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PubMedDate not supplied

The remnant liver dysfunction after 84% hepatectomy in dogs.

BACKGROUND/AIMS: We have been investigating the mechanism of remnant liver dysfunction after extensive hepatectomy in a canine model since 1990. This study focused on the role of heat shock protein and hepatocyte apoptosis. METHODOLOGY: Adult mongrel dogs were randomly divided into 3 groups: Group 1, sham operation; Group 2, 70% hepatectomy; and Group 3, 84% hepatectomy. Heat shock protein and hepatocyte apoptosis after hepatectomy were examined by using isolated hepatocytes and Kupffer cells. RESULTS: Heat shock protein significantly increased in Groups 2 and 3, but rose much higher in Group 3. Examination of pure hepatocyte culture showed no apoptosis in Group 2, but significant apoptosis occurred in Group 3. In co-cultures of hepatocytes and Kupffer cells, induction of apoptosis in Group 2 was mild, but it increased earlier and reached very high levels in Group 3. The TNF-alpha level in co-culture supernatant was significantly higher in Group 3 than Group 2. CONCLUSIONS: After extensive (84%) hepatectomy, apoptosis signal transduction predominates over anti-apoptosis signal transduction, despite high expression of heat shock protein in the remnant liver. Accordingly, the cytotoxic mechanism overcomes the cytoprotective mechanism, leading to significant induction of hepatocyte apoptosis and severe liver damage.

Animals↗
PubMed2002

Adverse effects of liver dysfunction and portal hypertension on intestinal adaptation in short bowel syndrome in children.

BACKGROUND: The effects of liver dysfunction and portal hypertension on intestinal adaptation in short bowel syndrome are generally unknown. The presence of these disorders may adversely affect the ability to wean these patients from parenteral nutrition. METHODS: Forty-two infants with short bowel syndrome were placed in one of three Child's classifications, depending on serum bilirubin, prothrombin time, ascites, albumin, and liver biopsy, and compared for time to diet tolerance, time required for parenteral nutrition, and survival. A subgroup of these patients also underwent portal pressure measurement, which was combined with liver biopsy results to compare three groups for the same parameters. RESULTS: Survival was Child's class A 100%, B 84%, C 61%, while time to feeding tolerance was A 16.3 days, B 20.0 days, C 28 days, and total parenteral nutrition time was A 80.0 days, B 98.0 days, C 100.0 days. In the groups that underwent portal pressure measurement, the survival was group I (normal biopsy and pressure) 100%, group II (abnormal biopsy and normal pressure) 90%, group III (abnormal biopsy and pressure) 66%, while time to feeding tolerance was I 15.0 days, II 18.0 days, III 24.0 days, and total parenteral nutrition time was I 72.0 days, II 94.0 days, III 184.0 days. CONCLUSIONS: Cholestatic liver disease, especially associated with portal hypertension adversely affects bowel adaptation in short bowel syndrome.

Cholestasis, Intrahepatic↗
PubMed1995

Determination of galactose in human blood by high-performance liquid chromatography: comparison with an enzymatic method and application to the pharmacokinetic study of galactose in patients with liver dysfunction.

Galactose, the C-4 epimer of glucose, is an agent of choice for the quantitation of liver function. A simple, precise, and accurate high-performance liquid chromatographic (HPLC) assay with refractive index detection was developed for the determination of galactose in human whole blood. The method consists of organic solvent-heavy metal deproteinization procedures and reversed-phase chromatography on a cation-exchange column in the calcium form. Calibration graphs were linear over the concentration range 100-2500 microgram/mL, with correlation coefficients > 0.999. The within-day coefficient of variation (CV) ranged from 2.08 to 8.94%, and the between-day CV ranged from 1.61 to 10.9%. The limit of quantitation was 100 micrograms/mL in whole blood. However, the limit of detection was 75 micrograms/mL based on a signal-to-noise ratio of > or = 3. Eight structurally related sugars and polyols were investigated to check for potential interferences using the analytical condition of the assay. The possible metabolites of galactose present in the body were also checked to determine the specificity of this assay. The proposed HPLC assay was compared with an enzymatic assay and an excellent correlation was observed (HPLC = 1.0299Enz. - 12.907, r = 0.952, p < 0.001). This HPLC method has been successfully applied to the pharmacokinetic study of galactose in six patients with liver dysfunction. Following the intravenous administration of a dose of 0.5 g/kg body weight, galactose pharmacokinetics followed a nonlinear two-compartment model with Michaelis-Menten elimination from the central compartment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Effect of moderate or severe liver dysfunction on the pharmacokinetics of gamma-hydroxybutyric acid.

