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PubMedDate not supplied

Amikacin nephrotoxicity in patients with chronic liver disease.

Chronic liver disease is a risk factor for aminoglycoside nephrotoxicity. We conducted this study to identify the incidence and risk factors associated with it. A total of 45 patients with liver disease and 329 controls were included, with a toxicity incidence of 17.7%, similar to that in controls. Chronic liver disease patients received lower amikacin doses than calculated on the basis of creatinine clearance (498 +/- 1187 vs 611 = 313 mg/day). Serum albumin, both at the beginning of the treatment and at the end was lower in patients who developed toxicity, and bilirubin levels were higher in these patients at the end of the treatment. Apparently, a dose reduction may lessen the risk for amikacin nephrotoxicity in patients with chronic liver disease. We conclude that hypoalbuminemia and hyperbilirubinemia are risk factors in this complication.

Amikacin↗
PubMed2004

Model for end stage liver disease score predicts mortality across a broad spectrum of liver disease.

BACKGROUND/AIMS: The utility of the model for end stage liver disease (MELD) score in non-transplant patients, particularly in those with less severe chronic liver disease remains uncertain. We studied and compared the predictive abilities of the MELD score and the Child-Turcotte-Pugh (CTP) score for intermediate (1-year) and long-term (5-year) mortality. METHODS: One thousand six hundred and eleven patients with chronic liver disease were studied. Observed and predicted survival curves were plotted to evaluate the predictive ability of the MELD score for survival. Receiver operating characteristic (ROC) curves was used to compare the MELD and CTP score. A multivariable model was constructed to examine predictors of mortality. RESULTS: The MELD score was a good predictor of 1-year mortality in chronic liver disease (c-statistics for all subgroups >/=0.75) and of 3- and 6-month mortality in alcoholic hepatitis (c-statistic >/=0.83). The CTP score had similar predictive abilities as the MELD. Hepatic encephalopathy was a strong independent predictor of death (Hazard ratio-2.8, P<0.0001). CONCLUSIONS: The MELD score is a valid prognostic score for intermediate term mortality in a heterogeneous population with chronic liver disease although the CTP score is equivalent in predicting survival. Inclusion of hepatic encephalopathy adds additional prognostic value to the MELD score.

Female↗
PubMed2000

Superoxide dismutase activity in children with chronic liver diseases.

BACKGROUND/AIMS: Liver disease in infancy has multiple etiologies. As reactive oxygen intermediates are involved in several types of tissue damage, we have investigated whether different forms of liver disease in infancy are associated with increased free radical generation, using an indirect approach in which superoxide dismutase (a free radical scavenger) activity is determined in the liver tissue. METHODS: A total of 48 liver biopsies performed at diagnosis were evaluated retrospectively. Nine infants had biliary atresia, eight Alagille syndrome, seven alantitrypsin deficiency and 12 cryptogenic hepatitis. As controls we studied 12 biopsies with normal histology obtained from seven children with portal vein thrombosis and five children who underwent biopsy for management reason but had no liver disease. Superoxide dismutase activity in liver biopsy specimens was measured using the cytochrome C method by spectrophotometry and expressed as U SOD/mg protein. RESULTS: Superoxide dismutase activity was significantly increased in biliary atresia (1.25 +/- 0.56 U SOD/mg protein, p<0.0001) and Alagille syndrome (1.31 +/- 0.56 U SOD/mg protein, p<0.0001) as compared with al-antitrypsin deficiency (0.75 +/- 0.3 U SOD/mg protein), neonatal hepatitis (0.72 +/- 0.37 U. SOD/mg protein) and normal controls (0.4 +/- 0.7 U. SOD/mg protein). The highest level of SOD activity was found, however, in control children with portal vein thrombosis (2.09 +/- 0.96 U SOD/mg protein; p<0.0001 as compared to the other groups). CONCLUSION: Superoxide dismutase, a key enzyme in free radical protection, is increased significantly in the liver tissue of infants with cholestatic liver disease due to bile duct damage and in children with portal vein thrombosis, suggesting that products of free radical reactions are involved in the pathogenesis of these disorders.

Alagille Syndrome↗
PubMed1994

Pathological spectrum of alcoholic liver disease.

