Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Liver Dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed2001

Ruscogenin glycoside (Lm-3) isolated from Liriope muscari improves liver injury by dysfunctioning liver-infiltrating lymphocytes.

The effects of ruscogenin 1-O-[beta-D-glucopyranosyl(1 --> 2)] [beta-D-xylopyranosyl(1 --> 3)]-beta-D-fucopyranoside (Lm-3) and its aglycone, ruscogenin, on liver injury induced in mice by delayed-type hypersensitivity to picryl chloride have been investigated. Lm-3 and ruscogenin significantly decreased liver injury when given during the effector phase of the delayed-type hypersensitivity reaction. The pretreatment of nonparenchymal cells, but not hepatocytes, with Lm-3 or ruscogenin in-vitro caused a concentration- and time-dependent inhibition against the damage. Lm-3 showed a stronger inhibition against the damage than ruscogenin (IC50: Lm-3 6.3 x 10(-10) M, ruscogenin 3.9 x 10(-7) M). However, neither Lm-3 nor ruscogenin blocked the hepatotoxic potential of CCl4, when used to pretreat hepatocytes. Moreover, Lm-3 and ruscogenin inhibited concanavalin A-induced lymphocyte proliferation only at high concentrations. These results suggested that Lm-3 and ruscogenin improved the immunological liver injury by selectively causing dysfunction of the liver-infiltrating cells rather than by protecting hepatocyte membranes. Such characteristics would be significant for treating immunologically related liver diseases as well as for developing new drugs.

Animals↗
PubMed1998

Discontinuous total parenteral nutrition prevents postischemic mitochondrial dysfunction in rat liver.

Although discontinuous total parenteral nutrition (d-TPN) has recently been favored for clinical use over continuous total parenteral nutrition (c-TPN) to ameliorate liver dysfunction, mechanisms for the protection against postoperative liver dysfunction remain unknown. This study aimed to examine differences in mitochondrial function in d-TPN- and c-TPN-pretreated livers during ischemia-reperfusion. Rat livers pretreated with d-TPN or c-TPN were perfused with Krebs-Ringer buffer and were exposed to 25% low-flow hypoxia followed by reperfusion. Intrahepatic mitochondrial membrane potential (triangle up) and cell viability were assessed by dual-color digital microfluorography using rhodamine 123 (Rh123) and propidium iodide (PI), respectively. In response to hypoxia, livers pretreated with c-TPN, d-TPN, and an ordinary chow diet exhibited a significant triangle up reduction among the entire lobules. Upon reperfusion, the regional triangle up values further decreased in the c-TPN liver, whereas those in the d-TPN-treated or chow-treated livers displayed a rapid recovery toward the control levels. The severity of cell injury did not differ among the groups, showing that the reperfusion-induced triangle up drop in the c-TPN-pretreated liver is not a consequence of cell injury. Differences in the triangle up drop among the groups appear to occur irrespective of those in the glycogen storage, because the livers undergoing d-TPN display a marked triangle up recovery even when reperfused at the end of a fasted state. These results indicate that c-TPN, but not d-TPN, jeopardizes mitochondrial re-energization and suggest that a circadian pattern of the TPN serves as a potentially beneficial strategy to reduce the risk of postischemic mitochondrial dysfunction in the liver.

Animals↗
PubMed1999

Effect of hepatic dysfunction due to liver metastases on the pharmacokinetics of capecitabine and its metabolites.

Capecitabine (Xeloda) is a rationally designed oral, tumor-selective fluoropyrimidine carbamate aimed at preferential conversion to 5-fluorouracil (5-FU) within the tumor. Because capecitabine is extensively metabolized by the liver, it is important to establish whether liver dysfunction altered the pharmacokinetics of capecitabine and its metabolites. This was investigated in 14 cancer patients with normal liver function and in 13 with mild to moderate disturbance of liver biochemistry due to liver metastases. They received a single oral dose of capecitabine (1255 mg capecitabine/m2) with serial blood and urine samples collected up to 72 h after administration. Concentrations of capecitabine and its metabolites were determined in plasma by high-performance liquid chromatography or liquid chromatography coupled to mass spectrometry and in urine by 19F-nuclear magnetic resonance spectroscopy. Although plasma concentrations of capecitabine, 5'-deoxy-5-fluorouridine, 5-FU, dihydro-5-FU, and alpha-fluoro-beta-alanine were, in general, higher in patients with liver dysfunction, the opposite was found for 5'-deoxy-5-fluorocytidine. These effects were not clinically significant. Total urinary recovery of capecitabine and its metabolites was 71% of the administered dose in patients with normal hepatic function and 77% in patients with hepatic impairment. The absolute bioavailability of 5'-deoxy-5-fluorouridine was estimated as 42% in patients with normal hepatic function and 62% in patients with impaired hepatic function. In summary, mild to moderate hepatic dysfunction had no clinically significant influence on the pharmacokinetic parameters of capecitabine and its metabolites. Although caution should be exercised when capecitabine is administered to patients with mildly to moderately impaired hepatic function, there is no need for, a priori, adjustment of the dose.

