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At least 1,495 records · Page 83Linked to original sources
PubMed1994

Transient hepatic dysfunction in two brothers receiving heparin and streptokinase: a genetic predisposition?

Two brothers with acute myocardial infarction are presented. Subsequent to a standard thrombolysis treatment with streptokinase and heparin, both developed abnormal liver tests, with elevated transaminases only. This liver dysfunction resolved promptly. The occurrence of such side-effects in two siblings raises the question of genetic predisposition to the otherwise uncommon hepatic complications of thrombolysis treatment.

Alanine Transaminase↗
PubMed1997

The protective effects of L-arginine after liver ischaemia/reperfusion injury in a pig model.

Hepatic ischaemia/reperfusion is characterized by circulatory and metabolic derangement, liver dysfunction, and tissue damage. To evaluate the role of L-arginine, a substrate of nitric oxide, in ischaemia/reperfusion injury, total liver ischaemia was induced for 120 min in 22 Landrace x Large White female pigs, which were randomly assigned to a treatment group (10 animals) or a control group (12 animals). An L-arginine bolus (540 mg/kg i.v.) was administered to the treatment group 1 h before clamping the hepatic hilum, at clamping, at reperfusion, and at 1 and 2 h after reperfusion. The control animals received normal saline and an i.v. infusion. Liver function tests and analysis of serum, erythrocyte, and tissue malondialdehyde contents were performed at commencement of laparotomy, before reperfusion, and at 30 min and 7 days after reperfusion. Liver biopsies were taken at laparotomy, at 30 min, and at 7 days after reperfusion for histological and ultrastructural examination. Assessment of apoptosis included in situ end-labelling analysis and DNA gel electrophoresis. Survival at 7 days was better in the treated animals than in the controls (9/10 vs. 7/12). Tissue malondialdehyde content, aspartate aminotransferase, and lactate dehydrogenase levels were lower in the treatment group, in which morphological changes were significantly less evident than in the controls 30 min after reperfusion. At 7 days, differences between the groups with respect to cell integrity were apparent only on ultrastructural analysis. Glycogen content, 7 days after reperfusion, was higher in the treatment group than in the controls: 70.25 per cent vs. 21.66 per cent positive hepatocytes (score 3 vs. score 1). Multiparametric analysis showed fewer apoptotic cells in the treatment group at all times. Our data show that the administration of L-arginine reduces damage to liver tissue after ischaemia/reperfusion injury in a pig model. This may be explained not only by the known vasodilator, anti-aggregation, and superoxide inactivation effects of increased nitric oxide release, but possibly also by some other action of L-arginine, such as its influence on cellular metabolism.

Animals↗
PubMed2001

Multiorgan donation from a donor with unrecognized ornithine transcarbamylase deficiency.

Ornithine transcarbamylase (OTC) deficiency, the most common inherited urea cycle disorder, shows a spectrum of severity ranging from severe neonatal hyperammonemic coma to no symptoms among adults. We report on the multiorgan procurement from a donor who died of cerebral edema due to unrecognized late-onset OTC deficiency. The donor's OTC deficiency was diagnosed retrospectively since the liver graft recipient developed cerebral edema postoperatively due to hyperammonemia. Plasma ammonia was extremely elevated (3793 micromol/l), but was not accompanied by general liver dysfunction. Post mortem, the diagnosis of OTC deficiency was established by enzyme and molecular analysis in a biopsy of the transplanted liver. In contrast to the fatal course of the liver graft recipient, the kidney, lung, and heart transplantations were successful. Ten months after transplantation these recipients were alive and showed good graft function. This case demonstrates the importance of careful donor evaluation, particularly if the donor's cause of death is obscure.

Adult↗
PubMed1987

Peroxidative injury of the mitochondrial respiratory chain during reperfusion of hypothermic rat liver.

