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PubMed1986

Widely differing plasma digoxin values in patients with congestive heart failure and severe liver dysfunction. A method-dependent problem.

We studied plasma digoxin levels by three methods in patients with congestive heart failure who had no, mild to moderate, and severe liver dysfunction secondary to the heart failure. Our results indicate that in patients with severe liver dysfunction, marked discrepancies in plasma can occur, depending on the methodology employed. The discrepancy is likely due to the presence of a digoxinlike immunoreactive substance.

Adult↗
PubMedDate not supplied

Liver dysfunction in steady state sickle cell disease.

The liver is one of the organs involved in the multiorgan failure that occurs in sickle cell disease, the pathophysiology of liver disease in this condition is complex because of the interrelated multifactorial causes. Liver dysfunction was assessed in both paediatric and adult sickle cell disease patients in the steady state. The transaminases and alkaline phosphatase were analysed by automation while coagulation studies were done manually. The mean (range) of Alanine transaminase (ALT), Aspartate transaminase (AST) and alkaline phosphatase (ALP) were 23.0 (2-77) IU, 48.5 (15-120) IU, 227.5 (37-1200) IU respectively. ALT and AST levels were less than 100 IU in over 95% of the patients. The gender or age of the patients did not significantly affect the level of these three enzymes. There was close association between the liver size and elevation of the liver enzymes except for alkaline phosphatase (ALT=.017, AST=.009, ALP=.056). Twenty-five percent of the patients had normal enzymes while 13% had derangement of the three enzymes, 19%, 50% and 74% had abnormal ALT, AST and ALP respectively. Only 22% and 5% had deranged PT and APTT respectively. In conclusion minimal elevation of the tramsaminases which is not gender or age dependent were observed in steady state sickle cell disease, higher levels of alkaline phosphatase may be due to associated vasoocclussive crises involving the bones rather than a pathology of the liver.

Adolescent↗
PubMed1986

[Clinical studies on the biliary excretion of mezlocillin, especially in cases with liver dysfunction].

To investigate efficacy of mezlocillin (MZPC) in the treatment of biliary tract infection, the time course concentrations of MZPC in the bile of patients with, in particular, liver dysfunction were measured. MZPC concentrations in the bile decreased with the increase in the severity of liver dysfunction. However, the bile concentration was maintained more than 50 micrograms/ml even in cases of severe cholangitis with obstructive jaundice. These results indicate that MZPC is an useful antibiotic for the treatment of biliary tract infection.

Aged↗
PubMed2005

[Liver dysfunction in recipients of hematopoietic stem cells. Impact on mortality].

Liver disease is a well-known cause of early morbidity and mortality affecting 80% of patients receiving allogeneic bone-marrow transplantation (BMT). Drug toxicity, veno-occlusive disease (VOD), acute graft-versus-host disease (GVHD), and fungal, bacterial, and viral infections are the most frequent hepatic complications during this period. The aim of this retrospective study was to determine the prevalence and etiology of liver disease and its impact on mortality as well as to assess the predictive value of pre BMT hepatic biochemical tests on the subsequent occurrence of acute and/or chronic GVHD and patient mortality. Of a total of 236 patients who underwent allogeneic BMT, 82 were analysed. Liver dysfunction was found in 88%. The causes of liver disease were: acute GVHD, 40.2%; chronic GVHD, 15.9%; unknown, 9.8%; sepsis, 7.3%; hepatotoxicity, 6.1%; VOD, 3.7%; acute hepatitis and disease recurrence, 2.4%. The mortality rate was 37%. We found acute liver failure (ALF) in 10% of the deaths (8 patients). The causes of ALF in these cases were acute GVHD progression in 5, herpetic hepatitis in 1, disease recurrence in 1, and VOD in 1. The correlation coefficients indicating positive predictive values of pre BMT hepatic biochemical tests for the subsequent occurrence of acute GVHD, chronic GVHD, and mortality were 0.27, 0.14, and 0.43, respectively. There was no significant difference between patients with abnormal or normal pre BMT liver function tests in the frequency of acute and chronic GVHD or mortality.

Adolescent↗
PubMed2000

Adult onset Still's disease with hemophagocytic syndrome and severe liver dysfunction.

