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At least 217 records · Page 12Linked to original sources
PubMed1998

Liver dysfunction in patients infected with hepatitis C virus undergoing chemotherapy for hematologic malignancies.

BACKGROUND: Reactivation of chronic hepatitis B virus (HBV) infection with the development of fulminant hepatitis induced by withdrawal of chemotherapy and/or corticosteroids (CS) is well known. However, less is known about liver dysfunction in patients with hepatitis C virus (HCV) who are undergoing chemotherapy. Thus, the authors conducted this study to determine whether chemotherapy for HCV positive patients with hematologic malignancies is associated with hepatic injury. METHODS: Thirty-three consecutive HCV positive patients were studied. Twenty-six had B-cell lymphoma, two had Hodgkin's disease, two had acute myeloblastic leukemia (AML), two had chronic myelocytic leukemia, and one had multiple myeloma. HCV infection was detected by anti-HCV antibodies (enzyme immunoassay) and HCV RNA (reverse transcription polymerase chain reaction). In 28 of 33 patients, CS were used as part of the chemotherapy regimens. Liver function tests (LFTs) were evaluated prior to chemotherapy, a mean of 19 days after each cycle of chemotherapy, and during the follow-up period after the completion of chemotherapy. Mean follow-up was 14 months (range, 7-26 months). RESULTS: Twenty-seven of 33 patients (82%) were positive for both anti-HCV and HCV RNA, 5 for HCV RNA only, and 1 for anti-HCV antibodies only. Fourteen patients (42%) had normal pretreatment LFTs. During treatment, 18 patients (55%) (7 with normal and 11 with abnormal pretreatment transaminase levels) had mild-to-moderate increases of alanine aminotransferase (ALT) (median, 156 U/L; range, 59-491) and aspartate aminotransferase (AST) (median, 121; range, 45-243), which occurred 2-3 weeks after the withdrawal of chemotherapy without associated hyperbilirubinemia. Only one patient with baseline ALT and AST of 182 IU/L and 117 IU/L had a severe "flare" of hepatitis C, with peak ALT and AST of 491 IU/L and 243 IU/L. No patient developed fulminant hepatitis or died of liver-related causes. Posttreatment levels of transaminases were not significantly different from pretreatment levels. Abnormal pretreatment transaminase levels did not predict further increase during treatment. CONCLUSIONS: Significant hepatic dysfunction is uncommon among HCV infected patients treated with chemotherapy for hematologic malignancies.

Acute Disease↗
PubMed2005

Fatty acid methyl esters are detectable in the plasma and their presence correlates with liver dysfunction.

BACKGROUND: Methanol is a component of certain alcoholic beverages and is also an endogenously formed product. On this basis, we have proposed that methanol may promote synthesis of fatty acid methyl esters (FAMEs) in the same way that ethanol promotes fatty acid ethyl ester (FAEE) synthesis. We tested the hypothesis that FAMEs appear in the blood after ethanol intake. METHODS: Patient plasma samples obtained from our laboratory (n=78) were grouped according to blood ethanol concentrations (intoxicated, blood ethanol >800 mg/l) and non-intoxicated. These samples were further subdivided into groups based on whether the patient had normal or abnormal liver function tests (abnormal, defined as > or =1 abnormality of plasma alanine and aspartate aminotransferase, albumin, total bilirubin, and alkaline phosphatase). A separate set of plasma samples were also divided into normal and abnormal groups based on pancreatic function tests (amylase and lipase). There were no patients with detectable ethanol in this group. Patients with abnormalities in pancreatic function tests were included upon recognition of endogenously produced FAMEs by patients with liver function test abnormalities. FAMEs were extracted from plasma and individual species of FAMEs quantified by gas chromatography-mass spectrometry (GC/MS). RESULTS: Increased concentrations of FAME were found in patient samples with evidence of liver dysfunction, regardless of whether or not they were intoxicated (n=21, p=0.01). No significant differences in plasma FAME concentrations were found between patients with normal (n=15) versus abnormal pancreatic function tests (n=22, p=0.72). CONCLUSIONS: The presence of FAMEs in human plasma may be related to the existence of liver disease, and not to blood ethanol concentrations or pancreatic dysfunction. The metabolic pathways associated with FAME production in patients with impaired liver function remain to be identified.

Esters↗
PubMed1985

Hyperbaric liver dysfunction in saturation divers.

