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: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HC II was functionally determined by thrombin inhibition in the presence of heparin in AT III-free plasma prepared by immunoadsorption on anti-AT III-Sepharose 4B column. HC II antigen concentration was assayed using specific antibodies to HC II. Simultaneously, AT III was measured. Plasma levels of HC II and AT III were determined in 110 patients with thrombotic tendency and two patients with obstetric complications and DIC. Highly significant correlations between activity and antigen prove the suitability of the methods. Reduced levels of HC II to about 50% with normal AT III values were repeatedly found in one patient with thrombotic tendency. The course of AT III and HC II during the process of DIC suggests that HC II may function as a thrombin inhibitor reserve when AT III becomes subnormally low.
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PMID:Methodology and clinical significance of heparin cofactor II. Probable heparin cofactor II deficiency in a patient with cerebrovascular thrombosis. 384 Sep 16

A synthetic thrombin inhibitor, MD-805, was used to anticoagulate 15 patients after cardiovascular surgery (CVS). A mean infusion rate of 0.71 +/- 0.1 (SD) microgram/kg . min maintained an activated coagulation time of about 150 sec in all patients, and significantly prolonged both activated partial thromboplastin time and prothrombin time. MD-805 was also administered to ten patients with disseminated intravascular coagulation (DIC), eight of whom had not responded to either heparin or gabexate mesilate (FOY), and eight of whom had circulating antithrombin III levels below 20 mg/dl. MD-805 therapy was successful in nine DIC patients. These results recommend MD-805 anticoagulant therapy after CVS and for treatment of DIC, especially when circulating levels of antithrombin III are low.
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PMID:Anticoagulation with a synthetic thrombin inhibitor after cardiovascular surgery and for treatment of disseminated intravascular coagulation. 643 71

In weaned pigs endotoxin infusion caused pathological changes in the clotting system typical of consumption coagulopathy and DIC resulting in circulatory disturbances. Infusion of the specific thrombin inhibitor hirudin prevented the endotoxin-induced disorders such as haematological changes, microthrombosis in various organs and the increase in right ventricular pressure and in respiratory rate.
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PMID:Influence of hirudin on endotoxin-induced disseminated intravascular coagulation (DIC) in weaned pigs. 743 13

The new thrombin inhibitor CRC 220 was characterized in vivo for its antithrombotic effects. CRC 220 led to a dose-dependent prolongation of clotting parameters as determined in rats, rabbits, dogs, sheeps, pigs and monkeys. We evaluated the efficacy of CRC 220 to prevent thrombus formation in arteries and in the microcirculation in different animal models. In a rabbit model of tissue factor-induced coagulation activation, infusion of 0.5 mg/kg x h CRC 220 (3 hours) led to a significant prevention of fibrinogen decrease. In a rat model of lethal LPS-induced DIC CRC 220 significantly prevented the mortality rate after a 4h-infusion of 0.75 mg/kg x h. Thrombin-induced platelet aggregation in rat lungs could be prevented by the i.v. bolus injection of CRC 220. A dose of 0.3 mg/kg leads to a reduction of more than 80% of platelet deposition in the lung, significant inhibition was still observed 90 minutes after CRC 220 administration; at this time the inhibitor had already been cleared from plasma. Arterial thrombosis was induced in rabbits by squeezing and stenosis of the A. carotis. The i.v. bolus administration of CRC 220 dose-dependently prevented thrombus formation, an ED50 of 0.03 mg/kg was calculated. This dose was associated with only a minor prolongation of aPTT.
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PMID:Pharmacological characterization of a new 4-amidinophenyl-alanine thrombin-inhibitor (CRC 220). 774 May 26

Rats which were infected with the gramnegative pathogen Klebsiella pneumoniae develop disseminated intravascular coagulation (DIC), multi-organ failure (MOF) and finally die in a septic shock. We investigated the therapeutic effect of antibiotic (tobramycin) treatment combined with the infusion of the highly specific thrombin inhibitor rec. hirudin. Although administration of 2 mg/kg tobramycin alone leads to a decrease of the bacterial burden, DIC could not be prevented. Infusion of rec. hirudin (0.25 mg/kg x h) for 4 h (start of treatment 1 h post infection), in addition to a bolus administration of tobramycin, led to an amelioration of DIC parameters as fibrinogen, thrombin-antithrombin complex (TAT) and platelets. Serum transaminase levels (GOT, GPT) as a marker of MOF were significantly improved by rec. hirudin, the T50 value increased from 17 h in the tobramycin group to 42 h in the tobramycin+rec. hirudin group, mortality rates were 90% or 60%, respectively. Combination of heparin (100 U/kg x h) and tobramycin was not effective on survival.
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PMID:Combination of antibiotic treatment with the thrombin inhibitor recombinant hirudin for the therapy of experimental Klebsiella pneumoniae sepsis. 797 45