We report the case of a 55-year-old Japanese woman with adult onset Still's disease in whom hemophagocytic syndrome and severe liver dysfunction developed. High serum levels of ferritin, macrophage colony stimulating factor and interferon-gamma, which imply the presence of hemophagocytic syndrome, were detected. It is known that hemophagocytic syndrome is associated with adult onset Still's disease. In our case, many markedly swollen Kupffer cells with phagocytized red blood cells were found in the liver, as well as macrophages in the bone marrow and spleen. Accordingly, we believe that severe liver dysfunction in this case may have been related to hypercytokinemia due to hemophagocytic syndrome.

Journal Article↗
PubMed2006

Plasma disappearance rate of indocyanine green in liver dysfunction.

The presence of hepatic dysfunction significantly affects the length of hospital stay and the outcome in critically ill patients. Considering the important partial hepatic functions of metabolism, synthesis, detoxification, and excretion, the worse clinical course of patients suffering from hepatic dysfunction is not surprising. The most often used indicator of hepatic dysfunction is bilirubin. However, bilirubin and other commonly used static laboratory tests provide only indirect measures of hepatic function. In contrast to these static tests, dynamic liver tests, such as indocyanine green (ICG) disappearance rate should provide better direct measures of the actual functional state of the liver at the time of assessment. The ICG is a water-soluble inert compound that is injected intravenously. It mainly binds to albumin in the plasma. ICG is then selectively taken up by hepatocytes, independent of adenosine triphosphate (ATP), and later excreted unchanged into the bile via an ATP-dependent transport system. The ICG is not metabolized; it does not undergo enterohepatic recirculation. Thus, ICG excretion rate in bile reflects the hepatic excretory function and hepatic energy status. Because of these features, ICG has been found to be useful to assess liver function in liver donors and transplant recipients, in patients with chronic liver failure, and as a prognostic factor in critically ill patients. Further trials concerning liver dysfunction have applied the noninvasive bedside assessment of ICG among other clinical variables to monitor the progress and/or the reversal of liver dysfunction.

Bilirubin↗
PubMed1997

Successful treatment with cyclosporine in a case of hemophagocytic syndrome manifesting as severe liver dysfunction.

Forms of hemophagocytic syndrome, which affects mainly children, vary from mild to very severe and often fatal. We describe an adult patient with hemophagocytic syndrome in whom severe liver dysfunction developed. The condition continued to deteriorate despite treatment with plasma exchange, high-dose gamma globulin, and corticosteroid therapy. Treatment with cyclosporine (2.3 mg/kg/day) dramatically improved the condition and normalized liver function. Cyclosporine reduced the serum levels of ferritin, interferon-tau, interleukin-6, and soluble interleukin-2 receptor. These findings suggest that hemophagocytic syndrome accompanied with severe liver dysfunction results from hypercytokinemia, and cyclosporine is useful in preventing a fatal outcome during the acute phase.

Adult↗
PubMed1992

Radiation hepatology of the rat: microvascular fibrosis and enhancement of liver dysfunction by diet and drugs.

Prior to whole-liver irradiation (0, 15, 25 Gy) rats were not treated, placed on a protein-deficient diet for 2 weeks, administered cyclophosphamide, and/or depleted of intracellular glutathione by injection with buthionine sulfoximide and diethyl maleate. At various times (0 to 84 days) after 0- and 25-Gy liver irradiation, liver function, liver mass, and hydroxyproline content were measured in nontreated animals. Liver function was measured in all other preirradiation regimens 2 to 3 months postirradiation. Histology and/or India ink perfusion of the liver were done on ascitic and jaundiced animals from all treatment groups. Approximately 20% of the 25-Gy whole-liver-irradiated animals in each preirradiation treatment group developed clinical signs of acute hepatitis (ascites, jaundice, and elevated liver enzymes in the plasma) 70 to 100 days after irradiation. Twenty-five-gray whole-liver irradiation also resulted in significant liver fibrosis that preceded the onset of liver dysfunction. Fibrotic changes were most dramatic in and around hepatic veins, sometimes resulting in complete or partial occlusion that disrupted intrahepatic blood flow and diminished liver function. In addition, a substantial accumulation of fluid in the liver of 25-Gy-irradiated livers occurred, resulting in a lower dry/wet liver weight ratio. Functional hepatic injury was enhanced by preirradiation treatment with a protein-deficient diet, cyclophosphamide, and/or depletion of intracellular glutathione. This enhancement of functional injury was pronounced after 15-Gy whole-liver irradiation when injury from radiation alone was minimal.