OBJECTIVES: To assess the effect of moderate or severe liver dysfunction on the pharmacokinetics of gamma-hydroxybutyric acid (GHB). METHODS: The absorption and disposition kinetics of GHB were studied in eight cirrhotic patients without ascites (Child's class A) and eight cirrhotic patients with ascites (Child's class C), after administration of a single oral dose of 25 mg.kg-1. The liver metabolic function of each patient was evaluated by measuring antipyrine clearance and the formation rate of the lidocaine metabolite monoethylglycinexylidide (MEGX). RESULTS: Compared to those previously determined in eight healthy control subjects given the same GHB dose, mean AUC values were double or greater in the cirrhotic patients. Accordingly, apparent oral clearance was markedly reduced (from 9.1 to 4.5 and 4.1 ml.min-1.kg-1 in nonascitic and ascitic patients, respectively). Terminal half-life (t1/2), was significantly longer in nonascitic patients than in control subjects (32 vs 22 min). A further significant prolongation of t1/2, most likely due to an increased distribution volume, was observed in patients with ascites (56 min). Nonetheless, GHB plasma concentrations fell to either undetectable or negligible levels by the end of the usual dosing intervals (6-8 h). More limited changes were noted in the absorption parameters. The peak level (Cmax) increased only in nonascitic patients, but not proportionally to the increase in AUC. The time to Cmax increased from 30 to 45 min in both cirrhotic groups. These findings are consistent with a slowed rate of GHB absorption in cirrhotic patients. Adverse effects were similar, for intensity and duration, to those recorded in healthy volunteers, i.e., mild and transient. CONCLUSIONS: Although liver cirrhosis causes significant modifications of GHB disposition kinetics, the increase in t1/2 is not such as to cause drug accumulation on repetitive dosing. However, in consideration of the higher mean plasma levels observed in cirrhotic patients, it appears wise to keep the initial GHB daily dose at the lower end of the therapeutic range and to carefully monitor the patients if upward dose adjustments are required.

Aged↗
PubMed1983

Liver dysfunction associated with gold therapy for rheumatoid arthritis.

Hepatic toxicity is rarely associated with gold therapy. Three patients with rheumatoid arthritis who developed jaundice during the course of chrysotherapy are described. Jaundice occurred both early and late in the course of therapy. differing grades of severity of dysfunction were encountered. Liver biopsy revealed intrahepatic cholestasis. Significance of jaundice occurring during gold therapy is discussed.

Aged↗
PubMed1976

Liver dysfunction following whole-body Co-60 irradiation in gerbil (Meriones Hurrianae Jerdon) and house rat (Rattus rattus Rufescens).

Liver dysfunction following whole-body Co-60 irradiation has been studied in domestic and desert rat species. A significant elevation in the serum transaminases activity was noticed both in gerbil and house rat. Alkaline phosphatase and plasma cholesterol levels were also increased indicating an early radiation impairment of the liver tissue, which was later confirmed by histological studies. A steady fall in liver glycogen in irradiated gerbils was strikingly in contrast to an increase in irradiated house rat. Drastic depletion in liver glycogen, changes in the serum enzyme levels and the severity of the hepatic necrosis in gerbils point out that desert mammalian species are much more sensitive to radiation hazard as compared with domestic ones.

Alanine Transaminase↗
PubMed2006

Incidence, etiology, and risk factors for liver dysfunction in children following hematopoietic stem cell transplantation.

AIMS: To identify risk factors which predispose children to develop liver dysfunction (LD) during the initial 100 days following hematopoietic stem cell transplantation (HSCT). METHODS: Retrospective analysis of all patients (<21 yr) who had undergone HSCT from July 1998 to June 2003. LD was defined by the presence of clinical jaundice and/or elevated alanine aminotransferase (ALT) or gamma-glutamyl transferase (GGT) (1.5 times normal). RESULTS: One hundred and six patients underwent HSCT during the study period. LD was seen in 91 (85.5%) patients and the majority (58.2%) had moderate to severe LD. The primary cause of LD could be ascertained in 2/3 of patients and was multifactorial in the rest. The odds ratio and 95% CI for risk factors associated with LD following HSCT on univariate analysis were as follows: allogeneic source of stem cells 4.2 (1.2-14.2), engraftment >12 days 4.3 (1.3-14.2), total parenteral nutrition >35 days 8.2 (1.1-66.2), pretransplant ALT >40 U/L 7.4 (0.9-58.6), use of cyclosporine and methotrexate 9.5 (1.2-77.9), and use of amphotericin-B 3.1 (0.9-10.6). On multivariate analysis only elevated pre transplantation ALT and delayed engraftment were associated with post-HSCT LD. LD was seen in all 13 patients who died within 100 days following HSCT, and it was felt to be the primary cause of death in six (46%) patients. The factors associated with increased risk of mortality were: allogeneic source of stem cells, delayed engraftment (>18 days), higher mean peak GGT (>250 U/L), and total bilirubin (>6 mg/dL). CONCLUSION: LD was common and severe in the majority of children following HSCT. Risk of LD was higher in children who had elevated pretransplantation ALT or had delayed engraftment. LD contributes significantly to morbidity and mortality following HSCT.

