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At least 145 records · Page 8Linked to original sources
PubMed2000

Gastro-intestinal complement activation during human liver transplantation: impact on postoperative liver function.

BACKGROUND: Liver transplantation elicits a systemic inflammatory response and eventually a multiple organ failure syndrome. Gastro-intestinal inflammatory activation with release of proinflammatory cytokines and complement activation may occur. This study evaluates gastro-intestinal complement activation and the association with postoperative parenchymatous liver cell injury and liver dysfunction. METHODS: In 17 patients undergoing liver transplantation, blood samples were collected from radial artery and portal vein for analysis of complement SC5b-9 and endotoxin concentration. Portal venous-arterial SC5b-9 plasma concentration gradients at 30 min after reperfusion were calculated. Outcome parameters included postoperative organ failure and serum concentrations of aspartate aminotransferase, alanine aminotransferase, bilirubin and factor II-VII-X. RESULTS: Patients with gastro-intestinal SC5b-9 release (n=7) had higher postoperative serum aspartate aminotransferase and alanine aminotransferase concentrations [49 (32-80) microkat/l vs 8 (6-14) microkat/l, P<0.01 and 33 (15-54) microkat/l vs 8 (4-23) microkat/l, P<0.04, respectively] and lower factor II-VII-X concentrations [46 (21-48)% vs 60 (47-69)%, P<0.02] compared to patients without gastro-intestinal SC5b-9 release (n=10). The ICU stay was prolonged in patients with gastro-intestinal complement release. There was no difference in number of organ failures and serum bilirubin concentration between the groups. The endotoxin concentration in arterial and portal vein blood was low and the association between endotoxaemia and complement activation was poor. CONCLUSION: Gastro-intestinal complement activation may contribute to postoperative parenchymatous liver cell injury and liver dysfunction in patients undergoing liver transplantation.

Adult↗
PubMed1995

Evaluation of liver function tests to predict operative risk in liver surgery.

Despite numerous studies in the past it is not possible yet to predict postoperative liver failure and safe limits for hepatectomy. In this study the following liver function tests ICG-ER (indocyaninegreen elimination rate), GEC (galactose elimination capacity) and MEGX-F (monoethylglycinexylidid formation) are examined with regard to loss of liver tissue and prediction of operative risk. Liver function tests were assessed in 20 patients prior to liver resection and on the 10th. postoperative day. Liver and tumor volume were measured by ultrasound and pathologic specimen and the parenchymal resection rate was calculated. In patients without cirrhosis (n = 10) ICG-ER and MEGX-F remained unchanged after resection, GEC was reduced but did not correspond to the resection rate. Patients with cirrhosis (n = 10) had a significantly lower ICG-ER and GEC before resection than patients without cirrhosis. After resection these tests were unchanged. Patients with liver related complications and cirrhosis (n = 5) had lower ICG-ER and GEC than patients with cirrhosis and no complications. In the postoperative course all liver function tests in these patients were significantly lower compared to preoperative results. Comparing liver function tests ICG serves best to indicate postoperative liver failure. Liver function tests do not correspond with loss of liver tissue.

Galactose↗
PubMed2005

Haemostatic abnormalities in liver disease: could some haemostatic tests be useful as liver function tests?

The liver plays a central role in haemostasis, being the site of synthesis of most of the clotting factors, coagulation inhibitors and fibrinolytic parameters, in addition to its clearance of activated clotting and fibrinolytic factors. Nonetheless, no haemostatic test(s) is included among the routine liver function tests and this study aims to probe this possibility. The liver disease group (n=258) included acute hepatitis (n=25), chronic viral hepatitis (n=128), hepatitis B (HB) carriers (n=25), liver cirrhosis (n=67), and hepatocellular carcinoma (HCC) (n=13). The prothrombin time was significantly prolonged in acute hepatitis, liver cirrhosis and HCC. However, the reptilase time was prolonged in all the groups except in HB carriers, while the thrombin time was prolonged only in the HCC group. Antithrombin III and protein C levels exhibited significant reduction in acute hepatitis, liver cirrhosis and HCC. On the other hand, protein S levels (total and free) were reduced significantly in all the patients groups, including HB carriers when compared with healthy controls. Derangement of haemostatic tests is a common feature in liver disease, being most significant in acute hepatitis, liver cirrhosis and hepatocellular carcinoma. The most sensitive markers of hepatocyte malfunction are protein S (total and free) and the reptilase time as they were abnormal, in the mildest liver affections, when other biochemical tests as well as other haemostatic tests were normal. Further studies are needed to see whether these two tests qualify for inclusion among the routine liver function tests.