Animals↗
PubMed2003

Inhibition of heme oxygenase ameliorates sepsis-induced liver dysfunction in rats.

PURPOSE: The disintegration of heme produces carbon monoxide (CO), a known vasodilator, which is catalyzed by heme oxygenase (HO). This study aimed to clarify the effect of HO inhibition on septic rat livers using two types of HO inhibitors; Sn-protoporphyrin (Sn-PP) and Zn-protoporphyrin (Zn-PP). METHODS: Sepsis was induced in male Sprague-Dawley rats by cecal ligation and puncture (CLP). Either NaOH or HO inhibitors were injected intraperitoneally; first 18 h prior to CLP, then immediately after CLP. The animals were killed 12 and 24 h after CLP and the liver tissue and plasma were harvested. RESULTS: Using Northern blotting, we found that mRNA of the stress-inducible isozyme, HO-1, was dramatically induced 12 h after CLP. Administering the HO inhibitors, Sn-PP and Zn-PP (5 micromol/kg), induced a significant inhibition of the elevation of aspartate aminotransferase plasma levels, the elevation of cyclic guanosine monophosphete (cGMP) in the liver tissue, and the increase in the sinusoidal space ratio, 24 h after CLP. Both Sn-PP and Zn-PP decreased the mortality rate 24 h after CLP compared with normal saline. CONCLUSIONS: CO produced by excessively induced HO-1 after CLP promotes an immoderate dilation of the sinusoidal space through the up-regulation of cGMP, resulting in liver dysfunction. Therefore, administering HO inhibitors at appropriate doses could be beneficial for the amelioration of sepsis-induced liver dysfunction.

Animals↗
PubMed1990

The effect of liver dysfunction on colchicine pharmacokinetics in the rat.

Recent work has shown that colchicine may benefit patients with primary biliary or alcoholic cirrhosis. However, very little is known about its pharmacokinetics in the presence of impaired liver function. To study this we examined the effects of three models of experimental liver dysfunction and one of cytochrome P-450 inhibition on colchicine elimination in the rat. The models of experimental liver dysfunction included bile duct ligation (with sham-operated controls), alpha-naphthylisothiocyanate-induced intrahepatic cholestasis and galactosamine-induced diffuse hepatocellular necrosis. The control group had a colchicine clearance of 77.33 ml/min.kg +/- 8.27 ml/min.kg, a half-life of 16.68 min +/- 0.97 min and a volume of distribution of 1.84 L/kg +/- 0.15 L/kg. Cimetidine administration, 120 mg/kg intraperitoneally 15 min before colchicine administration, caused clearance to decrease by 32% (p less than 0.05) and half-life to increase by 38% (p less than 0.05). Volume of distribution did not change. At 48 hr after bile duct ligation, colchicine clearance decreased by 84% (p less than 0.05), terminal half-life increased to 513.7 min +/- 106.6 min (p less than 0.05) and volume of distribution increased by 175% (p less than 0.05). Colchicine pharmacokinetics in sham-operated rats were not statistically different from the above mentioned controls.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Naphthylisothiocyanate↗
PubMed2001

Schizophrenia and liver dysfunction.

It is suggested that a non-hepatocellular liver dysfunction, caused by the presence of a congenital or acquired portal-systemic shunt, constitutes a major predisposing factor in the pathogenesis of schizophrenia. In addition to the common occurrence of schizophrenic reactions observed in liver disease, this suggestion is supported by autoptic findings in addition to the fact that a considerable number of abnormal biochemical and biological phenomena are shared by patients suffering from schizophrenia and portal-systemic shunting. The frequency of abnormal portal-systemic shunts in schizophrenia is unknown. Recent advances in non-invasive Doppler-sonographic techniques should enable an elucidation of this question.

