Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In our current study, we examined the antithrombotic effect of Chinese hamster ovary cell-derived human recombinant tissue factor pathway inhibitor (h-rTFPI) by intravenous injection of h-rTFPI with or without antithrombin into endotoxin-treated rats. An injection of h-rTFPI at a high dose (4 mg/kg of h-rTFPI or three doses of 1 mg/kg) significantly prevented the decrease of fibrinogen and factor VIII and the increase of fibrin/fibrinogen degradation products and glutamic-pyruvic transaminase in rats, while a single injection of 1 mg/kg of h-rTFPI or 250 U/kg of antithrombin did not significantly prevent intravascular coagulation. However, a simultaneous injection of 1 mg/kg of h-rTFPI and 250 U/kg of antithrombin did significantly prevent intravascular coagulation. From the studies on the clearance rate and immunohistochemical staining of injected h-rTFPI into normal rats, we found that most of the intravenously-injected h-rTFPI was localized on the central vein and sinusoids in the liver and catabolized via the proteoglycan-mediated pathway with a half-life of 48 min. These results suggest that h-rTFPI and antithrombin prevented endotoxin-induced intravascular coagulation in concert by binding to the vascular walls of the liver and by inhibiting fibrin formation on Kupffer cells in hepatic sinusoids.
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PMID:Antithrombotic effect of human recombinant tissue factor pathway inhibitor on endotoxin-induced intravascular coagulation in rats: concerted effect with antithrombin. 890 6

Previous results demonstrated that rats given Escherichia coli lipopolysaccharide (LPS; 4 mg/kg, i.v.) experience hepatocellular necrosis that begins within 4 hr and that prior treatment with anticoagulants (e.g., heparin) which target thrombin prevents the liver injury. In this study, hepatocellular injury, as marked by increased plasma alanine aminotransferase (ALT) activity and histologic changes, was prevented when heparin or hirudin was administered to rats shortly before the onset of injury. These results suggest that thrombin is a critical mediator that acts distally in the series of inflammatory events that culminates in hepatocellular damage. To explore further this hypothesis, livers isolated from rats 2 hr after LPS administration were perfused with various media. Perfusion of livers with medium comprising diluted blood from heparin-treated donors resulted in no release of ALT activity. By contrast, perfusion with similar medium anticoagulated with ancrod, which prevents clotting by depleting fibrinogen but does not inhibit thrombin, resulted in hepatocellular injury evidenced as a time-dependent appearance of ALT activity in the medium. Moreover, when livers from rats treated 2 hr previously with LPS were perfused with buffer to which thrombin had been added, injury resulted. No injury resulted when thrombin was omitted from the buffer or when livers from saline-treated rats were used. These results indicate that thrombin is a critical and distal mediator of LPS-induced liver damage and contributes to hepatocellular injury through a mechanism that is independent of clot formation. Furthermore, inflammatory events triggered by LPS exposure are a prerequisite for thrombin-induced injury.
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PMID:Thrombin is a distal mediator of lipopolysaccharide-induced liver injury in the rat. 890 62

In a prospective study 40 perimenopausal women with climacteric complaints between 45 to 52 years of age were examined. Twenty three (100%) were assigned to treatment with hormonal replacement therapy (Climen fy Schering-estradiol valerate cyproteron acetate) for 6 months. The therapy had to be stopped in 5 women (22%) for side effects. The drug was contraindicated in 17 patients because of non-treated hypertension, varices, hepatopathy and uterine fibroids with repeated metrorrhagia. In 18 patients (78%) Climax score, ALT, AST, bilirubin, total cholesterol, HDL-Chol, LDL-Chol, triglycerides, haemogram, fibrinogen, APTT, Quick test, serum Ca2+ and P2+ and urine C2+ and P2+/24 hours, weight and arterial blood pressure before and after the treatment were examined. The results confirm the benefical effect of Climen on the Climax score (p < 0.0001), total cholesterol (p < 0.01), HDL-Chol (p < 0.05) and LDL-Chol (p < 0.0001). After administration of Climen a significant decrease of P2+ serum concentration was demonstrated. Climen is suitable for treatment of acute climacteric complaints and has benefical effects on lipid metabolism.
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PMID:[Estradiol valerate/cyproterone acetate in the treatment of climacteric syndrome]. 900 75