Adult↗
PubMed1999

Hepatic sickling: an unusual cause of liver allograft dysfunction.

Orthotopic liver transplantation can be performed successfully in thalassemia. In this article, we describe a case of liver transplantation in a patient with sickle cell/beta-thalassemia complicated by liver sickling. Intrahepatic sickling must be considered in case of allograft dysfunction. This condition can easily be diagnosed by biochemical investigation and liver ultrasonography.

Adult↗
PubMed2000

Virus-associated haemophagocytic syndrome responsive to steroid pulse therapy and double filtration plasmapheresis.

We present an adult patient with haemophagocytic syndrome (HPS) successfully treated with a combination of steroid pulse therapy and double filtration plasmapheresis (DFPP). A 58-year-old male was admitted with high fever, severe renal dysfunction, liver dysfunction and an increased level of lactate dehydrogenase. A serological test for Epstein-Barr (EB) virus showed an elevation of EBNA-IgM antibody titre. There were increased haemophagocytic histiocytes in the bone marrow in addition to thrombocytopenia and disseminated intravascular coagulation (DIC) accompanied by organ dysfunction. EB virus associated haemophagocytic syndrome was diagnosed. On admission, interferon (IFN)-gamma, interleukin (IL)-6, IL-8, granulocyte colony-stimulating factor (G-CSF) and macrophage (M)-CSF were elevated, and were promptly normalized after steroid pulse therapy was initiated. G-CSF and M-CSF gradually decreased after DFPPs was started. To control hypercytokinaemia until treatment for the underlying disease is initiated, steroid pulse therapy and double filtration plasmapheresis are useful.

Antibodies, Viral↗
PubMed1994

Structural organization and analysis of the human fumarylacetoacetate hydrolase gene in tyrosinemia type I.

Fumarylacetoacetate hydrolase (FAH) is a metabolic enzyme functioning at the last step of tyrosine catabolism. Deficiency in this enzyme activity is associated with tyrosinemia type I, characterized by hypertyrosinemia, liver dysfunction, renal tubular dysfunction, liver cirrhosis, and hepatic tumors. We isolated from a human gene library a chromosomal gene related to FAH. The human FAH gene is 30 kilobases long and is split into 14 exons. All of the splice donor and acceptor sites conform to the GT/AG rule. We also analyzed findings in a patient with tyrosinemia type I with respect to the mutation responsible for defects in the enzyme. A nucleotide change from T to G was found in the exon 2 of the gene and this change was accompanied by an amino acid substitution (Phe62Cys). Transfection and expression analysis of the cDNA in cultured BMT-10 cells with the nucleotide substitution demonstrated that the substitution was indeed responsible for the decreased activity of the enzyme in the patient. These results confirmed that the T to G mutation was one of the causes of tyrosinemia type I. Structure of the FAH gene and tests for expression of the mutant FAH will facilitate further understanding of various aspects of FAH.

Base Sequence↗
PubMed1997

Chronic hepatitis in an infant, in association with human herpesvirus-6 infection.

A 20-month-old boy was investigated for persistent liver dysfunction. Liver histologic findings showed chronic hepatitis. The presence of human herpesvirus-6 DNA in liver tissue was demonstrated both by in situ hybridization and by polymerase chain reaction. Human herpesvirus-6 may be a causative agent of chronic hepatitis in this case.

Biopsy↗
PubMed1981

Persistent non-A, non-B hepatitis in experimentally infected chimpanzees.

Non-A, non-B (NANB) hepatitis was transmitted to six chimpanzees by intravenous inoculation of antihemophilic (factor VIII) materials, acute-phase chimpanzee liver, and chronic-phase plasma obtained from two NANB hepatitis-infected chimpanzees 10 and 16 months, respectively, after their inoculation. Five of six experimentally infected chimpanzees observed for more than one year demonstrated persistent or intermittent elevations in levels of serum alanine aminotransferase (ALT) indicative of continuing liver dysfunction. Liver biopsy specimens obtained from three chimpanzees with persistent elevations in levels of ALT were positive for hepatocyte cytoplasmic structures associated with NANB hepatitis for as long as 27 months after inoculation. Liver biopsy specimens obtained from four infected animals 13-30 months after inoculation also showed mild but persistent histopathologic lesions of undefined character. The detection of circulating immune complexes in one chimpanzee with persistent elevations in levels of ALT suggests that these complexes may be involved in the pathogenesis of NANB hepatitis.