Mitochondrial dysfunction in ischemic liver has been demonstrated to be due to decrease in the intramitochondrial level of ATP and the subsequent disruption of the proton barrier of the inner membrane (Watanabe, F., Hashimoto, T. and Tagawa, K. (1985) J. Biochem. 97, 1229-1234). In this study, another injury process, impairment of the electron-transfer system, which occurred during reoxygenation of ischemic liver, was studied during reperfusion of cold preserved liver and during cold incubation of isolated rat-liver mitochondria. The sites of the respiratory chain that were sensitive to peroxidative damage were ubiquinone-cytochrome c oxidoreductase and NADH-ubiquinone oxidoreductase. These enzymic activities decreased with increase in lipid peroxidation. Incubation of submitochondrial particles with t-butyl hydroperoxide or with an NADPH-dependent peroxidation system decreased the enzymic activities of the electron-transport system. These data strongly suggested that lipid peroxidation during reoxygenation of ischemic liver impaired the electron-transfer system. Thus, mitochondria of ischemic liver suffer from two different types of injury: increase in proton permeability during anoxia, and decrease in enzymic activities of the electron-transport system during reoxygenation.

Animals↗
PubMedDate not supplied

Antidotal therapy of severe acute organophosphate poisoning: a multihospital study.

Out of 859 consecutive cases treated for exposure to organophosphate (PO) insecticides, 53 were included in the study. Criteria for inclusion were severe OP poisoning necessitating artificial ventilation, intensive care monitoring and treatment according to a standard protocol. The protocol was based on relatively high doses of obidoxime, relatively low doses of atropine and overriding with a pacemaker in cases of ventricular arrhythmias and prolonged Q-T interval. Seven patients died during hospitalization. Thirty-two patients (60%) had major central nervous system (CNS) involvement. Five (9.4%) presented severe psychiatric sequelae. Twenty-two patients (41.5%) presented cardiac arrhythmias. Five (9.4%) had liver dysfunction. High frequency of cardiac arrhythmias was observed in patients who received high cumulative doses of atropine and obidoxime; impairment of liver functions was significantly higher in patients who received high cumulative doses of obidoxime. We conclude that each drug should be titrated separately: atropine dosage should be adjusted to the severity of tracheobronchial secretions and bronchospasm, while full doses of obidoxime are justified for the period before "aging" sets in.

Adolescent↗
PubMed2004

Evaluation of liver function for hepatic resection for hepatocellular carcinoma in the liver with damaged parenchyma.

BACKGROUND: Liver functional parameters, including the Child-Pugh score and indocyanine green clearance (ICG), and volumetric parameters influencing postoperative liver function were evaluated with the aim of obtaining standardardized criteria for selecting patients for, and deciding the extent of, hepatectomy for hepatocellular carcinoma (HCC). MATERIALS AND METHODS: The study population consisted of 120 patients with HCC undergoing hepatic resection excluding those with more than 3000 ml of intraoperative bleeding. Patients were classified as grades A, B, or C on the basis of, respectively, a Child-Pugh score of 5 or 6, 7-9, or >or=10 and were assigned to group D (postoperative liver dysfunction) or group N (no complication). Postoperative complications included massive ascites, pleural effusion, or hyperbilirubinemia. For each grade, the standardized estimated liver remnant ratio (STELR) was determined as the ratio of the liver remnant volume (estimated by computerized tomography) to the standardized total liver volume (STLV), estimated from the body surface area using the equation: liver volume [cm(3)] = 706 x body surface area [m(2)] + 2.4. The ICG retention rate at 15 min after injection (ICGR15) was then plotted against the STELR for each grade and a demarcation line separating patients in groups N and D was determined statistically by discriminant analysis. RESULTS: For grade A patients, the equation of the demarcation line was ICGR15 = 27.5 x STELR + 1.9 (Wilks' Lambda: 0.667, P < 0.001), indicating that, for safe hepatic resection in patients with an ICGR15 of 10%, the STELR should be greater than 0.29. In contrast, for grade B patients, the equation was ICGR15 = 72 x STELR - 22.1 (0.589, P < 0.001), indicating that, in patients with a 10% ICGR15, the STELR should be greater than 0.44, a larger value than in grade A patients. The number of grade C patients was too small for analysis. CONCLUSIONS: By combining the Child-Pugh score, ICG clearance, and liver volumetric parameters, criteria for the selection of patients for hepatic resection for HCC were established.

