of patients. Combined assessment of 13 C-GBT and 13 C-ABT increased the diagnostic accuracy (80% positive predictive value) of either test alone and reached 92.5% specificity and 100% sensitivity for the diagnosis of cirrhosis. CONCLUSIONS: In patients with chronic liver disease, both 13 C-GBT and 13 C-ABT are useful for the diagnosis of cirrhosis. Combination of the tests increases the diagnostic yield of each test alone.

Adult↗

PubMed2006

The combined elevation of tumor markers CA 19-9 and CA 125 in liver disease patients is highly specific for severe liver fibrosis.

Increased tumor markers in patients with liver cirrhosis are often considered to be unspecific. The use of this unspecific elevation to discriminate minimal fibrosis from severe fibrosis has never been explored. We aimed to answer the question, Do tumor markers predict severe liver fibrosis? The study group consisted of 125 patients with alcoholic liver disease, hepatitis B, or hepatitis C with available liver biopsy. Tumor markers CA 19-9, CA 15-3, and CA 125 were determined using routine laboratory methods and correlated with the extent of liver fibrosis. Fibrosis stages 1 and 2 were classified as minimal fibrosis; stages 3 and 4, as severe fibrosis. Tumor markers CA 19-9, CA 125, and CA 15-3 increased with stage of fibrosis. For separating patients with mild fibrosis (F1+F2) from patients with severe fibrosis (F3+F4), CA 19-9 had a sensitivity of 70.5% and a specificity of 88.6, CA 125 had 38.1% and 89.7%, and CA 15-3 had 19.0% and 93.0%, respectively. Logistic regression of a combined score of CA19-9 and CA 125 values revealed that an increase of 1 point of the CA 19-9/CA125 score resulted in a 1.6 times increase in likelihood of the presence of severe fibrosis. The CA 19-9/CA 125 score achieved a similar specificity (97.1% vs. 100%) but a higher sensitivity (42.9% vs. 33.3%) than the widely used cirrhosis discriminant score of Bonacini. A specificity (98.5%) similar to that of the CA 19-9/CA 125 score was reached by the easier determination of the combined elevation of CA 19-9 and CA 125, which had the best positive predictive value, 92.9%. The excellent predictive ability of the combined elevation of CA 19-9 and CA 125 for severe liver fibrosis (F3+F4) was confirmed in an independent group of patients with liver disease. The combined elevation of CA 19-9 and CA 125 is useful for identifying patients with advanced fibrosis or cirrhosis with high specificity. Patients without a combined elevation of CA 19-9 and CA 125 still require histological examination to identify severe fibrosis or cirrhosis.

Adolescent↗

PubMed1999

Screening for cerebral aneurysm in patients with polycystic liver disease.

BACKGROUND: Polycystic liver disease (PCLD) is an autosomal dominant disease characterized by multiple macrocystic lesions throughout the liver. The association between PCLD and cerebral aneurysm is well documented, and approximately 20% of patients with PCLD have demonstrable cerebral aneurysms at autopsy. The prevalence reported from autopsy series, however, may not reflect the true prevalence in patients with PCLD. We undertook this study to evaluate the prevalence and diagnosis of cerebral aneurysms in screening cerebral studies in patients with PCLD. METHODS: Patients were identified by searching the hepatobiliary surgical service data base and hospital medical records. Hospital charts were reviewed to confirm presence of PCLD and to identify screening studies for cerebral aneurysms. RESULTS: Ten patients with PCLD received screening studies of the cerebral vasculature during a 10 1/2-year period. One patient was found to have an asymptomatic cerebral aneurysm. A 45-year-old woman with no other significant medical history was referred for evaluation of PCLD. Screening magnetic resonance angiography (MRA) revealed a 5 mm aneurysm extending anteriorly near the origin of the right ophthalmic artery, without evidence of rupture. Cerebral angiography confirmed these findings, and the aneurysm was clipped. CONCLUSIONS: Because cerebral aneurysms can be an important source of morbidity and mortality in PCLD, we recommend screening by MRA or by computed tomographic angiography (CTA) of the cerebral vasculature in all patients who have PCLD.

Adult↗

PubMed1979

Histological changes in testicular biopsies from chronic alcoholics with and without liver disease.

Testicular and liver biopsies were obtained from thirty consecutive patients at the age of 30 and 64 years with chronic alcoholism (daily consumption of 72 g of alcohol or more for at least five years). The spermatogenesis was normal in 12 patients (40 per cent), moderately reduced in 15 patients (50 per cent) and severely reduced in 3 patients (10 per cent). No relation between the presence of liver disease as assessed by histological examination of the liver biopsy and the impairment in the spermatogenesis could be demonstrated.

Adult↗

PubMed1976

Carbohydrate metabolism in liver disease.

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.