An experimental disseminated intravascular coagulation (DIC) was induced in female CD rats by the intravenous administration of living bacteria (9.5 x 10(7) cfu Klebsiella pneumoniae), sublethal (5 mg/kg) or lethal (50 mg/kg) lipopolysaccharide (LPS), or tissue factor (1.5 micrograms/kg i.v. bolus or 0.4 micrograms/kg x hr i.v. infusion). We used a new fibrin monomer (FM) assay to follow the course of DIC. FM were detected by their ability to stimulate the tissue-type (t-PA) plasminogen activator dependent conversion of plasminogen to plasmin by a chromogenic assay. Miniplasminogen was used instead of plasminogen to avoid interference of the assay by alpha 2-antiplasmin. As a marker of DIC, elevated levels of FM were observed with all DIC-inducing agents (plasma levels were up to 90 micrograms/ml). The kinetics of FM formation were similar to the course of thrombin-antithrombin III (TAT) levels (maximal plasma levels 70 ng/ml); however, in the bacterial infection group, both parameters rose after a lag phase of about 1 hr. A 4 hr infusion of the highly specific thrombin inhibitor recombinant (rec.) hirudin (0.125 mg/kg x hr) resulted in a decrease of FM levels from 89.2 +/- 14.4 micrograms/ml in the LPS group (n = 10) to 27.4 +/- 11.2 micrograms/ml in the rec. hirudin group (n = 10; P < 0.001). The respective values for TAT levels were 73.1 +/- 19.7 micrograms/ml in the LPS group and 52.7 +/- 15.7 ng/ml in the rec. hirudin group (P < 0.001). Other coagulation parameters, such as platelets, fibrinogen, and fibrin(ogen) degradation products, were ameliorated accordingly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Formation of fibrin monomers in experimental disseminated intravascular coagulation and its inhibition by recombinant hirudin. 805 64

C1-Inhibitor (Berinert, C1 INH), a 104 kDa protein, inhibits complement components (C1 esterase) as well as enzymes of the contact phase of coagulation (Factor XII, Factor XI) and kallikrein, thus regulating kinin generation. C1 INH is used for the treatment of the hereditary angioneurotic edema. This paper will give a survey about the evidence in recent literature concerning the potential efficacy of the compound on other diseases associated with shock, capillary leakage and inflammation as well. In our own experiments we evaluated whether the compound could influence acute inflammatory reactions or the severe systemic inflammatory response syndrome (SIRS) as a consequence of an experimental septic shock. To prevent the sepsis-induced DIC we co-infused the thrombin inhibitors AT III or rec. hirudin in combination with C1 INH. Coinfusion of C1-inhibitor (50-200 U/kg x h) with either rec. hirudin or AT III significantly improved survival rate compared to thrombin inhibitor alone.
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PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80

Several lines of evidence suggest that coagulation may induce the release of thrombopoietin (TPO) into plasma and that TPO levels are higher in disseminated intravascular coagulation. Therefore we set out to illuminate the mechanism of TPO release in the setting of experimental endotoxemia, which induces activation of coagulation and platelets. Endotoxin (lipopolysachharide [LPS], 2 ng/kg) was infused into a total of 54 healthy men in two subsequent studies. Volunteers received infusions of unfractionated heparin, low-molecular-weight heparin, lepirudin, or placebo in a randomized, placebo-controlled fashion after bolus injection of LPS. TPO levels increased on average by 27% to 38% in all groups at 6 hours (P <.05 vs baseline), although all active drugs effectively blocked coagulation. Platelet counts dropped by about 15% at 1 hour after LPS infusion, recovered after 2 days, and exceeded baseline values by 8% to 18% after 7 days (P <.001 vs baseline for all groups). Yet lepirudin blunted the LPS-induced increase in circulating P-selectin by one half (P <.005 vs placebo), whereas both heparins did not diminish the increase in this platelet or endothelial activation marker as compared with placebo. Endotoxemia enhances TPO plasma levels independent of the degree of coagulation induction, which eventually results in increased platelet numbers. Of potential clinical interest is the observation that the direct thrombin inhibitor lepirudin, in contrast to heparins, mitigated LPS-induced platelet activation.
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PMID:Effects of anticoagulation on thrombopoietin release during endotoxemia. 1115 25

HIT type II is one of the severe complications of heparin therapy. The antibody for the heparin-PF 4 complex, which causes thrombocytopenia of less than 100 x 10(3).microliter-1, thrombosis and DIC-like symptoms, is produced. We managed the patient with HIT type II, who underwent off-pump CABG using argatroban, a direct thrombin inhibitor, as an anticoagulant. Intraoperative activated coagulation time (ACT) was maintained above 250 sec with 5.0 micrograms.kg-1.min-1 of argatroban infusion and all the procedures were successful. We also investigated the platelet count in the 100 patients with heparin therapy in CCU. The incidence of the platelet depression after heparin administration was as high as 59%, and in 12% of the patients the platelet count dropped below 100 x 10(3).microliter-1. In conclusion, thrombocytopenia by heparin therapy is not rare, and argatroban as an anticoagulant during off-pump CABG is thought to be useful.
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PMID:[Intraoperative management for a patient with heparin-induced thrombocytopenia (HIT) undergoing off-pump coronary bypass surgery using argatroban, a direct thrombin inhibitor]. 1184 Jun 59

The current management of thrombotic and vascular disorders has been strongly influenced by the introduction of several new drugs. 1. One of the major impact in the management of venous thromboembolic disorders has been the LMWHs. The newest, third generation heparin, the pentasaccharide inhibits specifically FXa. The elimination half-life of pentasaccharide is about 17 h, which allows a convenient once-daily dosing regime. The effects of pentasaccharide needs antithrombin. 2. Melagatran dipeptid is a specific, reversible direct thrombin inhibitor. It inhibits free and clot bound thrombin. Ximelagatran is a prodrug of melagatran. It is the first clinically used orally acting direct thrombin inhibitor. 3. Recombinant human activated protein C (rh-APC) has some advantages in patients with septic DIC. Qualities of the three new anticoagulants and clinical experiences with them have been summarized.
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PMID:[New anticoagulants in clinical practice]. 1563 34


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