Adult↗
PubMed1997

[Fatal acute liver failure: a rare complication of exertion-induced heat stroke].

Liver injury is a well-known complication of exertional heat stroke. However severe acute irreversible liver dysfunction is rarely associated. Persistent centrolobular hepatocellular necrosis without any regeneration remains very uncommon. We report a case of fatal acute liver failure occurring after exertional heat stroke. Despite the conventional symptomatic treatment, especially active cooling, the patient experienced multiple organ failure with brain death 6 days after his admission. In this case, a chronic treatment with neuroleptic and anticholinergic agents may be considered as a predisposing factor.

Adult↗
PubMed2000

Portal vein thrombosis and liver disease.

Portal vein thrombosis can occur secondary to infection, surgical intervention, or as a result of liver dysfunction. Its development can precipitate the need for emergency interventions including endoscopy, transjugular intrahepatic portosystemic stents (TIPS), portacaval shunts, or even liver transplantation. Portal vein thrombosis occurs slowly and silently. Portal vein thrombosis is not discovered until gastrointestinal hemorrhage develops in the patient unless the thrombosis is diagnosed on routine surveillance diagnostic testing. Portal vein thrombosis can be diagnosed by Doppler ultrasonography, computed tomography scan, or magnetic resonance imaging. Late identification of portal vein thrombosis can lead to increased morbidity and mortality of the patient population. Patients with portal vein thrombosis can be successfully managed with early identification and collaboration between the patient and the health care team for ongoing monitoring and treatment. Patient education involves assisting the patient in the understanding of esophageal varices, the various treatment modalities, their physical limitations, and the need for monitoring and management of the portal hypertension.

Adult↗
PubMed1999

Hepatitis: implications for dental care.

Patients with hepatitis and liver dysfunction present an array of pathophysiologic alterations for the practitioner to evaluate. An understanding of how treatment may be affected by liver disease is essential before dental treatment is begun.

Blood Coagulation Factors↗
PubMed1999

Epithelioid hemangioendothelioma with marked liver deformity and secondary Budd-Chiari syndrome: pathological and radiological correlation.

A case of malignant epithelioid hemangioendothelioma of the liver in a 48-year-old woman with severe portal hypertension and marked deformity of the liver is presented. This woman had a history of mild liver dysfunction since the age of 30 years, and abdominal distention, esophageal varices, splenomegaly and ascites since October 1996. Imaging examinations revealed liver deformity with severe atrophy of the left lobe and the anterior segment of the right lobe. Celiac arteriography showed narrowing and upward deviation of the proper hepatic artery, and occlusion of the left and right anterior hepatic arteries. Since March 1997, hepatic venography showed stenosis in the right hepatic vein truncus. Budd-Chiari syndrome was clinically diagnosed. She died in June 1997. The autopsy disclosed massive tumor embolism in the left and right anterior portal branches, few in the hepatic artery, and occlusion of the left and right anterior hepatic arteries. The extensive tumor embolism resulted in portal hypertension, and atrophy of the left lobe. The anterior segment of the right lobe was probably caused by the occlusion of both the hepatic arteries and the portal veins. The posterior segment of the right lobe, without massive tumor embolism in its portal branch, appeared hypertrophic.

Budd-Chiari Syndrome↗
PubMed1987

Carbohydrate metabolism in infants with biliary atresia.