Alanine↗

PubMed2000

13C-phenylalanine and 13C-methacetin breath test to evaluate functional capacity of hepatocyte in chronic liver disease.

BACKGROUND: To grade liver damage, Child-Pugh classification is used but these tests do not reflect the quantitative functional hepatic reserve. AIMS: 13C-Phenylalanine Breath Test and 13C-Methacetin Breath Test are evaluated as possible tools, being both safe and easy to perform, to quantify functional hepatic reserve in chronic liver disease patients. PATIENTS: Both tests were performed in 48 healthy volunteers and 48 chronic liver disease patients. METHODS: Breath samples were collected after taking 13C-Phenylalanine (100 mg) and 13C-Methacetin (75 mg). 13CO2 enrichment was measured using mass spectrometry RESULTS: Both tests discriminated the hepatic function, decreasing results of the 13CO2 enrichment agreeing with the increasing severity of the hepatic patient (13C-Phenylalanine Breath Test multiple correlation coefficient: 0.72, global p<0.001; Methacetin Breath Test: 0.73, p<0.001). Correlation between 13C-Phenylalanine Breath Test and Methacetin Breath Test was 0.63, p<0.001. If both tests were pathological, the sensitivity for the diagnosis of hepatic dysfunction was high (98%), although the specificity decreased to 60%. Best results were obtained at 30 minutes with 13C-Phenylalanine Breath Test and at 10 minutes with Methacetin Breath Test. CONCLUSIONS: Both 13C-Phenylalanine Breath Test and Methacetin Breath Test are safe and easy tests to perform and both are able to discriminate the hepatic functional capacity between the different groups studied.

Acetamides↗

PubMed2004

Diagnostic and therapeutic approach to cholestatic liver disease.

When cholestatic liver disease is present, liver ultrasound should be performed to ascertain if cholestasis is extrahepatic or intrahepatic. If bile ducts appear dilated and the probability of interventional treatment is high, endoscopic retrograde cholagio-pancreatography (ERCP) or trans-hepatic cholangiography (THC) should be the next step. If the probability of interventional therapeutics is low, cholangio-MRI should be performed. Once bile duct dilation and space occupying lesions are excluded, a work up for intrahepatic cholestasis should be started. Some specific clinical situations may be helpful in the diagnostic strategy. If cholestasis occurs in the elderly, drug-induced cholestatic disease should be suspected, whereas if it occurs in young people with risk factors, cholestatic viral hepatitis is the most likely diagnosis. During the first trimester of pregnancy cholestasis may occur in hyperemesis gravidorum, and in the third trimester of gestation cholestasis of pregnancy should be suspected. A familial history of recurrent cholestasis points to benign recurrent intrahepatic cholestasis. The occurrence of intrahepatic cholestasis in a middle-aged woman is a frequent presentation of primary biliary cirrhosis, whereas primary sclerosing cholangitis should be suspected in young males with inflammatory bowel disease. The presence of vascular spider nevi, ascites, and a history of alcohol abuse should point to alcoholic hepatitis. Neonatal cholestasis syndromes include CMV, toxoplasma and rubinfections or metabolic defects such as cystic fibrosis, alpha1-antitrypsin deficiency, bile acid synthesis defects, or biliary atresia. The treatment of cholestasis should include a management of complications such as pruritus, osteopenia and correction of fat soluble vitamin deficiencies. When hepatocellular failure or portal hypertension-related complications occur, liver transplantation should be considered.

Cholestasis, Extrahepatic↗

PubMed1981

Detection of liver IgG Fc receptors using soluble immune complexes of peroxidase-antiperoxidase. I. Detection in liver tissue from patients with liver diseases.

The presence of liver IgG Fc receptor sites was demonstrated in the liver tissue from 23 patients with liver diseases and 2 patients without liver lesions by the localization of soluble immune complexes of peroxidase-antiperoxidase (PAP). Cryostat sections of liver tissues were incubated with the complexes and the peroxidase activity was revealed histochemically. In the normal liver tissue, PAP were localized on the liver cell membrane, the Kupffer cells, and some of the sinusoidal walls. In acute hepatitis, a strongly positive reaction on swollen Kupffer cells was remarkable but positive reaction on the liver cell membrane was very weak. In chronic aggressive hepatitis, PAP were strongly positive on multiplied Kupffer cells and many PAP-positive infiltrated cells were observed at the area of piecemeal necrosis. However, the positive reaction on the liver cell membrane in patients with chronic aggressive hepatitis was generally fainter than in the normal cases without liver diseases. These results correlated well with the severity of liver cell necrosis. In chronic persistent hepatitis, the number of PAP-positive infiltrated cells in the portal area and positive Kupffer cells were fewer than in chronic aggressive hepatitis. Similar results were obtained with liver cirrhosis, and in particular, the liver cell membrane with regenerative nodules gave a positive reaction. A negative result was obtained by incubation with PAP-F(ab')2 alone. PAP reaction was significantly inhibited by pretreatment with aggregated human IgG, trypsin, and pronase but not with neuraminidase.