Humans↗
PubMed1986

Carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) in pancreatic cancer. Role of age and liver dysfunction.

In order to ascertain the clinical usefulness of CA 19-9 in detecting pancreatic cancer in comparison with CEA, and to verify the influence of age and liver dysfunction on serum levels of these two antigens, serum CA 19-9 and CEA were assessed in 32 control subjects, 32 patients with pancreatic cancer, 26 with chronic pancreatitis and 43 with gastrointestinal extra-pancreatic diseases. Sensitivity, specificity and diagnostic accuracy of CA 19-9 and CEA in detecting pancreatic cancer were: 69% and 44%, 91% and 75%, 60% and 19% respectively. Linear correlations were observed between the age of the subjects on the one hand and CA 19-9 or CEA on the other. Significant relationships were also noticed between alanine-amino-transferase or bilirubin serum levels and CA 19-9 values. Serum CA 19-9 seems to be a better diagnostic tool than CEA in the assessment of pancreatic cancer; nevertheless the influence of liver dysfunction and age to some extent limits the diagnostic value of CA 19-9.

Adult↗
PubMed2001

Liver dysfunction elicited by gut ischemia-reperfusion.

Gut ischemia and reperfusion (I/R) has been implicated as a prime mechanism in the pathogenesis of multiple organ failure and in initiating remote organ failure. Although it has long been known that gut I/R elicits liver dysfunction, only recently has the kinetics of leukocyte accumulation in the hepatic microcirculation and mechanisms of the liver injury after gut I/R been investigated. These studies reveal that the magnitude of gut I/R-induced liver injury depends on the duration of ischemic period and animal species. Gut I/R-induced accumulation of leukocytes, both neutrophils and lymphocytes, in the liver results in an oxidative stress in proximity to non-perfused sinusoid that contributes to subsequent hepatocellular injury. The gut I/R-induced leukosequestration in the liver is mediated by adhesion molecules that are induced by different cytokines, endotoxin, and oxidants. Kupffer cells also play an important role in the gut I/R-induced leukosequestration and liver injury. Nitric oxide and anti-oxidants such as superoxide dismutase protect the liver against the deleterious effects of gut I/R. Furthermore, agents such as ethanol can alter the hepatic responses to gut I/R. The results of these studies provide novel information and potential therapeutic strategies for reducing the liver dysfunction and multiple organ failure induced by gut I/R.

Journal Article↗
PubMed1991

Serum DU-PAN-2 in the differential diagnosis of pancreatic cancer: influence of jaundice and liver dysfunction.

The usefulness of serum DU-PAN-2 in diagnosing pancreatic cancer and in distinguishing between this cancer and other benign and malignant diseases, and to assess the role of liver dysfunction in altering the serum levels of this marker were investigated. DU-PAN-2 was measured in the sera of 31 patients with pancreatic cancer, 32 with chronic pancreatitis, 20 with benign and 21 with malignant extra-pancreatic diseases. DU-PAN-2 was found to be above 300 U ml-1 in 21/31 patients with pancreatic cancer (sensitivity 68%). Only 3/32 patients with chronic pancreatitis had abnormal values. A substantial number of patients with both benign and malignant extra-pancreatic diseases had an elevated serum DU-PAN-2 (9/20 and 15/21, respectively). Correlations were found between DU-PAN-2 and (1) total bilirubin, (2) alanine-amino-transferase and (3) alkaline phosphatase. Of the patients with high DU-PAN-2 values, jaundice was found in: 2/3 with chronic pancreatitis, 9/10 with benign and 12/14 with malignant extra-pancreatic diseases. In conclusion, the serum DU-PAN-2 test for pancreatic malignancy is not completely satisfactory, because it is not sensitive enough. While the test for chronic pancreatitis has an acceptable specificity, the assay cannot distinguish between pancreatic cancer and other extra-pancreatic diseases, mainly of the liver and biliary tract. Liver dysfunction as well as jaundice seem to considerable affect the levels of this marker, as reported elsewhere for CA 19-9.

Adult↗
PubMed1999

Rapid estimation of creatinine clearances in patients with liver dysfunction.