Earlier demonstration of elevated blood thyroid hormones and transaminase activities during controlled chamber dives to 540 and 660 msw [at AMTE(PL), Gosport, England; 1980 and 1981] led to the suspicion that high compression may interfere with liver function. Further studies, here described, of blood thyroid hormone level changes during the course of subsequent dives indicate that thyroxine and reverse triiodothyronine elevations are to be expected during any period of sustained compression, to depths as shallow as 61 msw. Moreover, blood levels of thyroxine-binding globulin (TBG), measured in the 540 and 660 msw dives, were also shown to rise, probably accounting for the hormone changes. This elevation is not confined to TBG, being demonstrable in at least six other glycoproteins (sex hormone-binding globulin, transferrin, ceruloplasmin, haptoglobin, alpha 1 acid glycoprotein, and alpha 2 macroglobulin). Since all these proteins share identical or very similar metabolic fates within the liver, these findings lend further weight to our hyperbaric liver dysfunction theory. How such disturbances may come about is discussed, together with its possible implications apropos high pressure nervous syndrome and divers' well-being and capabilities while at depth.

Diving↗
PubMed2001

[Acute isoniazid poisoning presenting convulsion and liver dysfunction].

A-19-year-old girl ingested 7.4 g of Isoniazid (INH) and 14.5 g of Ethambutol (EB) intentionally. She presented repetitive generalized convulsions with metabolic acidosis, treated with diazepam and 7.5 g of Pyridoxine (Vitamin B6). During day 4 and 5, liver dysfunction worsened and prothrombin time declined below 5%. She was treated with infusion of fresh frozen plasma and fully recovered on day 13. Serum concentration of INH and EB at 5 hours after ingestion was 7.6, 0.94 micrograms/ml respectively.

Acute Disease↗
PubMed2000

Effects of coffee consumption against the development of liver dysfunction: a 4-year follow-up study of middle-aged Japanese male office workers.

The association of coffee consumption with the development of increased serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) activities over 4 years was studied in 1221 liver dysfunction-free (serum AST and ALT < or = 39 IU/l and no medical care for or no past history of liver disease) Japanese male office workers aged 35 to 56 years. From the analysis using the Kaplan-Meier method, the estimated incidence of serum AST and/or ALT > or = 40 IU/l, > or = 50 IU/l, and > or = 60 IU/l decreased with an increase in coffee consumption. From the Cox proportional hazards model, coffee drinking was independently inversely associated with the development of serum AST and/or ALT > or = 40 IU/l (p = 0.019 by test for tendency), > or = 50 IU/l (p = 0.002), and > or = 60 IU/l (p = 0.007), controlling for age, body mass index, alcohol intake, and cigarette smoking. These results suggest that coffee may be protectively against the liver dysfunction in middle-aged Japanese men.

Adult↗
PubMed1996

Liver dysfunction in the early post-bone marrow transplant period.

In the paper hepatic dysfunctions occurring in more than 80% recipients of HLA-matched bone marrow transplants (BMT) in the early post-transplant period (< 100 days) is described. They involve veno-occlusive disease (VOD) and acute graft-versus-host disease (aGVHD). Liver dysfunctions can be also caused by unfavourable effects of drugs and by infections. Etiopathogenesis, clinical and laboratory findings, diagnosis, therapy and prophylaxis of the dysfunctions in question is being described in detail.

Acute Disease↗
PubMed1994

Allopurinol dose is important for attenuation of liver dysfunction after normothermic ischemia: correlation between bile flow and liver enzymes in circulation.

We have investigated the effect of two doses of allopurinol (ALL) (100 and 50 mg/kg) administered i.v. on liver function after 1 h of normothermic ischemia. ALL given in a concentration of 100 mg/kg significantly improved bile output after 1 and 24 h of reperfusion. Hepatocyte injury reflected by alanine aminotransferase (ALT) and lactic dehydrogenase (LDH) in plasma was also significantly reduced at 24 h, but not at 1 h of reperfusion compared with controls. ALL administered at a concentration of 50 mg/kg had some protective effect. Significant correlation between circulating liver enzymes and bile output at 24 h after reperfusion indicates an important pathophysiologic link between hepatocyte function and injury in this time window.

Alanine Transaminase↗
PubMed2002

The roles of ATF3 in liver dysfunction and the regulation of phosphoenolpyruvate carboxykinase gene expression.

