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)

Both deep venous thrombosis and DIC are intermediate mechanisms of disease--both are a consequence of the deposition of fibrin-rich material in blood vessels some distance from the primary site of tissue destruction. The great difference in the sites of fibrin deposition may depend on the extent and site of activation of the clotting mechanism. DIC likely occurs in the fluid phase of the blood as a consequence of massive fibrin formation while thrombosis results from limited fibrin formation at the interface between blood and vessel wall. Leukocytes may be essential for attaching thrombi to the vessel wall in many places.
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PMID:The intravascular generation of fibrinogen derivatives and the blood vessel wall in venous thrombosis and disseminated intravascular coagulation. 14 74

44 patients were treated with subcutaneous ancrod (Arwin) for peripheral arterial occlusive disease (Fontaine stage III). An acute fulminating arterial occlusion occurred in two patients on the 10th and 23rd days respectively, and in a third patient a deep venous thrombosis developed in the leg on the 45th day after beginning treatment. Accordingly, vascular occlusion must be expected during defibrination in the presence of poor peripheral drainage conditions and if the serum fibrinogen can no longer be maintained below 1.0 g/1 in spite of increasing the ancrod dosage. Under these circumstances the treatment must be terminated.
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PMID:[Thrombotic arterial and venous obstructions under ancrod (Arwin) therapy (author's transl)]. 65 69

Seventeen patients undergoing elective total hip or knee joint replacement were given enoxaparin prophylaxis against deep vein thrombosis. Four patients developed clinical evidence of deep vein thrombosis, confirmed by venography. Two patients developed disseminated intravascular coagulation.
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PMID:Enoxaparin prophylaxis for deep vein thrombosis in orthopaedic surgery. 131 65

Low molecular weight heparins are increasingly prescribed in France. Prepared from standard heparin by depolymerisation, they show a markedly decreased anti IIa activity and a anti Xa/anti IIa ratio ranging from 2 to 4. Their mode of action in the coagulation system is still not well known and it is difficult to explain the mechanism of their antithrombotic effect, demonstrated in vivo. They seem to inhibit the first traces of thrombin and then counteract the priming and amplification of coagulation. Their fibrinolytic activity is also a disputed question, but seems to be lower than that of standard heparin. The pharmacological studies show a venous as well as arterial antithrombotic activity of a low molecular weight heparin on several animal models, a lower but not negligible bleeding risk as compared to unfractionated heparin. Furthermore heparin fragments have a weak interaction with platelets, which allow to foresee a greater efficacy of LMWH than standard heparin in arterial thrombosis. Some very rare cases of thrombocytopenia in patients treated with LMW heparins have been recently reported. The compared pharmacokinetics of heparins gave proof of a renal elimination of low molecular weight heparin and a bio availability of about 90% after subcutaneous injection. Many clinical studies allowed to define indications of heparin fragments in prophylactic treatment after surgery as well as in medical patients and in curative treatment in case of deep vein thrombosis. However, others studies must be carried out to define the real efficacy of such a treatment during pulmonary embolism, disseminated intravascular coagulation and myocardial infraction, or during thrombotic complications after vascular surgery.
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PMID:[The new heparins]. 131 47

An unusually prolonged case of heparin-induced severe thrombocytopenia and decompensated disseminated intravascular coagulation (DIC) is described. The patient, treated with heparin at a dosage of 25,000 units/day for 3 days and 12,500 units/day for an additional 4 days because of a clinically suspected deep venous thrombosis, developed (4 days after the discontinuation of heparin) a clinical and laboratory picture of severe DIC, manifested by subcutaneous hematomas and ecchymoses. Platelet count was 24 x 10(9)/l, fibrinogen level 89 mg/dl and fibrin-degradation products between 3,200 to 6,400 ng/ml. A thorough laboratory and instrumental evaluation failed to demonstrate any underlying disorder. No heparin-dependent aggregating factor was detected in the serum of the patient. The patient recovered spontaneously. Whereas fibrinogen and fibrin-degradation products reverted to normality within four weeks, platelet count normalization was delayed until the sixth week after heparin discontinuation.
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PMID:An unusually prolonged case of heparin-induced thrombocytopenia and disseminated intravascular coagulation. 139 4