Alcoholic liver disease encompasses three main forms of liver injury: fatty change, alcoholic hepatitis and cirrhosis. However, there are many other types of injury, including perivenular fibrosis, venous occlusive lesions, microscopic cholangitis and chronic active hepatitis. The pathological spectrum is reviewed in this paper, and the contribution of other injurious agents to the pathological features is identified. Alcoholic liver disease can be mimicked by a variety of non-alcoholic liver diseases. However, features such as fatty liver with perivenular fibrosis, giant mitochondria, spotty hepatocyte necrosis, Mallory bodies, a micronodular pattern of cirrhosis, and iron deposition are strongly suggestive of an alcoholic aetiology. Correlation of clinical findings, and especially the alcohol history, and histopathological factors is necessary for the definitive diagnosis.

Fatty Liver, Alcoholic↗
PubMed2001

High prevalence of osteoporosis in patients with chronic liver disease prior to liver transplantation.

Osteoporosis is a common complication of liver transplantation. Its pathogenesis is multifactorial, but preexisting bone disease in patients with chronic liver disease is likely to play an important role. The aim of this study was to evaluate bone mineral density in adult patients with chronic liver disease prior to liver transplantation. A total of 243 consecutive patients (128 male, 115 female; mean age 51.1years) with chronic liver disease undergoing assessment for transplantation, were recruited over a 4-year period. BMD measurements were made using dual energy X-ray absorptiometry in the lumbar spine (L1-L4) and femoral neck (FN). Osteoporosis and osteopenia were defined by WHO criteria. Osteoporosis at either L1-L4 or FN was present in 36.6%, osteopenia in 48.1%, and normal BMD in only 15.2% of patients. There was no difference in prevalence of osteoporosis between males and females (P = 0.442). Women with osteoporosis were on average 10 years older (56.2 +/- 1.4 years) than those with normal bone density (46.4 +/- 2.3 years) P = 0.002; in men, no statistically significant age effect was found. Patients with osteoporosis had on average lower body weight than those with normal bone density (64.9 +/- 1.8 kg vs 74.2 +/- 2.2 kg) P = 0.003. T-scores in patients with cholestatic liver disease were lower than in non-cholestatic disease and the lowest BMD values were found in patients with cystic fibrosis. Logistic regression revealed that in women, increasing age (P = 0.004; OR = 1.12; CI 1.04-1.21) and lower body weight (P = 0.01; OR = 0.95; CI 0.91-0.99) were significant independent risk factors for osteoporosis but menopausal status (P = 0.1; OR = 0.24; CI 0.05-1.32) and presence or absence of cholestasis (P = 0.326; OR = 1.54; CI 0.65-3.67) were not. There were no independent risk factors in men. This study demonstrates a high prevalence of osteoporosis in patients with chronic liver disease prior to liver transplantation, men and women being equally affected. With the exception of increasing age and lower body weight in women, no independent risk factors were found, emphasizing the importance of BMD measurements in these patients and the need for prophylactic measures to optimize bone health.

Absorptiometry, Photon↗
PubMed2005

Cystatin C, an easy and reliable marker for assessment of renal dysfunction in children with liver disease and after liver transplantation.

Renal dysfunction of variable severity is being increasingly recognized as a major complication of calcineurin inhibitors (CI), in some patients even necessitating renal transplantation. Close and effective monitoring of the renal function is indicated. Current methods for this monitoring are calculation of the glomerular filtration rate (GFR) based on creatinine or exogenous substances like 51Cr-EDTA. The first method is unreliable in children and the second is expensive and cumbersome. Cystatin C has been shown to be an accurate marker of glomerular filtration but has not been evaluated in a large cohort of pediatric patients before and after liver transplantation (LT). We evaluated the accuracy of cystatin C in 62 children (30 male) with LT, who had their 51Cr-EDTA measured on 40 occasions prior to LT and on 47 occasions after LT. The reciprocal of cystatin C correlated better with 51Cr-EDTA GFR (r = .78) than the reciprocal of creatinine (r = .40). Diagnostic accuracy in the identification of reduced GFR was assessed by ROC analysis. Cystatin C yielded the highest area under the ROC curve (AUC) in all groups assessed. From these data a cutoff level of cystatin C predicting 51Cr-EDTA GFR < 80 ml/min/1.73 m2 was calculated. A level of 1.06 mg/L was found to have a sensitivity of 91% and a specificity of 81%. Applying this cutoff level in our patient group would have avoided 51Cr-EDTA GFR estimation in 43 of the 87 estimations. In conclusion, the use of this simple test could be recommended as screening of renal dysfunction in children with liver disease and after LT.