Activating transcription factor 3 (ATF3), a member of the ATF/cAMP-responsive element-binding protein family of transcription factors, is a transcriptional repressor, and the expression of its corresponding gene, ATF3, is induced by many stress signals. In this report, we demonstrate that transgenic mice expressing ATF3 in the liver had symptoms of liver dysfunction such as high levels of serum bilirubin, alkaline phosphatase, alanine transaminase, aspartate transaminase, and bile acids. In addition, these mice had physiological responses consistent with hypoglycemia including a low insulin:glucagon ratio in the serum and reduced adipose tissue mass. Electrophoretic mobility shift assays indicated that ATF3 bound to the ATF/cAMP-responsvie element site derived from the promoter of the gene encoding the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK). Furthermore, transient transfection assays indicated that ATF3 repressed the activity of the PEPCK promoter. Taken together, our results are consistent with the model that the expression of ATF3 in the liver results in defects in glucose homeostasis by repressing gluconeogenesis. Because ATF3 is a stress-inducible gene, these mice may provide a model to investigate the molecular mechanisms of some stress-associated liver diseases.

Activating Transcription Factor 3↗
PubMed1996

[Death due to cold of a 63-year-old male associated with hepatocellular carcinoma--bibliographic consideration on alcohol metabolism of the patients with liver dysfunction].

In the early morning of late December, a 63-year-old man was found dead in front of his apartment house. At medico-legal autopsy, subcutaneous hemorrhages of the occipital region and linear fractures of the occipital bone was observed, but there was no cerebral contusion leading him to death. Many white tumors, ranging from 0.5 to 2.0 cm in diameter, were observed in the liver. On sections of the liver, hepatic parenchyma was found entirely occupied by the tumors, which were histopathologically diagnosed as moderately- or well-differentiated hepatocellular carcinoma. Alcohol concentrations of the mixed intracardiac blood and the urine were determined to be 1.9 and 3.6 mg/ml, respectively. Through the police investigation, it became clarified that the male had been sleeping in front of his apartment house about at 10:30 p.m. on the day before he was found dead. The cause of his death was, therefore, considered due to cold, and the authors gave a bibliographic consideration on blood and urine alcohol concentrations and alcohol metabolism of a patient with liver dysfunction due to hepatocellular carcinoma.

Alcohol Drinking↗
PubMed2000

Rebound hypersecretion of GH following octreotide withdrawal due to liver dysfunction in an acromegalic patient.

Octreotide usually induces long-acting inhibition of GH secretion without rebound hypersecretion. We report a patient with acromegaly who showed rebound elevation of GH and insulin-like growth factor-1 (IGF-1) after octreotide withdrawal. The patient responded remarkably to octreotide therapy with normalization of GH and IGF-1 and shrinkage of pituitary macroadenoma. Octreotide therapy was stopped when he developed liver dysfunction. GH and IGF-1 were markedly elevated for two weeks after cessation of octreotide.

Acromegaly↗
PubMed2002

A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition.

Ovarian hyperstimulation syndrome (OHSS) is a potentially fatal condition associated with the use of ovulation-inducing drugs. We describe a 28-year-old woman who presented with ascites, oliguria and vomiting. Over 2 weeks, the combination of intractable vomiting, intravenous rehydration, paracentesis, hypercatabolism and proteinuria led to severe hypoalbuminaemia with gross oedema and progressively worsening liver function. The patient's albumin dropped to 9 g/l with liver function abnormalities peaking at: alanine aminotransferase, 462 IU/l; alkaline phosphatase, 706 IU/l; bilirubin, 26 micromol/l; and prothrombin time, 19 s. The judicious use of paracentesis and commencement of total parenteral nutrition coincided with a rapid clinical improvement. One month after discharge, the patient was asymptomatic with normal liver function. This case demonstrates the severity of malnutrition and liver dysfunction that can occur with severe OHSS. Increasing use of in-vitro fertilization techniques makes it mandatory for clinicians to be aware of the clinical features, complications and treatment of this condition, and we would suggest that patients with severe OHSS should be jointly managed by physicians and obstetricians.

Adult↗
PubMed2000

High susceptibility to bacterial infection, but no liver dysfunction, in mice compromised for hepatocyte NF-kappaB activation.

Based on the essential involvement of NF-kappaB in immune and inflammatory responses and its apoptosis-rescue function in normal and malignant cells, inhibitors of this transcription factor are potential therapeutics for the treatment of a wide range of diseases, from bronchial asthma to cancer. Yet, given the essential function of NF-kappaB in the embryonic liver, it is important to determine its necessity in the liver beyond embryogenesis. NF-kappaB is normally retained in the cytoplasm by its inhibitor IkappaB, which is eliminated upon cell stimulation through phosphorylation-dependent ubiquitin degradation. Here, we directed a degradation-resistant IkappaBalpha transgene to mouse hepatocytes in an inducible manner and showed substantial tissue specificity using various means, including a new method for live-animal imaging. Transgene expression resulted in obstruction of NF-kappaB activation, yet produced no signs of liver dysfunction, even when implemented over 15 months. However, the transgene-expressing mice were very vulnerable both to a severe immune challenge and to a systemic bacterial infection. Despite having intact immunocytes and inflammatory cells, these mice were unable to clear Listeria monocytogenes from the liver and succumbed to sepsis. These findings indicate the essential function of the hepatocyte through NF-kappaB activation in certain systemic infections, possibly by coordinating innate immunity in the liver.