Adolescent↗
PubMed1995

[Increased gamma-GT, minimal changes in liver histology, abdominal complaints--a functional liver liver disease].

Of 1,756 liver biopsies performed in the years 1987-1991, in 139 cases the patients exhibited both a nearly normal liver histology and elevated GGT values. After exclusion of patients with known causes for an elevated GGT 15 patients were selected, who over at least one year, were documented as having at least 3 measured GGT values with an average of over 40 U/l. In the follow-up of 1-15 years a typical constellation was detectable: longterm elevation of GGT (average 47-156 U/l, moreover a smaller degree of elevation of GLDH and GPT), minimal deviations from norm in liver histology (periportal fibrosis and/or fatty liver degeneration), and functional abdominal complaints. This triad occurred predominantly in middle-aged males, did not exhibit laboratory-chemical or histological signs of progression or regression tendencies and could be interpreted as a "functional" liver disorder with parelleles to M. Gilbert-Meulengracht.

Abdominal Pain↗
PubMed1999

Change of liver function in hypertrophying lobe of rabbit liver after portal branch ligation.

Preoperative portal embolization (PE) is useful for the prevention of postoperative liver failure after extended hepatectomy. However, clinical evaluation of liver function in the hypertrophying lobe after PE has not been studied. Here we report functional changes in the hypertrophying lobe using a 80% portal-branch-ligation rabbit model. Liver function was evaluated by the expression of liver-specific genes detected by Northern blot analysis and plasma disappearance rate of indocyanine green (ICG). The weight of the unligated lobe after portal ligation increased about twofold on the 7th postoperative day (POD) and about threefold on the 14th POD. The mRNA levels of the liver-specific genes (albumin, aldolase B, and tyrosine aminotransferase) in the unligated lobe decreased to about 50% on the 1st POD and returned to the preoperative levels on the 7-14th POD. In contrast, the expression of histone H2B mRNA increased on the 3rd-7th POD. The plasma disappearance rate of ICG (K-ICG) in the rabbit that has only the unligated lobe did not significantly change during the first 7 days, but then improved and recovered to 80% of that in the rabbit that has whole liver on the 14th POD. These results indicate that liver function of the hypertrophying lobe after portal branch ligation does not increase during the first 7 days despite an increase in liver weight. This finding suggests that the compensatory hypertrophying liver is enlarging without functional augmentation in the early period after PE.

Animals↗
PubMed2006

Improved liver function in patients with liver cirrhosis after autologous bone marrow cell infusion therapy.

We here report nine liver cirrhosis (LC) patients that underwent autologous bone marrow cell infusion (ABMI) from the peripheral vein. Subjects were patients with LC with total bilirubin of less than 3.0 mg/dl, platelet count of more than 5 (10(10)/l), and no viable hepatocellular carcinoma on diagnostic imaging. Autologous bone marrow (BM; 400 ml) was isolated from the ilium under general anesthesia. Mononuclear cells (MNCs) were separated by cell washing and were infused via the peripheral vein. MNC characteristics were confirmed by fluorescence-activated cell sorting analysis (CD34, CD45, and c-kit). After ABMI therapy, liver function was monitored by blood examination for 24 weeks. From 400 ml of BM, we obtained 7.81 +/- 0.98 x 10(9) MNCs. After washing, 5.20 +/- 0.63 x 10(9) MNCs were infused into patients with LC. Significant improvements in serum albumin levels and total protein were observed at 24 weeks after ABMI therapy (p < .05). Significantly improved Child-Pugh scores were seen at 4 and 24 weeks (p < .05). alpha-Fetoprotein and proliferating cell nuclear antigen (PCNA) expression in liver biopsy tissue was significantly elevated after ABMI therapy (p < .05). No major adverse effects were noted. In conclusion, ABMI therapy should be considered as a novel treatment for patients with decompensated LC.

Aged↗
PubMed2004

The relationship between nevirapine plasma concentrations and abnormal liver function tests.