The D-Dimer (D-D) assay for measuring cross-linked fibrin degradation products is now available for the clinical laboratory. We combined this assay with other tests to assess patients with diagnosed or suspected DIC. Also, a small group of patients (20) with deep venous thrombosis (DVT) were studied. The D-D test, antithrombin-III assay, FDP titer, fibrinopeptide-A level, protamine sulfate test, fibrinogen, prothrombin time, and activated partial thromboplastin time were used. The D-D test was abnormal in 93.7%, the AT-III level was abnormal in 87.5%, the fibrinopeptide-A level was abnormal in 89.5%, and the FDP titer was elevated in 83.7% of patients with DIC. When assessing patients found not to have confirmed DIC the D-D assay was abnormal in 20%, the AT-III level was abnormal in 6%, and the fibrinopeptide-A level was elevated in 13%. We conclude the D-Dimer assay to be a useful molecular marker of hemostasis in diagnosing DIC and this test will often discriminate between those patients with or without DIC, especially when used with the AT-III and fibrinopeptide-A assays. Of the battery of tests used in this study, the most useful, in descending order of efficacy, appear to be the D-dimer assay (93.7% abnormal), the fibrinopeptide-A titer (89.5% abnormal), the AT-III level (87.5% abnormal), and the FDP titer (83.7% abnormal). Of the global tests, the diagnostic efficacy of the prothrombin time activated partial thromboplastin time, and protamine sulfate test were no greater than chance and appear to be of little use in aiding in a diagnosis of DIC. Also, the D-Dimer assay is similar in cost to the FDP titer and is cost effective for the routine clinical laboratory.
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PMID:Diagnostic efficacy of the D-dimer assay in disseminated intravascular coagulation (DIC). 163 67

The haemostatic balance can basically be described as the equilibrium between fibrin formation (coagulation) and fibrin lysis (fibrinolysis). The status of this balance may therefore be reflected by the products of these two processes. Until recently, the tests for assessment of fibrin(ogen) degradation products were performed in serum since they were based on polyclonal antibodies, which cross-react with fibrinogen. However, the use of serum introduces many artefacts so the utility of these serum tests is limited. New assays have now become available, which can be divided into quantitative enzyme immunoassays (EIAs) and semi-quantitative latex agglutination assays. The new assays can be carried out in plasma since they use highly specific monoclonal antibodies, the majority of which do not cross-react with fibrinogen. This makes it possible to avoid the serum artefacts. Furthermore, these plasma assays can discriminate between degradation products of fibrin and those of fibrinogen (FbDPs and FgDPs, respectively). The possible clinical utility of the new assays is discussed on the basis of literature data on the following clinical states: deep venous thrombosis (DVT) and pulmonary embolism, liver disease and liver transplantation, sickle cell disease, renal diseases, pregnancy and preeclampsia, disseminated intravascular coagulation (DIC), malignancy, coronary artery disease and thrombolytic therapy. Fibrinolysis appears to be accompanied by fibrinogenolysis. Detection of fibrin(ogen) derivatives may be used to rule out DVT and to monitor efficacy of anticoagulant treatment for DVT or DIC, and reflects severity of renal disease but not renal function. High levels of FgDPs were found during orthotopic liver transplantation and thrombolytic therapy. Fibrin(ogen) degradation products cannot be used to predict reperfusion following thrombolytic therapy. The fibrinolytic system remained active during normal and complicated pregnancy and in patients with malignancies. The new assays provide valuable information on fibrin(ogen)olysis in several diseases. More information on the haemostatic balance may be obtained by using these new assays for fibrin(ogen)olysis products in combination with assays for coagulation products.
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PMID:Monoclonal antibody-based plasma assays for fibrin(ogen) and derivatives, and their clinical relevance. 210 91