Different methods are available for rapid assessment of renal function using the patient's serum creatinine concentration and body weight without obtaining urine collection over 24 hr. However, the reliability of these methods in patients with liver diseases has not been established. The purpose of this study was to determine the accuracy and precision of the estimated creatinine clearances obtained by the methods of Cockcroft-Gault, Jelliffe, Mawer, and Siersbaek-Nielsen in patients with liver diseases who have different degrees of renal function. Creatinine clearances obtained from 24-hr urine collection were used as the standard. The different methods for rapid renal function estimation had limited accuracy and reliability in patients with severe liver dysfunction (Child-Pugh class C) and also in those with creatinine clearances of less than 60 ml/min. Creatinine clearances were overestimated by about 40-100%. Using lean body weights, instead of total body weights, reduced the prediction errors. In patients with mild liver dysfunction (Child-Pugh class A), all four estimation methods provided reasonable estimation of the creatinine clearances.

Adult↗
PubMed1989

High-molecular-mass ("biliary") isoenzyme of alkaline phosphatase and the diagnosis of liver dysfunction in cystic fibrosis.

The high-Mr isoenzyme of alkaline phosphatase (AP, EC 3.1.3.1), a highly sensitive index to cholestasis, was measured by liquid chromatography in 45 patients with cystic fibrosis. Results of serum tests for liver dysfunction--including gamma-glutamyltransferase, aspartate aminotransferase, alanine aminotransferase, total AP, bilirubin, and bile acids--were compared with those for high-Mr AP. Values for high-Mr AP were increased in 44.4% of our patient population, with activities ranging from 0.4 to 17.3 U/L. The upper limit in the control group was 2.5 U/L. We find increased high-Mr AP to be a more sensitive indicator of liver dysfunction in patients with cystic fibrosis than are other tests.

Adolescent↗
PubMed2000

Erythropoietic protoporphyria with severe liver dysfunction and acute pancreatitis.

A case of erythropoietic protoporphyria associated with severe hepatic dysfunction and acute pancreatitis is reported. The patient, a 33-year-old man, was admitted to our hospital complaining of upper abdominal pain, nausea, and vomiting of 3 days' duration. Laboratory tests on admission demonstrated liver dysfunction, anemia, and thrombocytopenia. On the third hospital day, the intensity of the upper abdominal pain increased, concomitantly with elevated levels of serum amylase. Ultrasonography and computed tomography scanning revealed a slightly enlarged pancreas. During this episode, he also complained of various neurological symptoms, including reduced mental alertness, weakness of extremities, constipation, profound sweating, and urinary retention. Porphyrin studies demonstrated markedly elevated erythrocyte and fecal protoporphyrin levels. Laparoscopic findings obtained after the attack subsided were compatible with porphyric liver cirrhosis. We therefore concluded that neurologic disorders and acute pancreatitis could develop in patients with erythropoietic protoporphyria with severe liver dysfunction.

Adult↗
PubMed2005

Detection of autoantibody to aldolase B in sera from patients with troglitazone-induced liver dysfunction.

Troglitazone is a thiazolidinedione antidiabetic agent with insulin-sensitizing activities that was withdrawn from the market in 2000 due to its association with idiosyncratic hepatotoxicity. To address the suspected autoantibody production associated with troglitazone, we investigated autoantibodies in sera from patients with type II diabetes mellitus with troglitazone-induced liver dysfunction. Two female patients (47- and 70-year-old) ceased taking troglitazone (400 mg/day) after 23.5 and 16 weeks, respectively, due to increased serum ALT. Using two-dimensional electrophoresis and amino acid sequence analyses, aldolase B was identified as an autoantigen that reacted with antibodies in sera from both patients. The titer of anti-aldolase B remained high for several weeks after stopping troglitazone administration. The mean reactivity of autoantibodies to aldolase B determined by ELISA with sera of patients with chronic hepatitis (n = 40) and liver cirrhosis (n = 40) was significantly higher (p < 0.05 and p < 0.001, respectively) than with sera of healthy subjects (n = 80). These findings suggest that liver injury may cause the appearance of autoantibodies to aldolase B which may then aggravate the hepatitis. In addition, the anti-aldolase B titer might indicate the severity of liver dysfunction.

Aged↗