Abnormal liver function tests are frequently observed in HIV-infected individuals receiving nevirapine (NVP). Here we investigate the relationship between total and unbound plasma concentrations of NVP and the liver enzymes alanine aminotransferase (ALT) and gamma-glutamyl transferase (gammaGT). HIV-infected individuals [n = 85, 22 female, 34 hepatitis C or B virus (HCV or HBV(+))] receiving NVP (200 mg bd; median duration 66 weeks, range 3-189) and two nucleoside reverse transcriptase inhibitors (NRTIs) were enrolled into this study. Blood samples were taken at C(trough) (12 hr postdose) for measurement of NVP and liver function tests (ALT and gammaGT). Plasma protein bound and unbound drug was separated using ultrafiltration and NVP concentrations quantified using HPLC-MS/MS. A linear relationship was observed between total and unbound NVP C(trough) (r(2) = 0.77, p < 0.0001). Patients with elevated ALT (>37 IU/liter; n = 31) had higher NVP unbound C(trough) than those with ALT within the normal range (median 2268 vs. 1694 ng/ml, p = 0.04) but there was no difference in total C(trough). Logistic regression revealed no association between higher NVP C(trough) and ALT elevations. Significantly higher NVP total and unbound C(trough) were observed in patients with increased gammaGT (>40 IU/liter; n = 63; total 6747 vs. 4530 ng/ml, p = 0.001; unbound 2113 vs. 1557 ng/ml, p = 0.03). Significantly higher unbound NVP C(trough) was observed in HCV/HBV(+) (median 2275 vs. 1726 ng/ml, p = 0.02) and on bivariate analysis, higher NVP C(trough) was associated with HCV/HBV coinfection (chi(2) = 4.228; p = 0.04). Overall we found no strong association between NVP concentrations and hepatotoxicity. Although in this study NVP was well tolerated in HCV/HBV coinfected patients, higher plasma concentrations were observed.

Alanine Transaminase↗
PubMed1990

Differential regulation of liver P-450III cytochromes in choline-deficient rats: implications for the erythromycin breath test as a parameter of liver function.

Progressive liver fibrosis in rats develops when they are fed a diet deficient in choline. This diet also results in a pronounced and selective decrease in the liver microsomal content of a phase I drug-metabolizing enzyme belonging to the cytochrome P-450III gene family. Because P-450III cytochromes characteristically catalyze the N-demethylation of erythromycin, we believed that the production of breath CO2 from erythromycin would be dramatically reduced in choline-deficient rats. However, when 12 choline-deficient rats were compared with 9 control rats, the reduction in CO2 production from erythromycin (mean decrease 71%) was essentially identical to that from aminopyrine (mean decrease 69%), a substrate believed to be metabolized normally by the hepatocyte in fibrotic liver disease. Furthermore, we found that the relative erythromycin and aminopyrine demethylase activities were comparable when measured in vitro in liver microsomes prepared from the choline-deficient rats. To determine the molecular basis for the erythromycin demethylase activity in the choline-deficient rats, the liver microsomes were subjected to immunoblot analysis using a variety of polyclonal and monoclonal antibodies capable of distinguishing individual P-450III-related proteins. Our studies confirm that a major erythromycin demethylase belonging to the P-450III family, termed P-450p, was greatly reduced in the choline-deficient rat liver. However, the specific concentration of a second P-450p-related protein was essentially normal and that of a third P-450p-related protein was actually increased in the choline-deficient rat liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗
PubMed2000

Effect of low flow ischemia-reperfusion injury on liver function.

The release of liver enzymes is typically used to assess tissue damage following ischemia-reperfusion. The present study was designed to determine the impact of ischemia-reperfusion on liver function and compare these findings with enzyme release. Isolated, perfused rat livers were subjected to low flow ischemia followed by reperfusion. Alterations in liver function were determined by comparing rates of oxygen consumption, gluconeogenesis, ureagenesis, and ketogenesis before and after ischemia. Lactate dehydrogenase (LDH) and purine nucleoside phosphorylase (PNP) activities in effluent perfusate were used as markers of parenchymal and endothelial cell injury, respectively. Trypan blue staining was used to localize necrosis. Total glutathione (GSH + GSSG) and oxidized glutathione (GSSG) were measured in the perfusate as indicators of intracellular oxidative stress. LDH activity was increased 2-fold during reperfusion compared to livers kept normoxic for the same time period whereas PNP activity was elevated 5-fold under comparable conditions. Rates of oxygen consumption, gluconeogenesis, and ureagenesis were unchanged after ischemia, but ketogenesis was decreased 40% following 90 min ischemia. During reperfusion, the efflux rates of total glutathione and GSSG were unchanged from pre-ischemic values. Significant midzonal staining of hepatocyte nuclei was observed following ischemia-reperfusion, whereas normoxic livers had only scattered staining of individual cells. Reperfusion of ischemic liver caused release of hepatic enzymes and midzonal cell death, however, several major liver functions were unaffected under these experimental conditions. These data indicate that there were negligible changes in liver function in this model of ischemia and reperfusion despite substantial enzyme release from the liver and midzonal cell death.