Biomarkers↗
PubMed1995

Hypothalamic-pituitary-testicular function in end-stage non-alcoholic liver disease before and after liver transplantation.

OBJECTIVE: Gonadal dysfunction is common in chronic liver disease, but most of the previous studies have been restricted to men with alcohol-induced liver disease. We have evaluated hypothalamic-pituitary-testicular function in patients with end-stage non-alcoholic liver disease before and at 6 and 12 months after hepatic transplantation. DESIGN: A prospective study of hypothalamic-pituitary-testicular endocrine function before and after cadaveric hepatic transplantation. PATIENTS: Fifty four consecutive patients with end-stage, non-alcoholic liver disease were evaluated before and after liver transplantation. MEASUREMENTS: Hypothalamic-pituitary-testicular (HPT) axis function was evaluated under basal conditions by single morning measurements of plasma total and free testosterone, sex hormone-binding globulin and by plasma LH and FSH responses to 100 micrograms i.v. GnRH. RESULTS: Men with chronic non-alcoholic liver disease had reduced levels of total and free testosterone and increased levels of SHBG compared with controls with normal liver function. Total and free testosterone were positively correlated with basal and stimulated LH (but not FSH) concentrations. Gonadotrophin responses to GnRH were preserved but delayed compared with healthy controls consistent with a predominantly hypothalamic defect in regulation of pituitary-testicular function. Increasing severity of underlying liver disease was associated with declining total and free testosterone as well as peak GnRH-stimulated LH concentrations. Spironolactone treatment was associated with decreased circulating testosterone levels only in men with liver disease of intermediate severity (Child-Pugh class B). Following hepatic transplantation, total and free testosterone and SHBG concentrations returned progressively towards eugonadal control levels over the first 12 months but total and free testosterone levels remained subnormal. CONCLUSIONS: Hypothalamic-pituitary regulation of testicular function is impaired in end-stage non-alcoholic liver disease in proportion to the severity of underlying liver disease. Spironolactone reduces circulating testosterone but only among men with Child-Pugh B liver cirrhosis. Gonadal function improves, but is not normalized, over the first year following successful liver transplantation.

Adolescent↗
PubMed1997

L-[1-(13)C] Phenylalanine oxidation as a measure of hepatocyte functional capacity in end-stage liver disease.

BACKGROUND: Liver disease is associated with impaired metabolism of these amino acids phenylalanine and tyrosine. Decreased metabolism of these amino acids leads to abnormal plasma elevations and impaired clearance rates. We have developed a noninvasive breath test that measures hepatic cytosolic enzyme activity. METHODS: The rate of hepatic phenylalanine metabolism was quantitatively calculated from the appearance of 13CO2 in the breath using the nonradioactive tracer L-[1-(13)C]phenylalanine. RESULTS: Normal controls (n = 47) oxidized phenylalanine more than twice that of end-stage liver disease patients (n = 117). Significant differences in the percent of phenylalanine oxidized per hour (mean +/- SEM) were found between controls (7.08% +/- 0.33%, 95% CI: 6.42%-7.74%) and Child Pugh classification patients, class A (4.96% +/- 0.69%, 95% CI: 3.50%-6.42%), class B (2.88% +/- 0.13, 95% CI: 2.39%-3.38%) and class C (1.75% +/- 0.13, 95% CI: 1.50%-2.01%). The phenylalanine breath test score significantly correlated with albumin levels, prothrombin time and total bilirubin. CONCLUSION: We have demonstrated that phenylalanine oxidation is significantly decreased with end-stage liver disease and is correlated with the best clinical measures of liver disease.

Adult↗
PubMed1994

Diagnostic utility of laboratory tests in alcoholic liver disease.