Animals↗
PubMed1990

Hypoproteinemia related with chronic lithium therapy in two patients.

We present here two cases of reversible hypoproteinemia which could have occurred as an adverse effect of chronic lithium administration. In the present cases, protein losing a renal dysfunction, liver dysfunction and malabsorption syndrome were not observed, and the relationship between their dietary volume and serum protein levels was poor. The mechanism of hypoproteinemia in these cases was not identified from previously obtained data. We suggested that this type of hypoproteinemia might be a new adverse effect of lithium.

Adult↗
PubMed2000

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by rathke's cleft cyst: a case report.

We report a case of a seventy-year-old woman with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by Rathke's cleft cyst. She experienced nausea, vomiting, diarrhea, and headache and disturbance of consciousness induced by hyponatremia at a serum sodium level of 100 mEq/l. In spite of severe hyponatremia, urinary sodium excretion was not suppressed and serum osmolality (270 mOsm/kg) was lower than urine osmolality (304 mOsm/kg), and arginine vasopressin (AVP) remained within normal range. SIADH was diagnosed because she was free from other diseases known to cause hyponatremia such as dehydration, cardiac dysfunction, liver dysfunction, renal dysfunction, hypothyroidism, and adrenal insufficiency. Cranial computed tomographic (CT) scan and cranial magnetic resonance (MR) imaging showed a cystic lesion of approximately 2 cm in diameter in the pituitary gland. These images suggested that the cystic lesion was a Rathke's cleft cyst, which was the cause of SIADH. Water restriction therapy normalized her serum sodium concentration and improved her symptoms. After one year, she suffered from general fatigue, appetite loss, fever, and body weight loss (5 kg/2 months). She had neither hypotension nor hypoglycemia, but her serum sodium level was low and serum cortisol, ACTH, and urine free cortisol were very low. Therefore, secondary adrenal insufficiency was suspected and diagnosed by stimulation tests. After start of hydrocortisone replacement therapy (10 mg/day), her symptoms disappeared. In conclusion, Rathke's cleft cyst should be kept in mind as a potential cause in a patient with SIADH, hypopituitarism, and/or adrenal insufficiency.

Adrenal Insufficiency↗
PubMed1976

[Further study on gentamicin in pediatrics (author's transl)].

Gentamicin (GM) was intramuscularly injected to 16 children with various infectious disease (1 septicemia, 1 purulent meningitis, 4 bronchopneumonia, 1 pyothorax, 3 pyelonephritis, 2 acute cystitis and 4 RITTER'S dermatitis). The results obtained are as follows: 1. The excellent and good clinical results were noted in all patients except for an indeterminate case with bronchopneumonia because of the concomitant therapy with CEZ. The effective rate was 100.0%. This was possibly because of quite high susceptibility (See Article) of all isolates to gentamicin. 2. Doses of GM were adjusted depending on the style of infectious diseases. The satisfactory clinical results were obtained in some cases by increasing its recommended dosage to about 5-8 mg per kg per day. 3. No kidney dysfunction, liver dysfunction, the 8th cranial nerve damage, etc. were observed by administering 5 to 8 mg per kg per day for at maximum 18 days, in this clinical trial. 4. It has been indicated in this clinical trial that GM is worthy to be used as a first-choice drug in chemotherapy of infectious diseases caused by Staphylococcus, gram-negative bacillus, etc., especially in patients who are hypersensitive to penicillin and cephalosporin derivatives. However, further study would be required for the safety of increase in its dosage and duration of administration.

Adolescent↗
PubMed2004

Body fat accumulation and postoperative complications after abdominal surgery.