Animals↗
PubMed1975

The effect of hepatic ischaemia on liver function and the restoration of liver mass after 70 per cent partial hepatectomy in the dog.

Partial hepatectomy was performed in dogs either as the only procedure or following a period of ischaemia of liver remnant produced by inflow occlusion for periods of 30-60 minutes before partial hepatectomy. Temporary portal decompression was maintained through the portion of liver subsequently excised. 1. Survival in dogs subjected to partial hepatectomy and ischaemia to the liver remnant was similar to that in animals after partial hepatectomy alone. 2. Metabolic changes were similar in both groups but dogs submitted to partial hepatectomy and ischaemia to the remnant had higher serum alkaline phosphatase and alanine amino-transferase levels with increased bromsulphthalein in the fourth to sixth post-operative weeks. 3. Replacement of liver mass proceeded rapidly in all groups of animals. It is concluded that ischaemia of the liver remnant for up to 60 minutes preceding partial hepatectomy in the dog is consistent with survival and produced little change in postoperative liver function or in the rate of restoration of liver mass.

Alanine Transaminase↗
PubMed1999

[Evaluation of the liver uptake rate measured by 99mTc-GSA SPECT to assess liver function].

Whether the global liver uptake rate of 99mTc-GSA directly measured by SPECT is useful as a new index of liver function was evaluated in comparison with biochemical test results (PT%, ChE, Alb, ICG R15, KICG) and Child classification. 99mTc-GSA SPECT was performed in 157 patients with diffuse hepatic disease or hepatobiliary tumor, and two indices, namely the global liver uptake rate measured by SPECT 15 minutes after intravenous injection of 99mTc-GSA (LUS 15) and liver uptake per volume (liver uptake density) were examined. Both LUS 15 and liver uptake density were significantly correlated with biochemical test results and Child classification. In particular, close relationships between LUS 15 and ICGR15 (r = -0.720, p < 0.0001), LUS 15 and KICG (r = -0.750, p < 0.0001), and between LUS 15 and ChE (r = 0.720, p < 0.0001), indicate that LUS 15 is a useful index to evaluate liver function. Moreover, the local liver uptake rate measured by SPECT represented regional liver function and was considered a useful index to predict the function of the remnant liver after invasive treatment such as surgery.

Adult↗
PubMed1985

Clinical application of the measurement of serum asialoglycoproteins to estimate residual liver function in patients with chronic liver diseases with or without hepatocellular carcinoma.

The correlation between the amount of asialoglycoproteins and results of conventional liver function tests was studied in patients with chronic liver diseases, with or without hepatocellular carcinoma. The objective was to determine the clinical significance of the measurement of levels of serum asialoglycoproteins. The levels were elevated in accordance with the progress of liver diseases, and correlated with the decrease in albumin content, cholinesterase activity, the ratio of esterified cholesterol to total cholesterol and to the increase of indocyanine green retention at 15 min (p less than 0.001). There was no correlation with values of glutamic oxaloacetic and pyruvic transaminases. The amount of serum asialoglycoproteins also correlated with survival time in fatal cases of cirrhosis and/or hepatocellular carcinoma. Bilirubin and bile acids did not interfere with the measurement of serum asialoglycoproteins in cases of hyperbilirubinemia. Serum asialoglycoprotein levels are a good indicator of hepatic functional reserve in patients with chronic liver diseases, with or without hepatocellular carcinoma.

Asialoglycoproteins↗
PubMed2001

Derivation of pharmacokinetics equations for quantitative evaluation of bioartificial liver functions.

A bioartificial liver (BAL) is an extracorporeal medical device incorporating living hepatocytes in a cartridge. A variety of BALs have been developed and new devices are being introduced. Some of them have been clinically applied and from the results obtained they are claimed to be useful devices for assisting the liver functions of patients. However, there is still uncertainty as to their efficacy and their limitations are not clear. It is important to establish methods to quantitatively evaluate the metabolic and synthetic functions of BAL. In this paper, we derive simple equations for the quantitative evaluation of BAL functions on the basis of pharmacokinetics. Pharmacokinetics was originally developed to understand the processes of absorption, distribution, and elimination of administered drugs. Metabolic functions of the natural liver have been analyzed using pharmacokinetics and values of the useful parameters, clearance (CL) and intrinsic clearance (CLint), have been reported. The metabolic functions of the BAL expressed using values of CL and CLint are easily compared with those of the normal human liver. We believe that our method provides a useful basis for estimating the clinical effectiveness of BAL.