Alcoholic liver disease is an important health problem in the US. A public health approach is proposed, using laboratory tests to identify patients with early fibrosis of the liver. A variety of serological markers of liver fibrosis based on collagen-related products (e.g., amino-terminal propeptides of type III procollagen) have been investigated. Further studies are needed to determine the optimal combination of tests for discriminating between steatosis and early fibrosis. Laboratory tests are also useful in excluding nonalcoholic liver diseases such as viral hepatitis, hemochromatosis, and Wilson disease. The monitoring of sobriety in patients with alcoholic liver disease by currently available tests is far from ideal. A new marker of excessive alcohol consumption, carbohydrate-deficient transferrin, is not usually affected by liver disease and thus shows promise as a marker of relapse in alcoholic patients. The development of reliable screening markers of fibrosis and sobriety could potentially reduce the health costs and suffering associated with the complications of alcoholic cirrhosis.

Clinical Laboratory Techniques↗
PubMed1987

The characteristics of alcoholic liver disease in Japan. Clinicopathologic comparison with alcoholic liver disease in the United States.

Alcoholic liver disease (ALD) in Japan was compared clinicopathologically with the occurrence in the U.S.A. ALD found in Japan was more frequently complicated by other hepatic diseases including non-A, non-B chronic hepatitis than ALD found in the U.S.A. (9.9% versus 21.9%). Patients with such complications were excluded from this study. The chief complaints of the total of 51 alcoholics studied in the U.S.A. were abdominal distension or jaundice and those of 98 alcoholics studied in Japan were non-specific: general fatigue, weakness or appetite loss. The U.S. patients exhibited more elevated levels of serum bilirubin (8.1 +/- 7.5 versus 1.9 +/- 2.4 mg/dl, mean +/- SD) and a higher incidence of leukocytosis (49.0% versus 5.1%). While the serum glutamic-oxalacetic transaminase (GOT) levels were not significantly different between the two groups (146.5 +/- 116.8 versus 140.8 +/- 147.7 IU/L), the serum glutamic-pyruvic transaminase (GPT) levels among Japanese alcoholics were higher (38.6 +/- 31.4 versus 87.4 +/- 99.1 IU/L) and in about one quarter of these patients, serum GPT was higher than serum GOT, a feature not seen in the patients in the U.S.A. Comparative histopathologic study of 337 U.S. patients and 210 Japanese patients disclosed a higher frequency of cirrhosis (46.9% versus 33.8%), the presence of Mallory bodies (58.5% versus 13.8%) and marked neutrophilic exudation (45.1% versus 6.2%). Thus, the majority of Japanese alcoholics exhibited progression of liver disease, eventually leading to cirrhosis, due to hepatocellular drop-out and fibrosis caused by a mechanism different from alcoholic hepatitis. In addition, ALD in the U.S.A. revealed more striking extension of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Lymphocyte cytotoxicity for autologous human hepatocytes in alcoholic liver disease.

Alcoholic liver disease has been shown to progress even after cessation of ethanol intake and the involvement of an immunological mechanism has been suggested. To study whether lymphocyte cytotoxicity for autologous human hepatocytes is involved in the pathogenic process of alcoholic liver disease, hepatocytes (target cells) obtained by a needle liver biopsy from 36 patients with alcoholic liver disease were isolated by enzymatic digestion and incubated with autologous peripheral lymphocytes (effector cells). Using a microcytotoxicity assay, a cytotoxic effect was observed in patients with active cirrhosis or alcoholic hepatitis, but not in those with inactive cirrhosis, hepatic fibrosis or fatty liver. When lymphocytes were separated into T cell enriched and non-T cell enriched fractions, this cytotoxic effect was significantly greater with the non-T cell enriched lymphocyte fraction than with the T cell enriched fraction. The addition of aggregated IgG reduced the cytotoxic effect of the lymphocytes. These results suggested that antibody-dependent cell-mediated cytotoxicity may be of pathogenic importance in alcoholic liver disease.

Antibody-Dependent Cell Cytotoxicity↗
PubMedDate not supplied

[Role of the liver in the regulation of glucose metabolism in diabetes and chronic liver disease].