Carbohydrate metabolism in 9 infants with biliary atresia (BA) was investigated preoperatively and during the early postoperative period when these infants were on parenteral nutrition for 7 days. Findings were compared with data on infants without liver dysfunction. Changes of plasma glucose, immunoreactive insulin (IRI) and C-peptide immunoreactivity (CPR) in the biliary atresia group with moderate liver fibrosis were the same as those in the control group. However, in one patient with marked liver fibrosis, the molar IRI/CPR ratio was significantly low, thereby suggesting an increased hepatic insulin extraction. This change, however, was transient and the molar IRI/CPR ratio gradually returned to the level of other BA patients and the control groups after the 1st postoperative day. This study shows that in infants with BA, the glucose intolerance seen in adults with obstructive jaundice is absent and the parenteral nutrition can be performed without severe changes of carbohydrate metabolism.

Biliary Atresia↗
PubMed1992

Substituent effects in the free radical reactions of silybin: radiation-induced oxidation of the flavonoid at neutral pH.

Silybin dihemisuccinate sodium salt, a flavonoid used in human therapy of liver dysfunction, has an inhibitory effect in vivo on radiation-induced deactivation of enzymes and peroxidation of membrane lipids in rat liver microsomes. The reactivity of silybin and its phenolic OH groups towards free radicals (OH, N3., (SCN)2.-, Cl3CO2.) in aqueous solution was studied by pulse radiolysis. Absorption spectra for the phenoxyl-type radicals were assigned using structurally similar models. The one-electron reduction potential for silybin at pH 7 (E07 = 0.76 V), determined using the p-methoxy-phenoxyl/phenolate redox couple as reference standard (E07 = 0.72 V, Lind et al. 1990), is related to the 3'-methoxy-4'-OH structure, the exclusive target for one-electron oxidation at pH 7, while the 7-OH and 5-OH groups are prevented from oxidation by 4-keto substitution and intramolecular H-bonding, respectively. The free radical reactivity of silybin compares favourably with poly-OH-substituted flavonoids; however, the latter compounds have been reported to generate potentially toxic oxygen species at a biologically relevant pH.

Animals↗
PubMed1994

Serum laminin levels offer only a little additional information in liver disease.

We have measured serum laminin, a marker of portal hypertension, in 151 patients with nonmalignant liver diseases, to evaluate its utility in cirrhosis and portal hypertension. There were abnormal serum levels in 43.1% of the patients as a whole and in 62.7% of the cirrhotics. Laminin showed a correlation with many laboratory tests, especially those that reflect liver insufficiency and alcohol intake. Cirrhotics had higher laminin levels than noncirrhotics (p < 0.0001); an association was also found with portal hypertension (p < 0.0001), but laminin was also increased in patients without portal hypertension. Our results suggest that liver dysfunction can also lead to abnormal laminin concentrations, probably through slower metabolization rate. Laminin serum concentrations reflect the severity of the liver disease, and are also a marker of alcohol consumption. Determination of laminin serum levels could play an adjunctive role with respect to other liver tests in the evaluation of these patients although the measure does not really provide more useful information.

Adolescent↗
PubMed1988

Peliosis hepatis induced by 6-thioguanine administration.

A patient with acute myeloblastic leukaemia developed jaundice revealing peliosis hepatis after receiving 6-thioguanine for two months. Peliosis hepatis was severe and was associated with mild lesions of centrilobular veins. Withdrawal of 6-thioguanine was followed by a progressive improvement of liver dysfunction. This report shows that 6-thioguanine, a thiopurine already reported to be responsible for veno-occlusive disease of the liver, can induce peliosis hepatis. This suggests that some liver vascular disorders caused by thiopurines (6-thioguanine, azathioprine and 6-mercaptopurine), particularly peliosis hepatis, veno-occlusive disease, sinusoidal dilatation and perisinusoidal fibrosis, might be related syndromes caused by similar lesions at different sites.

Chemical and Drug Induced Liver Injury↗
PubMedDate not supplied

Beneficial effect of hyperbaric oxygen therapy on liver regeneration after 90% hepatectomy in rats.