Animals↗
PubMed2003

Propofol ameliorates liver dysfunction and inhibits aortic superoxide level in conscious rats with endotoxic shock.

Propofol, widely used as a sedative agent, is known to exert antioxidant and anti-inflammatory effects in vitro. We studied the effects of propofol on hemodynamics and the function of several organs in conscious rats with endotoxemia. Intravenous injection of rats with endotoxin (lipopolysaccharide) caused hypotension, vascular hyporeactivity and tachycardia as well as significant lung, liver and kidney damage. Hepatocellular damage caused by lipopolysaccharide for 6 h was significantly attenuated in the lipopolysaccharide+propofol group. Aortic superoxide anion (O(2)(radical)(-)) production, but not plasma nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) level, was also suppressed by propofol in lipopolysaccharide-injected rats. Light microscopy showed that propofol attenuated the marked infiltration of neutrophils in liver tissues from lipopolysaccharide-injected rats. Moreover, the survival rate of the lipopolysaccharide+propofol group at 16 h was significantly increased when compared with that of the lipopolysaccharide group (53% vs. 12%). These results suggest that inhibition of aortic O(2)(radical)(-) production and amelioration of liver dysfunction contribute to the beneficial effect of propofol in conscious rats with endotoxic shock.

Animals↗
PubMed1999

[A case of pulmonary metastasis from renal cell carcinoma with complete response to interferon-alpha and tegafur/uracil (UFT) but possibly UFT-induced liver dysfunction and leukoencephalopathy-like symptoms].

A 61-year-old man presented with gross hematuria. He underwent left radical nephrectomy under a diagnosis of left renal cell carcinoma without distant metastasis, but bilateral multiple pulmonary metastases appeared 2.5 months after the operation. Though the metastases responded well to combination therapy of interferon-alpha and a 1:4 mixture of tegafur and uracil (UFT), the side effects of liver dysfunction and leukoencephalopathy-like symptoms due to UFT appeared 7 months after the beginning of the chemotherapy. These side effects were improved after the cessation of UFT administration.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1990

The effect of metronidazole on TPN-associated liver dysfunction in neonates.

The effect of metronidazole (MNZ) on hepatic dysfunction associated with total parenteral nutrition (TPN) in neonates was investigated. Neonates receiving TPN for more than 2 weeks were divided into three groups. In group 1, TPN was given alone, in group 2, 25 mg/kg/d of MNZ was administered intravenously for the first 2 weeks of TPN, and in group 3, 50 mg/kg/d of MNZ was given for the first 3 weeks of TPN. Several parameters of liver function tests (LFTs) during the first 4 weeks of TPN were compared among these three groups. There was no significant difference of these parameters between group 1 and group 2. Although there was no significant difference of alkaline phosphatase, gamma-glutamyl transpeptidase, direct bilirubin, and total bile acid between groups 1 and 3, transaminase (glutamic oxaloacetic, glutamic pyruvic) of group 3 remained significantly lower than those of group 1. In conclusion, the administration of MNZ 50 mg/kg/d for 3 weeks, at least, prevented the elevation of transaminase during TPN in neonates, suggesting the possible involvement of intestinal anaerobic flora in the pathogenesis of TPN-associated liver dysfunction.

Cholestasis, Intrahepatic↗
PubMed1990

Anticonvulsant syndrome with multiple symptoms, including porphyria, IgA deficiency, and liver dysfunction.

A 19-year-old Japanese female who had been treated for epilepsy with a combined phenytoin-phenobarbital preparation for the past three years presented with increasing skin pigmentation and hirsutism. She had suffered two attacks of loss of consciousness after bilateral partial oophorectomy at the age of 16. Investigations revealed a marked increase in coproporphyrin levels in the urine and feces, a marked decrease in her serum IgA level, and liver dysfunction. All these manifestations gradually improved upon the withdrawal of her antiepileptic treatment. In vitro studies revealed B cell dysfunction producing IgA deficiency, which normalized within one year after discontinuation of the antiepileptic therapy. It was assumed that her treatment had worsened preexisting porphyria, which was misdiagnosed as epilepsy because of abnormal EEG findings. The type of porphyria appeared to be hereditary coproporphyria, despite the lack of a family history.

Adult↗
PubMed2005

Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation.

A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome.

Aged↗