The liver plays a major role in the regulation of glucose metabolism: plasma glucose concentration is the result of peripheral glucose utilization and liver production. Several hormones, including insulin, glucagon, growth hormone, cortisol, and catecholamines contribute to the regulation of glucose metabolism by the liver. In this review, we examine hepatic glucose metabolism, in particular the actions of insulin and contrainsular hormones on glucose hepatic uptake and production in patients with diabetes or chronic liver disease. The most frequent patterns of hepatic involvement that take place during diabetes, i.e. nuclear glycogenesis, steatosis, portal fibrosis, and diabetic steatonecrosis, are discussed. Also considered are anomalies of glucose homeostasis observed in chronic liver disease, including glucose intolerance, diabetes, and hypoglycemias. There is a strong correlation between diabetes mellitus and the liver: diabetic patients have typical histological lesions, while several glucose metabolism alterations are commonly found in subjects with chronic liver disease. The pathogenesis of impaired glucose metabolism during chronic liver disease has not yet been fully understood: further clinical and experimental studies should clarify this issue.

Chronic Disease↗
PubMedDate not supplied

Haematological disorders in liver disease.

The liver plays a central role in haemopoiesis and synthesis of coagulation proteins; liver disease is associated with a broad range of haematological abnormalities. Anaemia arises through multiple mechanisms, haem metabolism is disturbed, and liver disease causes alterations in red cell lipid metabolism. Defects of platelet number and function arise due to the effects of liver disease, immune mechanisms and hypersplenism. Coagulation disturbances are due to impaired vitamin K metabolism, defective synthesis of coagulation factors and regulatory proteins, impaired clearance of activated coagulation factors and increased fibrinolysis. Treatment, including blood component therapy, is discussed. Recent data indicate an emerging role for disturbances in Epo, cytokines (TNF, IL-6) and thrombopoietin in causing haematological changes in liver disease.

Anemia↗
PubMed1979

Nonalcoholic liver disease. Overlooked causes of liver injury in patients with heavy alcohol consumption.

Alcoholic subjects with abnormal liver chemistry studies are often assumed to have alcoholic liver disease, even though the diagnosis is not established by liver biopsy. To determine the magnitude of nonalcoholic liver disease in patients with heavy alcohol consumption, the data on 145 consecutive patients judged to consume at least 80 g of alcohol daily for prolonged periods, and who underwent liver biopsy at the University of Chicago, were reviewed. Nonalcoholic liver disease was suspected clinically and confirmed by liver biopsy in 40 (28 per cent), whereas alcoholic liver disease was suspected in 105 but confirmed in only 83 (80 per cent). The remaining 22 patients had liver disorders, including cholangitis or pericholangitis, acute hepatitis or some form of chronic hepatitis, for which they required appropriate therapy. Neither clinical features, hepatitis B surface antigen (HBsAg), anti-HBsAg nor serum glutamic oxaloacetic transaminase to serum glutamic pyruvic transaminase (SGOT:SGPT) ratios distinguished these 22 patients from those with alcoholic liver disease. Thus, liver biopsy is necessary for the identification of nonalcoholic liver disease in patients suspected of harboring alcoholic liver disease, since other clinical features do not allow identification of these patients.

Acute Disease↗
PubMed2004

Nonalcoholic fatty liver disease: Improvement in liver histological analysis with weight loss.

The effect of significant weight loss on nonalcoholic fatty liver disease remains unclear. In this case series of 36 selected obese patients, we examined the effect of weight loss on nonalcoholic fatty liver disease, including nonalcoholic steatohepatitis (NASH) and hepatic fibrosis. These 36 patients (11 males, 25 females) had paired liver biopsies, the first at the time of laparoscopic adjustable gastric band placement and the second after weight loss. Second biopsies were obtained from two groups: those requiring a subsequent laparoscopic procedure (n = 19) and those with index biopsy score of 2 or greater for zone 3-centric hepatic fibrosis (n = 17). All biopsies were scored, blinded to the patient's identity and clinical condition, for individual histological features and for NASH stage and grade. Initial biopsies demonstrated NASH in 23 patients and steatosis in 12 patients. Repeat biopsies were taken at 25.6 +/- 10 months (range, 9-51 months) after band placement. Mean weight loss was 34.0 +/- 17 kg, and percentage of excess weight loss was 52 +/- 17%. There were major improvements in lobular steatosis, necroinflammatory changes, and fibrosis at the second biopsy (P <.001 for all). Portal abnormalities remained unchanged. Only four of the repeat biopsies fulfilled the criteria for NASH. There were 18 patients with an initial fibrosis score of 2 or more compared with 3 patients at follow-up (P <.001). Those with the metabolic syndrome (n = 23) had more extensive changes before surgery and greater improvement with weight loss. In conclusion, weight loss after surgery provides major improvement or resolution of obesity and metabolic syndrome-associated abnormal liver histological features in severely obese subjects.