Hepatitis↗

PubMed1978

Erythrocyte lipid composition and sodium transport in human liver disease.

In patients with liver disease there are usually increases in erythrocyte cholesterol and phosphatidylcholine concentrations. This increase in membrane lipid changes the shape of the erythrocyte and "spur" or "target" cells may be present. Sodium fluxes were measured in erythrocytes from 17 patients with a variety of liver diseases and from 17 normal subjects and the values related to the lipid content of the membrane. Ouabain-insensitive and ouabain-sensitive effluxes were lower in patients than in normal subjects and the reduction in ouabain-insensitive efflux was more marked. Sodium influx was also significantly lower in erythrocytes from patients than controls. Ouabain-sensitive and ouabain-insensitive effluxes and sodium influx did not correlate with the cholesterol content of erythrocytes from patients. Significant negative correlations were noted between ouabain-insensitive sodium efflux (r=--0.63, P less than 0.01), sodium influx (r=--0.61, P less than 0.01) and intracellular sodium concentration (r=--0.66, P less than 0.01) and the cholesterol : phospholipid molar ratio of the cell but there was no significant correlation between this ratio and the ouabain-sensitive sodium efflux (r=0.41, P less than 0.05). These results support the hypothesis that an altered lipid composition may affect the permeability of the erythrocyte membrane in patients with liver disease.

Biological Transport↗

PubMed2001

Molecular analysis of the Pi*Z allele in patients with liver disease.

Alpha1-antitrypsin (AAT) is the main protease inhibitor in human plasma. There are more than 75 variants of this protein that differ from each other by their isoelectric point. Most of these alleles cause a reduction in AAT levels; the most common allele is Pi*Z. The main complications related to the Pi*Z allele are obstructive pulmonary disease and liver disease. Some Pi*Z allele carriers present cholestatic jaundice and cirrhosis. The Z type is associated with a secretion defect, which leads to deficiency of AAT and to the formation of intrahepatocytic inclusions in affected subjects. The diagnosis of AAT deficiency can be made by different techniques, including molecular analysis, although the final diagnosis should be done in conjunction with demonstration of the periodic acid-Schiff-positive globules on liver biopsy. In this study, specimens of 29 patients with cryptogenic cirrhosis between age 1 month and 18 years, and of 100 controls were submitted to polymerase chain reaction followed by digestion with TaqI enzyme. Five of the 29 patients had undergone liver transplantation. Three patients were heterozygous for the Pi*Z allele, and two were homozygous (allele frequency = 12.07%; 7/58). Among the controls, who represented the population of Porto Alegre, 1 in 100 individuals was heterozygous for the Pi*Z allele, resulting in an allele frequency of 0.5% (1/200). The high frequency of Pi*Z alleles among the patients indicates the usefulness of AAT molecular testing in children with cholestatic jaundice and cirrhosis.

Adolescent↗

PubMed2006

Role of Kupffer cells in the pathogenesis of liver disease.

Kupffer cells, the resident liver macrophages have long been considered as mostly scavenger cells responsible for removing particulate material from the portal circulation. However, evidence derived mostly from animal models, indicates that Kupffer cells may be implicated in the pathogenesis of various liver diseases including viral hepatitis, steatohepatitis, alcoholic liver disease, intrahepatic cholostasis, activation or rejection of the liver during liver transplantation and liver fibrosis. There is accumulating evidence, reviewed in this paper, suggesting that Kupffer cells may act both as effector cells in the destruction of hepatocytes by producing harmful soluble mediators as well as antigen presenting cells during viral infections of the liver. Moreover they may represent a significant source of chemoattractant molecules for cytotoxic CD8 and regulatory T cells. Their role in fibrosis is well established as they are one of the main sources of TGFbeta1 production, which leads to the transformation of stellate cells into myofibroblasts. Whether all these variable functions in the liver are mediated by different Kupffer cell subpopulations remains to be evaluated. In this review we propose a model that demonstrates the role of Kupffer cells in the pathogenesis of liver disease.

Animals↗

PubMed2006

[Extrahepatic manifestations of liver diseases: skeleton].

Since nowadays liver diseases are being diagnosed more frequently than in former years, an increasing number of patients with skeletal alterations is detected. Predominant is osteoporosis with the feared complications of bone fractures. The measurement of bone mineral density enables us to differentiate between normal, osteopenic and osteoporotic conditions. Despite the great number of data available on bone disease we are still incapable to predict which patients with liver disease will develop osteoporosis or bone fractures and when. Treatment should focus on the prevention of development of osteoporosis and fractures and rather not on the treatment of complications. We are still lacking convincing long-term treatment studies with a sufficient number of patients who are well stratified.

Bone Density↗