The contribution of subcutaneous or intra-abdominal fat (SCF, IAF) accumulation to postoperative mortality or morbidity after elective gastric or colorectal cancer surgery was studied. One hundred thirty-nine patients who underwent gastric or colorectal cancer surgery were investigated. Data were collected on the following preoperative comorbid conditions: lung dysfunction, cardiovascular dysfunction, liver dysfunction, or diabetes mellitus (DM). The IAF and SCF areas were determined at the umbilical level by preoperative CT scanning. We investigated whether IAF or SCF was independently associated with postoperative mortality or morbidity. The mortality rate was 0.7 per cent (1/139). Nineteen (14%) of 139 patients had medical complications (pneumonitis or arrhythmia) and 27 (19%) had surgery-related complications (anastomotic leakage, intra-abdominal collections, or abdominal wound infection) postoperatively. Age (> or =70 years), lung dysfunction, cardiovascular dysfunction, and IAF were significantly associated with medical complications, and surgical site (gastric/colorectal), DM, body mass index, IAF, and SCF were significant for surgery-related complications by univariate analysis. Multilogistic regression analysis showed that age, cardiovascular dysfunction, and IAF were significant for medical complications, and surgical site, DM, and SCF were independently related with surgery-related complications. Body fat accumulation is independently associated with postoperative morbidity after gastric or colorectal surgery, and assaying it may be useful for predicting postoperative complications.

Adipose Tissue↗
PubMed2005

[A case of idiopathic portal hypertension complicated with sepsis caused by Aeromonas hydrophila].

A 53 year old man with idiopathic portal hypertension (IPH) was admitted because of high fever and diarrhea. Nineteen years before admission, he had received splenic hilar renal shunt operation with proximal flush ligation of splenic vein due to gastric varices. Three months before admission, he had been admitted to our hospital for evaluation of liver dysfunction. Liver biopsy examination had revealed peri-portal fibrosis consistent with IPH. Aeromonas hydrophila was isolated from blood. Although he was treated with antibiotics plus dopamine, glucose-insulin therapy, and mechanical ventilation, he had severe septic shock, and died 29 days after admission. We have to take notice of A. hydrophila infection in cases of portosystemic shunt because they fall in severe septic shock.

Aeromonas hydrophila↗
PubMed1983

[Serum unconjugated 2-hydroxyestrone and erythrocyte catechol-O-methyltransferase activity in pregnancy toxemia].

To clarify the significance of catecholestrogens in toxemia of pregnancy, plasma unconjugated 2-hydroxyestrone (2-OHE1) was measured by a specific radioimmunoassay. In addition, catechol-O-methyltransferase (COMT) activity in erythrocytes was compared between normal and toxemic pregnancies. The following results were obtained. There was no significant difference in the plasma 2-OHE1 level between normal and toxemic pregnancies in the 3rd trimester, these being 220 +/- 53(SD,n = 7), 162 +/- 138(n = 9) pg/ml, respectively. However, the plasma 2-OHE1, level was quite low in all three subjects in toxemic pregnancy with placental dysfunctions. Liver dysfunction was found in only one case of toxemic pregnancy, whose plasma 2-OHE1 was within the normal range. In two cases of mild toxemia and one case of severe toxemia with placental dysfunctions there was no significant difference in COMT activity as compared with normal pregnancy. The COMT activity of a diabetic woman with pregnancy toxemia without placental dysfunctions was slightly higher than that of a normal pregnant woman. From these results it is suggested that the lower plasma 2-OHE1 level in toxemic pregnancy may be caused by placental dysfunctions.

Catechol O-Methyltransferase↗
PubMed1998

[Clinicopathological study of multiple myeloma associated with hyperammonemia].

Of 5 multiple myeloma patients with hyperammonemia, autopsy was performed in 4 patients, while amino acid metabolism was examined in 3 patients. As a result they were classified into the following 3 types; A, liver dysfunction and severe liver infiltration of myeloma cells. B, severe liver infiltration without liver dysfunction. C, Neither liver dysfunction nor severe liver infiltration. In one type A patient, isoleucine decreased. In two patients without liver dysfunction (one type C patient and another patient in whom autopsy was not performed) valine, leucine and isoleucine decreased, and tyrosine decreased slightly. The Fischer ratio decreased in these 2 patients, while it decreased slightly in a type A patient. Clinically, in 4 patients hyperammonemia was observed during periods of poor general condition and when refractory to chemotherapy. In an aggressive type case, consciousness disturbance was developed rapidly and multiple myeloma was diagnosed. In all patients, consciousness disturbance was noted. Hyperammonemia might have been caused by hepatic failure or systemic-portal shunt in patients with liver infiltration. In those without liver infiltration, it was suggested that hyperammonemia was caused by myeloma related humoral factors that influence amino acid metabolism.

Aged↗
PubMed1988

The role of liver biopsy in evaluating acute allograft dysfunction following liver transplantation: a clinical histologic correlation of 34 liver transplants.