Adolescent↗
PubMed1976

Liver dysfunction following small-bowel bypass for obesity. Nonoperative treatment of fatty metamorphosis with parenteral hyperalimentation.

A patient with liver dysfunction following small-bowel bypass for obesity was treated successfully with intravenous hyperalimentation. The hepatic steatosis and dysfunction were most likely caused by the preferential absorption of carbohydrate in the remaining small bowel, with resulting relative protein starvation. Routine use of high-protein, low-carbohydrate diets postoperatively until weight stabilization has occurred may prevent this complication.

Adult↗
PubMed1989

Leukocyte endogenous mediator fails to alter protein dynamics in a model of liver dysfunction.

This study examines the effect of a purified leukocyte-derived endogenous mediator (LEM) on protein metabolism during liver dysfunction and after sham surgery and the role of a nonsteroidal, antiinflammatory drug (indomethacin sodium trihydrate) in modifying this response. Febrile response, protein kinetics, urinary end products of protein metabolism, and plasma acute phase protein levels were studied in rats given a pyrogenic dose of LEM or saline solution, and these same indicators were studied after the administration of the same dose of LEM plus 2 mg/kg indomethacin 3 weeks after a portacaval shunt (PCS) or sham operation. In both surgical groups given LEM, a maximum of 1.1 degrees C fever was observed. LEM increased protein turnover and urinary excretion of nitrogen and urea in sham-operated rats but not in the PCS animals. Administration of indomethacin decreased the plasma oxidation of L[1-14C]leucine and prevented the increased excretion of total nitrogen and urea in sham-operated animals treated with LEM. PCS animals showed a constant excretion of nitrogen and urea independent of treatment. alpha 1-Acid glycoprotein levels increased significantly in sham-operated animals treated with LEM but not in the PCS group until indomethacin was added. The coadministration of LEM and indomethacin in shams also enhanced the levels of alpha 2-macroglobulin and alpha 1-acid glycoprotein over values found with LEM alone. These findings confirm the catabolic effect of LEM in normal animals and identify the essential role of the liver in the acute phase response. The data also suggest that indomethacin may modify the acute phase response by reducing plasma amino acid oxidation as well as enhancing the levels of some specific acute phase proteins.

Acute-Phase Proteins↗
PubMed1997

Mexiletine-induced severe skin eruption, fever, eosinophilia, atypical lymphocytosis, and liver dysfunction.

A 64-year-old man developed a severe generalized pruritic morbilliform skin eruption, fever, eosinophilia, atypical lymphocytosis, and liver dysfunction 30 days after ingestion of mexiletine, a sodium channel blocker, prescribed to treat postherpetic neuralgia. Following intravenous dexamethasone, body temperature normalized the next day. However, the skin eruption did not disappear completely for 4 weeks. The patch test was positive for mexiletine. Clinical features and the result of patch test indicated that the patient developed hypersensitivity syndrome, a severe adverse cutaneous drug reaction, caused by mexiletine. We propose that mexiletine be added to the list of drugs that can cause severe adverse cutaneous drug reactions and that patients receiving mexiletine be warned to stop taking the drug immediately if a skin eruption occurs.

Anti-Arrhythmia Agents↗
PubMed2004

Microscopic polyangiitis presenting with liver dysfunction preceding rapidly progressive necrotizing glomerulonephritis.

The authors describe a 52-year-old woman diagnosed with microscopic polyangiitis. She presented with abnormal liver function tests accompanied by fever, headache, and fatigue. Two months later, rapidly progressive necrotizing glomerulonephritis developed together with seropositivity for perinuclear antineutrophil cytoplasmic antibody. Although liver dysfunction from microscopic polyangiitis is very rare, especially at presentation, this diagnostic possibility should be kept in mind to permit prompt consideration of steroid therapy.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2001

[A case of acute renal failure and liver dysfunction induced by carbamazepine(CBZ)].

A 56-year-old female with symptomatic epilepsy was admitted to our hospital because of acute renal failure(ARF) and liver dysfunction(LD) after receiving CBZ for two months. She had suffered a drug eruption caused by phenobarbital and valproate six months previously. Renal and liver biopsies presented acute interstitial nephritis and active chronic hepatitis, respectively. Drug-induced lymphocyte stimulating test showed CBZ positivity. Steroid therapy resulted in recovery from ARF and LD. CBZ sometimes causes ARF or LD, but rarely induces both simultaneously, especially in adults. Pathological evidence of two lesions other than from autopsy seems to be the first step in this case. Cross reaction with other antiepileptic agents was also of interest, suggesting that one member of the cytochrome P450 subfamily, CYP3A, participated in the mechanism.