Angiotensin-converting enzyme (ACE) inhibitors have proven to be effective in the reduction of ischemia/reperfusion damage after myocardial ischemia. Whether this favorable effect can be related to other models of ischemia and reperfusion has not yet been investigated. Therefore, we studied in a model of syngeneic liver transplantation in the rat the effect of recipient enalapril treatment on postischemic liver injury. Untreated animals served as the control group. Treatment with enalapril was started 5 minutes before reperfusion by intravenous infusion of enalapril at a dosage of 5 mg/kg/h. By means of in vivo microscopy, the sinusoidal perfusion rate and leukocyte adherence in sinusoids and postsinusoidal venules were analyzed during 45 to 60 minutes of reperfusion. Liver function was monitored by measuring bile output over a period of 60 minutes. Analysis of coagulation factors (prothrombin time, factor V, fibrinogen) and liver enzymes (alanine transaminase [ALT], aspartate transaminase [AST]) served for the evaluation of organ dysfunction and damage secondary to ischemia/reperfusion injury. The sinusoidal perfusion rate was significantly improved by enalapril treatment (94.7% [1.0] vs. 75.3% [3.8]; mean [SEM]; P = .005). In addition, leukocyte-sticking in both liver sinusoids and postsinusoidal venules was remarkably reduced in enalapril-treated animals as compared with controls (stickers/lobule: 21.0 [3.3] vs. 59.2 [2.1]; P = .0004; stickers/mm2 venular surface: 20.5 [4.7] vs. 110.3 [18.1]; P = .0004). Moreover, bile output was increased (1.13 [0.35] vs. 0.43 [0.18] g bile/60 min x 100 g liver; P = .06). Values for PT (22.5% [2.1] vs. 9.7% [1.8]; P = .005), factor V 99.4% [9.5] vs. 49.5% [8.5]; P = .007), and fibrinogen (64.1% [7.7] vs. 12.8% [3.2]; P = .001) were significantly improved, paralleled by a remarkable reduction in serum ALT (1,428 U/L [190] vs. 2,315 [248]; P = .02). Our data show for the first time that ACE inhibition in the liver recipient by enalapril attenuates hepatic ischemia/reperfusion damage after experimental liver transplantation. Our results may offer a novel approach to reduce ischemia/reperfusion injury in clinical liver transplantation.
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PMID:Angiotensin-converting enzyme inhibition by enalapril: a novel approach to reduce ischemia/reperfusion damage after experimental liver transplantation. 904 13

The actiopathogenesis of leucocytoclastic vasculitis is still unknown, but recently hepatitis C virus (HCV) has been suggested as trigger of autoimmunity. We report a case of a 26-yr-old patient with purpura due to leucocytoclastic vasculitis associated with hepatitis C virus infection. Laboratory findings showed AST, ALT, gamma GT within normal limits, positive antibodies to HCV (IIF and Riba II) and polymerase chain reaction for HCV RNA. Anti-nuclear antibodies, IgG and IgM anti-cardiolipin antibodies, anti-platelet antibodies and anti-neutrophil cytoplasmic antibodies with perinuclear pattern were also present. A skin biopsy specimen of a purpuric lesion showed leucocytoclastic vasculitis with small vessel thrombosis and perivascular deposition of IgM and fibrinogen on immunofluorescence study. This case shows a role of HCV in leucocytoclastic vasculitis; it is possible that this HCV can induce autoimmunity independently of cryoglobulins and liver involvement.
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PMID:Leucocytoclastic vasculitis associated with hepatitis C virus antibodies. 911 52

The results of hematologic, biochemical research and research of clotting system after intraperitoneal implantation of absorbed synthetic threads Dexon S are presented in this work. The research was made on rats of Wistar type. Blood for the research was taken 3, 7, 14, 30 and 60 days after the implantation. Morphology (Ht, Hb, MCH, WBC, the number of platelets), activity of aspartic and alanine aminotransferase and antithrombin activity, concentration of comolete protein and its fraction and concentration of glucose, urea, creatinine and also concentration of ions Na+, K+, Mg2+, Ca2+ and fibrinogen, protein C3 and C4 of complement system as well as kaolin-kephalin time and prothrombin time of plasma were marked. On the basis of the obtained results of the research it was noticed that the used methods of research constitute supplement of biological estimation of absorbed grafting materials.
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PMID:[Usefulness of selected parameters from the diagnostic laboratory for evaluating absorbed grafting materials]. 912 61

In order to evaluate the clinical and prognostic significance of early hyperfibrinogenemia in patients with transient ischemic attack (TIA) and ischemic cerebral infarction (ICI), we analyzed the relationships between plasma fibrinogen, brain damage severity, clinical status on admission and intra-hospital mortality. Vascular damage severity was estimated by measuring the necrotic area by computed axial tomography (CT) and indirectly by means of changes in some plasma enzymes (CK, LDH, GPT/ALT, and GOT/AST). Plasma fibrinogen levels were statistically higher in ICI than in TIA and control subjects (p < 0.0005; analysis of variance). Moreover, plasma fibrinogen was directly related to the extension of the necrotic area at CT scan (p < 0.05) and in ICI patients was positively correlated with CK (r = 0.50, p < 0.01), LDH (r = 0.41, p < 0.05) and GOT/AST (r = 0.42, p < 0.05) serum levels, but not with GPT/ALT. A higher plasma fibrinogen value was observed in patients with stupor or coma compared with those with alert consciousness (p < 0.05). In patients who died during hospitalization, fibrinogen levels were higher than those of subjects who were discharged (p < 0.005). The results indicate that in the early phase of cerebral ischemia, plasma fibrinogen levels are related to the severity of the clinical status and to the extension of the brain vascular damage, thus representing a negative clinical and prognostic factor of the disease.
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PMID:Clinical and prognostic significance of hyperfibrinogenemia in cerebral ischemia. 986 53

