Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and the advances in preparation and sterilisation of the coagulation components on the other hand. Therefore, the indication for FFP and the various coagulation components deserves permanent consideration. FFP is still the therapeutical means of choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin dose required might cause an unacceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic agent, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity of accurate diagnosing is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement in the patient's therapy.
 ...
PMID:[Perioperative blood coagulation therapy and diagnosis]. 219 26

Early diagnosis and immediate treatment of the disease responsible for DIC are most important for successful therapy of DIC. Furthermore, it is also necessary to use anticoagulant agents in most cases of DIC. The agents may be classified on the basis of their mode of anticoagulant action into three groups: ones with antithrombin effect, ones with anti-Xa effect or ones with both effect, and each agent is hoped to be chosen appropriately for development of DIC in near future. At present, such anticoagulant agents as standard heparin, antithrombin-III concentrate, gabexate mesilate, nafamostat mesilate, MD-805, low molecular weight heparin, heparan sulfate, activated protein C, are known as drugs for DIC, and each of them was effective for improvement from DIC in our experience. Antifibrinolytic agents, which have been considered to be contraindicated for therapy of DIC, may be good indication for selected cases of DIC with enhanced fibrinolysis such cases as acute promyelocytic leukemia. Antiplatelet agents may be available for some cases of chronic DIC.
 ...
PMID:[Treatment of disseminated intravascular coagulation]. 221 66

Patients with acute myeloid leukemia have multiple hemostatic and thrombotic complications, which may or may not result from disseminated intravascular coagulation. Previous studies incorporating routine coagulation analyses failed to detect any clinically useful information in most of these patients. In this study, the first comprehensive evaluation of the various aspects of the hemostatic system in a population of patients with acute myeloid leukemia was performed. Eighteen patients (23-71 years of age) were studied at either diagnosis or relapse. Hemostatic studies were performed at onset and on days 3, 7, and 30 after initiation of therapy. The bone marrow blast counts ranged from 8% to 98%; prothrombin time and activated partial thromboplastin time showed only minor prolongations in a few of these patients. However, in all patients measurement of platelet-associated markers revealed elevated platelet factor 4 and thromboxane B2 and normal 6-keto-prostaglandin F1 alpha levels. Fibrinolytic markers showed an increase in D-dimer and tissue plasminogen activator and a decrease in alpha 2-antiplasmin levels. Plasminogen, plasminogen activator inhibitor, and fibrinogen levels were normal. Coagulation markers demonstrated a decrease in protein C and antithrombin III levels and an elevation of the thrombin-antithrombin complex. The pretreatment values for all hemostatic markers studied were similar to the values obtained on days 3, 7, and 30 during treatment. This investigation demonstrated a subclinical activation of the components of the hemostatic system possibly leading to a hypercoagulable state. Although only six patients (33%) experienced hemorrhagic complications, the risk of bleeding and/or thrombosis was strongly evident in all patients. The significance of finding abnormal levels of specific molecular markers of hemostasis will be established in the future application of such markers in clinical evaluations of leukemic patients known to be at risk for coagulation disorders.
 ...
PMID:Global and molecular hemostatic markers in acute myeloid leukemia. 222 Jun 67

41 patients with hereditary and acquired antithrombin II deficiency received a substitution therapy with human plasma fraction of antithrombin III from the GDR blood-transfusion service. In 6 patients a hereditary AT III deficiency was substituted and in this context the substitution in case of thromboses during pregnancy was explained. 35 patients with acquired AT III deficiency were substituted with AT III concentrate because of thromboembolic complication in the macro-circulatory system in case of AT III deficiency due to reduced synthesis, loss, increased consumption or a combination of these conditions or because of DIC. The substitution effect was good. Dosage and injection intervals depend on the clinical condition. Side-effects have not been observed.
 ...
PMID:Treatment with AT III concentrates in hereditary and acquired AT III deficiency. 246 21

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and advances in the preparation and sterilization of coagulation components on the other. Therefore, the indication for FFP and the various coagulation components deserves constant consideration; this is the intention of this paper. FFP is still the therapeutic choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin doses required might entail an unexceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic factor, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity for an adequate diagnostic procedure is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement of the patient's therapy.
 ...
PMID:[The status of blood coagulation preparations within the scope of modern hemotherapy in surgical patients]. 248 30

