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)

In Western countries, hepatic vein thrombosis (Budd-Chiari syndrome) is, as a rule, an uncommon though well-known complication of acquired or hereditary thrombophilia. It may be complicated by overt defibrination when secondary to deep venous thrombosis ascending to the vena cava. To be effective treatment should consist of early initial intensive thrombolysis for up to one week, followed without interruption by an APTT-controlled heparin infusion. Oral anticoagulant therapy is started together with the heparin, which should not be discontinued until the prothrombin times, expressed as international normalized ratios (INR), lie within a therapeutic range of 3-5 INR for 2 days, the target being 4 INR. After this intensity of anticoagulation has been maintained for three weeks, the range may be lowered to 2.5-4 INR, the target being 3 INR. Oral anticoagulation should be continued for as long as thrombophilia persists.
 ...
PMID:[Fibrinolytic and anticoagulation therapy in Budd-Chiari syndrome. Review and recommendations]. 312 3

Protein C and protein S serve as natural anticoagulants. Deficiencies of these proteins are often associated with recurrent deep vein thrombosis and coumarin induced skin necrosis. These two proteins function by selectively inactivating factors Va and VIIIa, two of the "cofactors" of blood coagulation. Hence, inhibition of coagulation by this pathway complements the better known inhibition mediated by the antithrombin III-heparin system. These observations suggest that protein C and/or activated protein C may prove useful in controlling thrombosis and/or DIC. We have developed a Ca2+ dependent monoclonal antibody which allows the rapid isolation of human protein C. This rapid isolation has allowed us to demonstrate that activated protein C can protect baboons from the lethal effects of E. coli/endotoxin and that protein C supplementation can minimize fibrinogen consumption following tissue factor infusion into dogs.
 ...
PMID:Protein C, isolation and potential use in prevention of thrombosis. 330 68

A four year old girl presented with varicella gangrenosa, and haematological investigations showed a disseminated intravascular coagulation. The child subsequently developed a unilateral deep venous thrombosis. She was treated with oral steroids and intravenous heparin and made a full recovery.
 ...
PMID:Varicella gangrenosa. 336 17

A simple assay method of heparin cofactor II (HC II) activity is described. The procedure is based on the following principle: Antithrombin III (AT III) in plasma is inactivated by addition of an IgG fraction of goat serum after immunization of the animals against human AT III. Complete inactivation of AT III could be shown by absence of an anti Xa-effect of heparinized plasma treated with this antibody. Thrombin was only partially inhibited after inactivation of AT III. The characteristics of this inhibition were typical for the action of HC II. This method was applied for an assay of HC II activity. After optimizing of the method practical application in clinical routine screening was carried out. A diminution of HC II was observed in liver cirrhosis and in DIC but not in AT III deficiency. In 15 out of 269 cases of recurrent DVT there were HC II activities below 70% of normal. In 4 out of these patients activities of HC II were repeatedly between 44% and 52%. In arterial obstructive disease there was an HC II activity of less than 60% in 18 out of 583 patients and in 11 of them the HC II levels were repeatedly between 45% and 54%.
 ...
PMID:Heparin cofactor II: a simple assay method and results of its clinical application. 342 87

We conducted an evaluation of the hemostatic integrity of patients with untreated cancer of the prostate. Of 60 patients analyzed retrospectively, only 1 had a mild case of disseminated intravascular coagulation, possibly associated with concomitant estrogen therapy, and in 1 patient mild deep vein thrombosis developed preoperatively, also possibly associated with multiple medications for concurrent disorders. Of 16 other patients prospectively evaluated on admission, only 1 had frankly abnormal levels of fibrinopeptide A unaccompanied by other coagulation abnormalities. Occasional individuals had minimal, negligible deviations of partial thromboplastin times, thrombin time, or antithrombin III values. In none of these patients did hemostatic complications develop during their hospital stay. These results demonstrate that although an occasional coagulation abnormality may occur in patients with cancer of the prostate (albeit with a lower incidence than in other neoplasms), this malignancy does not require increased precautions with respect to those given to the patient population at large.
 ...
PMID:Untreated prostatic carcinoma is not associated with frequent thrombohemorrhagic disorders. 360 3