Bioartificial Organs↗
PubMed1995

Novel galactose single point method as a measure of residual liver function: example of cefoperazone kinetics in patients with liver cirrhosis.

A novel, simple, clinically useful quantitative liver function test, called the galactose single point (GSP) method, was developed to assess residual liver function by measuring galactose blood concentration 1 hour after galactose was administered (0.5 g/kg). This method was applied to the study of cefoperazone kinetics in patients with hepatic cirrhosis. To study the influence of hepatic cirrhosis on the residual liver function and the correlation between the residual liver function and the pharmacokinetics of cefoperazone, a dose of 1 g of cefoperazone was administered to 11 healthy volunteers and 12 patients with liver cirrhosis. The GSP method, the galactose elimination capacity (GEC) test, and the modified galactose elimination capacity (MGEC) test were done for each volunteer and patient to measure residual liver function. The galactose concentrations were determined enzymatically. Cefoperazone was administered intravenously, and blood and urine samples were collected at appropriate intervals after drug administration. All blood and urine samples were stored at -30 degrees C until high-performance liquid chromatography analysis. Cefoperazone plasma concentrations were much higher in cirrhosis patients than in normal subjects at all times. The elimination half-life, hepatic clearance, mean residence time, and renal clearance of cirrhosis patients differed significantly from those of healthy volunteers. The plasma protein binding was unaltered in both groups. Urinary excretion of cefoperazone was significantly increased in cirrhosis patients (23.95 +/- 5.06% for normal men and 51.09 +/- 11.50% in cirrhosis patients). Hepatic clearance, fraction excreted in urine, and total clearance significantly correlated with GSP, GEC, and MGEC (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Transplanted liver: consequences of denervation for liver functions.

Following liver transplantation, all hepatic nerves are transected; thus, liver allografts are completely isolated from neural control of their hosts. Despite this absolute denervation, liver allograft function does not appear to be significantly impaired after successful transplantation. In experimental animal models, hepatic denervation has no major effects on bile acid production and biotransformation, while it increases blood pressure and salt retention; decreases the number of hepatic progenitor cells, cholangiocyte proliferation, and liver regeneration; and influences the hepatic microcirculation, diet behavior, and glycemic control. In humans, hepatic denervation after liver transplantation has no major deleterious effects on bile secretion, liver regeneration, and hepatic blood flow. Insulin resistance and postprandial hyperglycemia, changes in ingestion behavior, and reduced stimulation of hepatic progenitor cells in the canals of Hering are the major side effects of absent liver innervation. Despite these abnormalities, patients can lead a new life with improved quality of life.

Animals↗
PubMedDate not supplied

Natural history of hepatectomy regarding liver function: a study of both normal livers and livers with chronic hepatitis and cirrhosis.

BACKGROUND/AIMS: The cirrhotic liver has been shown to regenerate after hepatectomy based on the findings of various imaging techniques. However, little has been reported so far regarding the restorative process using the liver function test in a long series after hepatectomy of both normal and injured livers. METHODOLOGY: A retrospective review was performed of 48 patients who underwent hepatic resection due to either primary or secondary liver cancers. They were histologically divided into three groups of 6 normal, 23 chronic hepatitis and 19 cirrhotic liver patients. In addition, the hepatitis group was divided into two groups according to the resected volume, which were 16 of a small resected volume and 7 of a large volume. For these patients, both a complete blood count and normal liver function test were performed before operation, and 7 and 14 days, 1, 3, and 6 months, and 1, 2, and 3 years, postoperatively. RESULTS: In the normal patient group, almost all test results recovered to their preoperative levels by 14 days to 1 month postoperatively. In the cirrhotic group, however, the red blood cell count and hematocrit levels did not recover to preoperative levels until 3 months postoperatively, while the GPT levels, the total bilirubin and albumin all recovered by one month postoperatively. However, the total cholesterol level needed 6 months to recover. In the large resection hepatitis group, the GPT level needed 7 days to recover, while the albumin and total cholesterol level needed three months to do so. In addition, the platelet level decreased significantly at 3 months postoperatively and thereafter it seemed to remain at a lower level. CONCLUSIONS: We demonstrated that a hepatic resection in patients with chronic liver disease requires a longer period of time to recover to preoperative levels based on the type of underlying liver parenchymal disease and the extent of resection.

Aged↗