Fatal multiple organ failure after severe infection may be related to an early activation of protease cascade systems. This study aimed to relate changes in coagulation, fibrinolysis, and kallikrein to shock and outcome. Of 53 patients with severe infection, 30 did not develop shock, 12 survived septic shock, and 11 died from organ failure after septic shock. No patient had overt disseminated intravascular coagulation. We measured 17 components of the coagulation/fibrinolysis/kallikrein pathways on admission and on the next 2 days. High values for fibrinogen, factor VIII:C, von Willebrand factor antigen, and D-dimer were seen in all patients; factor XII, prekallikrein, factor VII, antithrombin, protein C, and fibronectin were low. The patients thus appeared to be hypercoagulable. These disturbances were more pronounced in septic shock survivors, who also had low plasminogen and antiplasmin, indicating ongoing fibrinolysis. Nonsurvivors of sepsis were distinguished mainly by high plasminogen activator inhibitor values; this suggests an impaired functional fibrinolysis in fatal sepsis, with possible therapeutic implications. Cryoprecipitate infusion increased the fibronectin concentration, but did not influence the other factors studied.
 ...
PMID:Coagulation, fibrinolysis, and kallikrein systems in sepsis: relation to outcome. 250 62

We have evaluated the quantitative relationship between lipopolysaccharide (LPS, endotoxin), fibrinopeptide A (FPA), antithrombin (AT), protein C (PC) and extrinsic pathway inhibitor (EPI) in plasma from 39 consecutively admitted patients with systemic meningococcal disease (SMD). The most severely ill patients with fulminant meningococcal septicemia (n = 13, 6 dead) had significantly (p less than 0.01) higher plasma levels of LPS and FPA and lower levels of PC and AT on admission as compared with the less severe clinical presentations (n = 26, 1 dead). The levels of EPI on admission were significantly (p less than 0.05) higher in nonsurvivors vs survivors with fulminant septicemia. As the disease progressed, the levels of LPS, FPA, AT and PC declined, while the levels of EPI increased. Three of six nonsurviving septicemic patients had levels of EPI greater than 200% within 16 hours of admission vs two of 30 survivors (p = 0.02). The results suggest that increasing levels of LPS in SMD elicit increasing consumption coagulopathy, contributing to the organ pathophysiology. The kinetics of EPI, inhibiting the thromboplastin-FVIIa-FXa complex, differs markedly from the kinetics of AT and PC i.e. increases as opposed to decreases.
 ...
PMID:The quantitative association of plasma endotoxin, antithrombin, protein C, extrinsic pathway inhibitor and fibrinopeptide A in systemic meningococcal disease. 251 Mar 54

Six adult specific-pathogen-free cats were inoculated intraperitoneally with a cell culture-adapted strain of feline infectious peritonitis virus. Plasma samples were evaluated for antithrombin-III (AT-III) activities at post-inoculation days (PID) 0, 4, and 11 and at termination on PID 16 (1 cat) or 21 (5 cats). Other hemostatic values evaluated were activated partial thromboplastin times, prothrombin times, thrombin times, fibrinogen, platelet counts, and fibrin/fibrinogen degradation products. Antithrombin-III activity remained within normal or above normal range (89 to 246%) in all cats, with the exception of one cat on PID 4 (AT-III, 70%). Mean baseline AT-III activity for 6 cats at PID 0 was 123%. Mean AT-III activity on PID 4, 11, and 16 or 21 was 98, 162, and 130%, respectively. On PID 4 and 16 or 21, results of coagulation screening tests indicated that all cats had disseminated intravascular coagulation. Histologically, cats also had severe fibrinonecrotizing thrombovasculitis.
 ...
PMID:Evaluation of antithrombin-III activity as a coindicator of disseminated intravascular coagulation in cats with induced feline infectious peritonitis virus infection. 255 30

Both congenital and acquired antithrombin-III (AT-III) deficiencies are amenable to replacement therapy. We describe two antithrombins produced by recombinant DNA techniques from human alpha 1-antitrypsin (alpha 1AT) cDNA in yeast. Alteration of the alpha 1AT active site, replacing methionine 358 with arginine, results in a thrombin inhibition rate similar to that of heparin-activated AT-III. Alteration of two further residues, to give a five-residue sequence identical to AT-III, does not increase this rate further. Neither antithrombin is activated by heparin; both are unglycosylated and have shorter in vivo half-lives (t1/2) than human alpha 1AT. These antithrombins should be suitable for therapeutic replacement of AT-III in cases of congenital deficiency and in conditions associated with acquired AT-III deficiency, such as disseminated intravascular coagulation.
 ...
PMID:Characterization of antithrombins produced by active site mutagenesis of human alpha 1-antitrypsin expressed in yeast. 264 77

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
 ...
PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>