Secondary haemostasis was evaluated in 26 dogs with leishmaniasis and 10 normal dogs by measurements of modified one-stage prothrombin time (m-OSPT), activated partial thromboplastin time (APTT), thrombin time, fibrinogen concentration and fibrin degradation products. There were no significant differences between the groups in the m-OSPT, fibrinogen concentration, or levels of fibrin degradation products. The APTT was significantly (P = 0.006) longer in the infected dogs than in the control group, and in infected dogs with alanine aminotransferase (ALT) activities > 50 U/litre. There was a significant linear regression between ALT and APTT. Thrombin time was significantly (P = 0.003) longer in the infected dogs than in the normal dogs. There were no significant differences between the thrombin times of sick dogs with different levels of creatinine or activities of ALT, or between male and female dogs, whether diseased or normal.
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PMID:Evaluation of secondary haemostasis in canine leishmaniasis. 1009 24

The mortality rate among children with acute liver failure (ALF) on the waiting list for liver transplantation is high. We present our experience with living related donor liver transplantation (LRD-LT) in children who required urgent transplantation for ALF. Between December 1995 and July 1997, 6 children underwent LRD-LT for ALF. Cause of liver failure, recipient and donor demographics, clinical and laboratory data, surgical details, complications, and 6-month and 2-year graft and patient survival were recorded. Five boys and 1 girl received left lateral segment grafts from their parents. The mean age was 4 +/- 2.8 years (range, 1 to 9 years). ALF was caused by Wilson's disease in 1 patient and sickle cell intrahepatic cholestasis syndrome in 1 patient; in 4 patients, the cause was unknown. All patients had mental status changes; 2 were on life support. Mean pretransplantation liver function test values were: alanine aminotransferase, 972 +/- 565 U/L (normal, 1 to 53 U/L), total bilirubin, 31.3 +/- 12.4 mg/dL (normal, 0.1 to 1.2 mg/dL), prothrombin time, 34.3 +/- 12.4 seconds (normal, 10.8 to 13.3 seconds), international normalized ratio, 8.46 +/- 5.4 (normal < 2), and fibrinogen, 109 +/- 23.9 mg/dL (normal, 175 to 400 mg/dL). The donors were 5 mothers and 1 father. The mean donor age was 32.5 +/- 7.6 years (range, 19 to 40 years). No donor required blood transfusion, and no donor had any early or late postoperative complications. The donors' mean hospital length of stay was 5 days. In five cases, grafts were blood group-compatible; 1 child received a blood group-incompatible graft. All grafts functioned immediately. No patient had hepatic artery or portal vein thrombosis or biliary complications. The child who received a mismatched graft died of infection of the brain caused by Aspergillus spp at 22 days posttransplantation with a functioning graft. The child with ALF caused by sickle cell intrahepatic cholestasis syndrome developed outflow obstruction 3 months posttransplantation and required retransplantation; he eventually died of vascular complications related to his primary disease. Four children are alive at a mean follow-up of 27 months (range, 14 to 36 months). LRD-LT for children with ALF facilitates timely transplantation without drawing on cadaveric donor resources. The established safety record of LRD-LT made this option appealing to both physicians and parental donors.
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PMID:Living related liver transplantation for acute liver failure in children. 1022 5

A 57-year-old woman with a 7-year history of Parkinson's disease was admitted to our hospital because of a high fever, disturbance of consciousness, increased muscular rigidity, tachycardia and hyperhidosis after she stopped taking her prescribed levodopa + carbidopa (Menesit) 400 mg/day. In the laboratory examinations, the erythrocyte sedimentation rate was 109 mm/h, thrombocytes 7.8 x 10(4)/mm3, fibrinogen 457 mg/dl, FDP 74.8 micrograms/dl, thus suggesting disseminated intravascular coagulation (DIC). According to her biochemical examination, the serum AST (253 IU/l), ALT (178 IU/l), CK (7115 IU/l) and BUN (25 mg/dl) levels were all increased. These laboratory data and the clinical course indicated the patient to be suffering from neuroleptic malignant syndrome (NMS) with DIC. She was diagnosed to have NMS associated with DIC. She was treated with dantrolene sodium, bromocriptine, and gabexate mesilate, and her symptoms thereafter gradually improved. On day 7, she developed status epilepticus in spite of the clinical improvement in her symptoms of NMS and DIC including a clouding of consciousness. The status epilepticus was also attenuated by the use of thiamylal sodium. Patients with Parkinson's disease associated with NMS are considered to have a low incidence of DIC, status epilepticus, and in Japan this may be the first case report of the successful treatment of NMS with DIC and status epilepticus in a patient with Parkinson's disease.
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PMID:[A successfully treated parkinsonian patient with neuroleptic malignant syndrome complicated by status epilepticus and disseminated intravascular coagulation]. 1050 92


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