BACKGROUND/AIMS: Hyperbaric oxygen therapy (HBOT) has been reported to augment oxygen delivery to ischemic tissues and improve the liver dysfunction in clinical cases. HBOT was performed after 90% hepatectomy in rats to determine its effect on the regeneration of remnant liver. METHODS: After 90% hepatectomy was performed in 8-week-old male Wistar rats, the animals were subdivided into an HBOT (2 atm abs., 80% O2, 1 h/day, 3 days) group and a non-HBOT group. Members of both groups were sacrificed, usually every 4 h until a maximum of 50 h after hepatectomy, and the liver regeneration rate, the proportion of PCNA-positive cells and the ATP volume in the remnant tissues were examined. RESULTS: In the HBOT group, the liver regeneration rate at 36 h and 50 h after operation and the proportion of PCNA positive cells at 8 h was significantly increased compared with the non-HBOT group. The ATP volume in the remnant livers in the HBOT group was also significantly increased at 12 h. CONCLUSION: HBOT augmented liver regeneration after hepatectomy by stabilization of energy metabolism induced by oxygen delivery in rats.

Animals↗
PubMed1995

Anti-tuberculosis medication and the liver: dangers and recommendations in management.

In the light of three deaths due to liver failure secondary to anti-tuberculosis therapy at the Royal Free Hospital, we have reviewed the current literature, and asked--How common is liver dysfunction with anti-tuberculosis medications and how might it be prevented? Anti-tuberculosis chemotherapy is associated with abnormalities in liver function tests in 10-25% of patients. Clinical hepatitis develops in about 3%, though estimates vary, and in these patients there is likely to be significant morbidity and mortality. On the basis of reported cases of tuberculosis, 160 patients in England and Wales can be expected to develop drug-induced hepatitis due to anti-tuberculosis therapy each year. There are published guidelines from the British and American Thoracic Societies regarding the choice of drug therapy for tuberculosis. Current recommendations with regard to monitoring liver function, and what to do when these tests become abnormal, vary considerably. We suggest a protocol for using liver function tests to monitor for liver damage, and give recommendations on what action to take when these become abnormal.

Antitubercular Agents↗
PubMed2006

Human herpesvirus-6 hepatitis associated with cyclosporine-A encephalitis after bone marrow transplantation for chronic myeloid leukemia.

A 31-year-old man referred to our hospital for treatment of his chronic myeloid leukemia (CML) in the first chronic phase by bone marrow transplantation. We pretreated him with cyclophosphamide and total body irradiation and bone marrow transplantation (BMT) was carried out. On day 31, the engraftment was confirmed and on day 52, acute graft versus host disease (GVHD) was observed. On day 189, he lost consciousness due to cyclosporine A-induced leukoencephalopathy and 375 mg cyclosporine A was changed to 100 mg prednisolone. On day 199, liver dysfunction (AST 410 IU/L, ALT 557 IU/L, gammaGTP 385 IU/L, ALP 363 IU/L, D-Bil 0.3 mg/dl) developed and a liver biopsy was performed. PCR analysis of DNA from the liver biopsy specimen was positive for HHV-6 and immunostaining using anti-HHV-6 and anti-HHV-6b antibodies showed positive staining in the cytosol of hepatocytes. No other viruses were found to induce hepatitis. From these results, he was diagnosed as having HHV-6 hepatitis and it was successfully treated with gancyclovir (GCV) administration.

Adult↗
PubMedDate not supplied

Diffuse intrasinusoidal liver metastasis of small cell lung cancer causing fulminant hepatic failure: CT findings-a case report.

A 65-year-old man with small cell lung cancer treated with two courses of chemotherapy manifested appetite loss and abdominal distention 10 days before admission. Helical CT scanning of the abdomen and pelvis disclosed marked hepatomegaly without any visible nodular lesion in the hepatic parenchyma. He died of severe liver dysfunction with multiorgan failure on the 20th hospital day. Autopsy revealed diffuse invasion of tumor cells into the sinusoid throughout the liver.

Aged↗