Acute Kidney Injury↗
PubMed2003

Epirubicin in patients with liver dysfunction: development and evaluation of a novel dose modification scheme.

This study aimed to develop an epirubicin dose modification scheme in women with breast cancer and liver dysfunction. We first identified target areas under the concentration-time curve (AUCs) of 2400 and 1600 ng/ml.h from pharmacokinetic studies in 15 women with normal liver tests. In a second group of 16 women with abnormal liver biochemistry, the relationship between raised asparate aminotransferase (AST) and epirubicin clearance was: dose=AUC (97.5-34.2xlog AST). Adaptive dosing was evaluated prospectively in a third group of 41 women with serum AST > or =2xnormal+/-raised bilirubin. The median AUCs were 2444 and 1608 ng/ml.h, close to the high and low target AUCs, respectively. Variability in AUC was lower with adaptive dosing than in a fourth group given an unadjusted dose of epirubicin (coefficient of variation=25.8, 30.0 and 46.5%, respectively; P=0.06). Epirubicin dosing based on AST is safe and may reduce pharmacokinetic variability.

Adult↗
PubMed1995

Allergic reaction involving liver dysfunction and disseminated intravascular coagulation caused by a health food, Proporis.

A 43-year-old woman was hospitalized with skin eruption and liver dysfunction complicated with disseminated intravascular coagulation (DIC) after taking Proporis, a so-called health food. Her clinical course was well correlated with discontinuation and the retaking of Proporis. No other reason for the development of DIC was detected except for allergic reaction to Proporis, as demonstrated by a patch skin test. DIC subsided after the discontinuation of Proporis and treatment with gabexate mesilate and heparin. The consumption of health foods with various ingredients is recently increasing. Thus, attention should be paid to any possible serious allergic reaction related to such foods.

Adult↗
PubMed2001

Two cases of lymphadenopathy with liver dysfunction due to Mycoplasma pneumoniae infection with mycoplasmal bacteraemia without pneumonia.

We present two cases of unusual manifestations of Mycoplasma pneumoniae infection: lymphadenopathy with liver dysfunction without pneumonia. One was diagnosed as an infectious mononucleosis-like syndrome and the other as Kawasaki disease. Polymerase chain reaction successfully detected Mycoplasma pneumoniae DNA using blood samples. Mycoplasma pneumoniae can be included in the panel of aetiological agents in patients with lymphadenitis and hepatitis even in the absence of pneumonia.

Bacteremia↗
PubMed1989

Pharmacokinetics of benzodiazepine antagonist Ro 15-1788 in cirrhotic patients with moderate or severe liver dysfunction.

Ro 15-1788, a benzodiazepine antagonist, has been advocated as a new treatment for hepatic encephalopathy. This drug is extensively metabolized by the liver in normal subjects. In the present study, we examined Ro 15-1788 disposition in eight healthy controls (Group I), eight cirrhotic patients with moderately impaired liver function (Pugh score less than 10, Group II) and eight patients with severe liver dysfunction (Pugh score greater than 10, Group III). The subjects of each group were age and sex matched. After an intravenous infusion of 2 mg Ro 15-1788 over 5 min, blood samples were taken at fixed intervals up to 7 hr after the infusion. Plasma levels of the drug were determined by capillary gas chromatography. In controls, Ro 15-1788 had a high plasma clearance [16.3 +/- 2.6 ml per min per kg (mean +/- S.D.)], a short half-life (45.7 +/- 8.5 min), a large volume of distribution (0.62 +/- 0.09 liter per kg) and a low plasma protein binding (45 +/- 6%). Plasma clearance was reduced markedly in both groups of cirrhotic patients (-57 and -74%, respectively); the volume of distribution was unchanged in Group II and moderately increased in Group III (+37%). The elimination half-life was markedly prolonged in Groups II and III (+66 and +210%, respectively). Plasma clearance and Pugh score were highly correlated in cirrhotic patients (r = 0.830, p less than 0.001). The plasma protein binding of Ro 15-1788 was lower in cirrhotics, resulting in a significant increase in the free fraction of the drug (+16% in Group II; +44% in Group III).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Liver dysfunction in haemophilia A, B and other hereditary haemorrhagic disorders.

Seventy patients with Haemophilia A, B, von Willebrand's disease and Factor V deficiency had their liver functions studied. Twenty-five patients (36%) were found to have significant "transaminitis" (elevated SGPT/SGOT). Nine patients (13%) had positive Hepatitis B surface antigen (HBsAg). The incidence of Hepatitis B surface antibody (anti-HBs) in the study group was 74%. All patients were asymptomatic at the time of study. This asymptomatic liver dysfunction will require close monitoring for clinical significance.

Adolescent↗