Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antithrombin III (Human) (AT III) was administered to 18 patients with documented hereditary AT III deficiency. In eight patients with no ongoing clinical symptoms of thrombosis, the percent increase per unit AT III infused per kilogram of body weight ranged from 1.56% to 2.74%, and the half-life from 43.3 to 77.0 hours. No significant difference was noted between patients receiving and those not receiving coumarin therapy. In clinically ill patients, the in vivo recovery was significantly lower and ranged from 0.64% to 1.90% increase per unit AT III infused/kg. Efficacy of AT III was evaluated in 13 patients for the prevention or treatment of thrombosis. AT III was efficacious as assessed by the absence of thrombotic complications after surgery and/or parturition, and the nonextension and nonrecurrence of thrombosis in patients exhibiting an acute thrombotic episode. No side effects were noted. Follow-up studies indicated no hepatitis B seroconversion and no alanine aminotransferase elevations in patients who were not transfused with other blood products.
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PMID:Evaluation of the safety, recovery, half-life, and clinical efficacy of antithrombin III (human) in patients with hereditary antithrombin III deficiency. Cooperative Study Group. 237 90

In order to assess thrombogenicity and liver toxicity of different coagulation factor concentrates, antithrombin III, soluble fibrin, alanine aminotransferase (ALAT) and gamma-glutamyl transpeptidase (GT) were measured in samples taken before, 30 min and 24 h after the infusion. Seventy-six studies were performed in 55 patients with haemophilia A (37), B (11) or von Willebrand's disease, type III (7). A sharp rise of soluble fibrin was observed in 2 patients with haemophilia B, indicating that modern factor IX concentrates may still be thrombogenic. A slight increase was also seen after infusion of factor VIII-von Willebrand factor concentrates of low purity. Antithrombin III, ALAT and GT did not change significantly after any of the factor concentrates. The alterations in those parameters did not correlate with the impairment of liver function.
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PMID:Acute effects with reference to thrombogenicity and liver toxicity after injection of different coagulation factor concentrates. 256 25

When Escherichia coli endotoxin was intravenously injected into rats given killed Corynebacterium parvum 6 days previously, fibrin deposition and endothelial cell injury occurred in hepatic sinusoids at 1.5 h and were intensified thereafter. Serum alanine aminotransferase values were increased along with prothrombin time and decreased plasma levels of antithrombin III and coagulation factor VIII:C at 5 h. Antithrombin III concentrate (plus heparin) or superoxide dismutase infused concurrently with injection of endotoxin significantly attenuated the derangements of these variables and the histologic extent of liver injury at 5 h. Intravascular coagulation, probably developing through the action of superoxide anion, may contribute to the development of massive hepatic necrosis induced by C. parvum and endotoxin in rats.
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PMID:Intravascular coagulation in the development of massive hepatic necrosis induced by Corynebacterium parvum and endotoxin in rats. 266 Feb 48

Carbon tetrachloride (CCl4) produces hepatic necrosis and Galactosamine (GALN) causes acute hepatocellular injury in dogs. 8 Beagle dogs were treated orally twice with 0.4 ml/kg CCl4 and 12 Beagle dogs with 200 mg/kg GALN i.v. After intoxication, groups of dogs were given antithrombin III (AT III) (Kybernin) from human plasma (25-100 U/kg i.v., days 1-3). Serum enzymes (GOT, GPT) were elevated, alkaline phosphatase values and serum bilirubin were increased in all animals. Dogs developed severe coagulation disorders reflecting intravascular coagulation and depressed levels of factors produced by the liver, such as AT III or fibrinogen. First toxic symptoms were seen after 48 h. Untreated dogs died between 48 and 72 h after GALN. AT III reduced the toxic effects on the coagulation system dose-dependently (minimal effective dose 3 X 50 U/kg). Decrease of fibrinogen and of platelet count were less pronounced, coagulation tests (Quick, TEG) less altered than in untreated dogs. Death rate was reduced. In CCl4 intoxicated animals also serum enzyme levels normalized after AT III. In GALN treated animals serum glucose levels were decreased in control dogs. These experimental results confirmed clinical effects of AT III in acute hepatic intoxications of humans.
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PMID:[Effect of antithrombin III on experimental hepatotoxin poisoning in dogs]. 653 7