One hundred six liver biopsy specimens from 34 orthotopic liver transplant (OLT) patients were examined and the histologic findings correlated with the clinical course of the patients to determine if specific morphologic patterns were associated with specific causes of acute allograft dysfunction. The principle causes of allograft injury in these patients appeared to be acute rejection and ischemic injury, with rarer cases of viral infection and biliary obstruction. Graft rejection causing transient liver dysfunction was associated with a mixed inflammatory infiltrate in the portal tracts and involving the interlobular bile ducts. Rejection resulting in severe, persistent dysfunction was associated with destruction and loss of the interlobular bile ducts or portal inflammation, followed by acute centrilobular hepatocyte necrosis. Ischemic liver injury was characterized by hepatocyte ballooning and/or hepatocyte necrosis. Ischemic injury causing transient graft dysfunction demonstrated focal, limited areas of hepatocyte necrosis or transient centrilobular hepatocyte ballooning. Severe ischemic injury resulting in persistent dysfunction caused diffuse hepatocyte necrosis or centrilobular ballooning followed by centrilobular hepatocyte loss and severe cholestasis with evidence of bile duct epithelial injury. The histologic patterns observed were not pathognomonic; radiologic studies, bile cultures, and other laboratory tests were necessary to rule out biliary or vascular obstruction and bacterial cholangitis. However, liver biopsies, especially serial biopsies, were helpful in suggesting the probable cause of liver dysfunction and in predicting subsequent allograft recovery or failure.

Adolescent↗
PubMed1991

Differentiation of liver graft dysfunction by transplant aspiration cytology.

Episodes of graft dysfunction are frequently observed after liver transplantation and can be due to different causes requiring specific therapy. In this study the usefulness and reliability of liver transplant aspiration cytology (TAC) for differential diagnosis of liver graft dysfunction is assessed. Out of more than 1500 TACs performed, 292 TACs, taken during episodes of liver dysfunction due to retrospectively defined causes, were analyzed. Immune activation and parenchymal damage in the aspirates were determined cytologically. In 63 episodes of acute rejection, marked immune activation was present in aspirate but not in blood, with varying degrees of hepatocyte damage and cholestasis. No or only minimal immune activation was observed in 86 cases of toxic, ischemic, or septic liver damage, but considerable parenchymal damage and cholestasis were observed. In 3 cases of hepatitis slight-to-moderate immune activation with large granular lymphocytes was found in the aspirate, while 17 cases of viral infection presented with slight-to-moderate immune activation in aspirate and blood. After successful treatment the cytologic patterns normalized, except when the cause of liver dysfunction persisted. Moreover, typical patterns of parenchymal changes were found for preservation damage of the liver (n = 108), fatty degeneration (n = 3), obstructive cholestasis (n = 5), and acute arterial ischemia (n = 2). One case of moderate subcapsular hematoma was the only complication observed (less than 0.1%). Thus, liver TAC is an easy, safe, and clinically useful method for differential diagnosis of liver graft dysfunction. In particular, differentiation between acute rejection and nonimmunologic causes of dysfunction is very reliable, but hepatitis and viral infections also present distinctive patterns in liver TAC.

Biopsy, Needle↗
PubMed1999

Primary dysfunction after liver transplantation. Is it possible to predict this complication?

OBJECTIVE: the aim of this study was to evaluate potential risk factors related to the development of primary liver graft dysfunction (PDF), including initial poor function (IPF) and primary nonfunction (PNF), and to describe a statistical predictive model for this complication. METHODS: to evaluate potential risk factors for the development of PDF (IPF and PNF), patients were classified into three groups on the basis of early postoperative graft function, and their medical charts were reviewed for donor, recipient and peroperative information. To evaluate the prognostic influence of potential risk factors, those that were statistically significant in the univariate analysis were subsequently studied by multivariate analysis using a Cox model. The study group comprised 214 liver transplants performed in 177 recipients. RESULTS: of the 214 liver transplants considered, 153 (71.5%) presented immediate graft function and 61 (28.5%) developed primary dysfunction. Initial poor function occurred in 43 (20.1%), while in 18 (8.4%) primary nonfunction of the liver was found. The severity of steatosis and preservation injury, recipient serum creatinine level, UNOS status, use of venovenous bypass, intraoperative coagulopathy and intraoperative bile output, reached statistical significance in the multivariate analysis and were predictors of PDF. CONCLUSIONS: the predictive model obtained is a useful tool to evaluate donors and recipients for liver transplantation, and for the early detection of primary dysfunction.

Adolescent↗