Adult↗
PubMed1993

[Apolipoprotein A-I, E, C-III and LDL-receptor mRNA expression in liver diseases].

The liver plays a major role in lipid metabolism, and quantitative and or qualitative changes in serum lipoproteins and apolipoproteins have been observed in various liver diseases. We investigated changes in hepatic mRNA expression of apolipoproteins A-I, C-III, and E and LDL receptor in human liver diseases, rat D-galactosamine, CCl4 induced liver failure and regenerating liver. The apolipoprotein mRNA expression were significantly decreased in liver and severe acute hepatitis as compared with controls and were correlated with serum albumin levels. LDL receptor mRNA expression were decreased in liver cirrhosis and rat liver failure. These findings indicated that liver biosynthesis of these apolipoproteins and LDL receptor are suppressed in liver disease. On the other hand, LDL receptor mRNA expression increased in regenerating liver, and this shows that serum cholesterol was needed for membrane biosynthesis.

Apolipoprotein A-I↗
PubMed1977

Liver protocollagen proline hydroxylase in human liver diseases and experimental liver fibrosis.

Liver protocallagen proline hydroxylase activity (PPH activity) was determined in patients with various liver diseases, CCl4-induced liver fibrosis rats and cholin deficiency (tcd) fatty liver rats. The following results were obtained: Liver PPH activity in patients with chronic hepatitis was higher than that in patients with acute hepatitis, while the activity in patients with liver cirrhosis was much higher than that in patients with chronic hepatitis. The activity was higher in patients with chronic active hepatitis than in those with chronic inactive hepatitis. Patients with active and progressive liver cirrhosis were found to have an especially high PPH activity, in whom the activity reflected well the degree of liver fibrosis. Even though fibrosis in persistent hepatitis was almost negligible or slight, the degree of liver PPH activity in persistent hepatitis was similar to that in liver cirrhosis. Liver PPH activities in CCl4-induced liver fibrosis rats and CD fatty liver rats elevated proportionally to the lapse of time. Whilst liver PPH activity in rats of CD fatty liver without fibrosis in 23 to 31 weeks after the start of the experiment was slightly lower than that in rats of CD fatty liver with fibrosis. But liver PPH activity of the former was considerably higher than that of control rats.

Acute Disease↗
PubMed2005

Liver histopathology in human immunodeficiency virus-hepatitis C virus co-infected patients with fatal liver disease.

BACKGROUND: Liver failure is an increasing cause of death in human immunodeficiency virus-hepatitis C virus (HIV-HCV) co-infected patients. Here, histopathological features of fatal liver disease in HIV-HCV co-infected patients were comparatively assessed. METHODS: Liver biopsies of seven HIV-HCV co-infected patients with clinically imminent liver death and advanced immune deficiency were studied. Biopsies of seven asymptomatic patients with stable hepatic and immune functions, who were matched according to their documented duration of HIV-HCV co-infection, served as controls. Inflammatory and fibrotic changes as well as hepatocellular steatosis and cholestasis were assessed semiquantitatively by established scores. RESULTS: All patients with fatal liver disease had severe immunodeficiency and jaundice, while biliary ducts were patent. Unexpectedly, the extent of hepatic steatosis, inflammatory activity and fibrosis was strikingly similar in both study groups. Importantly, liver failure was observed even in the absence of marked fibrosis. Lobular bilirubinostasis was the only feature that significantly distinguished patients with advanced immunodeficiency and fatal liver disease from the control group. CONCLUSION: Thus, rapid deterioration of liver function and death can occur in HIV-HCV co-infected patients with advanced immunodeficiency even when liver histology does not reveal markers of end-stage liver disease. Jaundice and marked bilirubinostasis in the absence of biliary tract obstruction seem to herald this complication of chronic hepatitis C in HIV infection.

Adult↗