Protein C (PC) is the central component of a major antithrombotic regulatory system with both anticoagulant and profibrinolytic properties. A deficiency of PC is one of several hereditary abnormalities of haemostatic proteins that have been described in patients with a propensity for thromboembolic complications. Major morbidity is often seen in these patients. The various aspects of hereditary PC deficiency in terms of clinical presentation, genetics, diagnosis and treatment of both homozygous and heterozygous states will be presented. In heterozygous deficiency, the levels of plasma PC are usually between 35% and 65% of normal, whereas the majority of normal individuals have levels between 70% and 130%. PC-deficient patients usually develop venous thrombotic complications between the ages of 15 and 40 years with a high incidence of DVT and pulmonary embolism. The majority of thrombotic lesions appear to develop spontaneously; others are associated with trauma, surgery or pregnancy. Treatment of symptomatic patients is initial heparin therapy followed by coumadin. After multiple thrombotic events, lifelong oral anticoagulant therapy is necessary. The potential complications of treatment are coumadin-induced skin necrosis, heparin-induced thrombocytopenia and bleeding. Homozygous PC deficiency, a rare but fatal hereditary condition, manifests itself with massive DIC and purpura fulminans in the newborn period. Effective treatment for these infants can be instituted with either oral anticoagulant therapy or PC replacement. The heterozygous deficiency of PC is similar to that found in other inherited disorders in that several genetic mechanisms are responsible for the expression of the disease. Both quantitative and qualitative decreases in PC exist, the former being type I deficiency and the latter, type II. The best initial diagnosis of either form involves a clotting (functional) assay while differentiation between the two also requires an antigenic (immunological) assay. Autosomal inheritance with significant variable penetrance is found with profound clinical implications. In summary, PC deficiency is one of a group of inherited disorders termed hereditary thrombotic disease, which may have serious implications for patient morbidity and mortality.
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PMID:Hereditary protein C deficiency: a review of the genetics, clinical presentation, diagnosis and treatment. 210 16

Changes of blood coagulation in 32 cases of SLE were investigated. Abnormalities frequently found were elevation of blood fibrinogen, FDP, V111R: Ag levels, prolonged or shortened KPTT time, and depressed AT-III value. Half of the patients with SLE showed laboratory changes compatible with the diagnostic criteria of DIC, but acute DIC was encountered clinically only in 2 cases hypercoagulation state or hypercoagulation with lower fibrinolysis, however were frequently seen. Lupus anticoagulant were detected in 6 patients and deep vein thrombosis of lower extremity in 1 patient. Examination of blood coagulation in patients with SLE was, therefore, of clinical importance.
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PMID:[Blood coagulation changes in systemic lupus erythematosus]. 212 40

We developed an ELISA to quantitate complexes of activated protein C (APC) with a major plasma APC inhibitor, alpha 1-antitrypsin (alpha 1AT) in human plasma based on the sandwich principle using two different antibodies directed towards protein C and alpha 1AT, respectively. This ELISA test was specific for APC:alpha 1AT complexes and sensitive to greater than or equal to 150 pg complex. Fifty-one of 56 healthy donors had APC:alpha 1AT complex levels above the detection limit (3 ng/ml) ranging from 4 to 14 ng/ml (mean value +/- SD: 7.6 +/- 2.5 ng/ml). Patients (n = 10) with disseminated intravascular coagulation (DIC) had detectable levels of APC:alpha 1AT complex ranging from 21 to 125 ng/ml (median: 69 ng/ml). Complexes of APC with plasma protein C inhibitor (PCI) were also measured using an ELISA sandwich assay. None of the 30 healthy donors had detectable levels (greater than or equal to 5 ng/ml) of APC:PCI complex, and plasma samples from 9 of 10 DIC patients had detectable concentrations of APC:PCI complex ranging from 10 to 63 ng/ml (median: 22 ng/ml). APC:alpha 1AT complex was detected in 25 of 26 patients with deep venous thrombosis (DVT), with levels ranging from 5 to 136 ng/ml (median: 23 ng/ml), whereas APC:PCI was detected in only 6 DVT patients, with levels between 11 and 105 ng/ml. PCI antigen levels in 70 normals ranged from 56 to 175% (mean +/- SD: 99.1% +/- 24.2%). PCI antigen levels were decreased in DIC patients, in patients with cerebral arterial thrombosis, and in DVT patients undergoing heparin therapy, but not in patients with myocardial infarction. PCI antigen levels were decreased much further in DVT patients receiving heparin compared to those not receiving heparin, showing that heparin therapy is associated with a decrease in PCI levels. The detection in normal subjects and in thrombotic patients of circulating APC:inhibitor complexes supports the view that the protein C pathway is activated during DIC and DVT. Moreover, it emphasizes that both PCI and alpha 1AT are physiologic inhibitors of APC. Thus, measurement of APC complexes may provide sensitive parameters for specific detection of activation of the clotting and protein C pathways.
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PMID:Determination of plasma protein C inhibitor and of two activated protein C-inhibitor complexes in normals and in patients with intravascular coagulation and thrombotic disease. 217 67


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