Numerous investigators have postulated that a hypercoagulable state exists in humans for a period of time before the development of thrombotic episodes. A clear biochemical definition of the prethrombotic state, however, has proved elusive due in part to the lack of reliable techniques for monitoring pertinent changes in blood coagulability. Based on recent advances in our knowledge of the biochemistry of the coagulation system, a series of highly sensitive and specific immunochemical tools has been developed that can quantitate the activities of various steps of the hemostatic mechanism in vivo at the subnanomolar level. We have established assays for F1+2 and the protein C activation peptide, which measure the cleavage of the prothrombin molecule by factor Xa and the scission of protein C by the thrombin-thrombomodulin complex, respectively. Nossel and coworkers had previously constructed similar assays for fibrinopeptide A (FPA) and fragment B beta 1-42, which monitor the cleavage of fibrinogen by thrombin and the proteolysis of fibrin I by plasmin, respectively. Substantial elevations in the levels of these markers have been found in patients with disseminated intravascular coagulation and many subjects with acute deep venous thrombosis. The F1+2 and FPA assays have been used to demonstrate that significant increments in factor Xa activity but not thrombin activity regularly occur in the blood of nonanticoagulated individuals with congenital deficiencies of antithrombin or protein C. These two disorders are known to be correlated with the subsequent development of thrombosis. Patients with protein C deficiency have also been noted to have significantly reduced plasma levels of protein C activation peptide. By using the immunoassays for FPA and B beta 1-42 in studies of postoperative patients, it has been shown that an imbalance between the procoagulant action of thrombin and the anticoagulant effect of plasmin on fibrin I polymer may induce an acquired thrombotic diathesis. Finally, we have recently demonstrated that prothrombin activation as measured by the F1+2 assay is suppressed by oral anticoagulants in the blood of patients with thrombotic diatheses. These investigations suggest that these assay techniques can be used to improve our understanding of the hypercoagulable state as well as to develop more effective treatment strategies for the prevention of thromboembolic events.
 ...
PMID:The pathophysiology of the prethrombotic state in humans: insights gained from studies using markers of hemostatic system activation. 360 75

Antithrombin-III assays are performed to assess response to heparin therapy and efficacy of antithrombin concentrate therapy and in diagnosing hereditary thrombophilia, deep venous thrombosis, pulmonary embolus, and disseminated intravascular coagulation. Synthetic substrate assays for antithrombin-III are the methods of choice; however, most existing assay systems are semiautomated. A fully automated, antithrombin-III assay using the Kabi Chromogenic Synthetic Substrate S-2238 COATEST on the MULTISTAT III has been developed. This assay was compared with the Dade Protopath fluorometric assay. The correlation (r-sq) between the two assay systems was 0.82. Additionally, a three-way assay comparison was also performed, incorporating a new fluorometric substrate for antithrombin-III. The three-way comparative assays revealed correlation as follows: MULTISTAT III fluorometric assay and the MULTISTAT III/Kabi COATEST assay r-sq = 0.90; MULTISTAT III fluorometric assay and the Dade fluorometric assay r-sq = 0.86; and the MULTISTAT III/Kabi COATEST assay and the Dade Protopath fluorometric assay r-sq = 0.95. These automated assays were extremely cost effective and were a fraction of the cost of performing other types of antithrombin-III assays.
 ...
PMID:Fully automated antithrombin-III assays by synthetic substrate on the Multistat III. 361 51

The significance of acquired antithrombin III (AT III) deficiency must be interpreted in close relation to the underlying disease process. In patients with acute or chronic liver impairment, the AT III activity is related to a decrease of procoagulatory factors, whereas, in protein loss syndromes such as nephrotic syndrome, the AT III indicates an increased risk of thromboembolic events. The effect of oral contraceptives (OC) on AT III levels in young healthy females (n = 30) was determined prospectively. AT III decreases during OC usage could not be related to the estrogen content of the examined oral contraceptives, and there was no parallel decrease of AT III activity and concentration in each type of OC. In a prospective study, the extent of AT III decrease was determined in patients undergoing cardiopulmonary bypass operations (CPB) receiving different anticoagulant schedules during extracorporeal circulation (n = 49). There was no significant influence on the effectiveness of anticoagulation by the observed AT III decreases. AT III deficiency during CPB was primarily the result of hemodilution. However, the AT III kinetics were significantly influenced by the different protamin dosages and were not affected by the different heparin dosages. Correction of diminished AT III levels by substitution of AT III concentrates is beneficial in cases, in which an interruption of an enhanced coagulatory process such as disseminated intravascular coagulation is necessary or in patients requiring high dosage heparinization as in deep vein thrombosis. In those cases the quality of AT III correction correlates to the course of the disease. However, the potency of concentrates as well as the individual AT III recovery and half-life must be considered for an appropriate treatment with AT III substitution.
 ...
PMID:[Clinical aspects of acquired antithrombin III deficiency]. 371 7

Heparin-induced thrombocytopenia with thromboembolism calls for an immediate substitution of the heparin with other potent anticoagulants, such as coumarin derivatives. The occurrence of this adverse effect in pregnancy poses an additional dilemma because the use of coumarin derivatives is not acceptable during pregnancy, while other medications may not be as effective. In a pregnant patient treated with mucous sodium heparin for deep vein thrombosis, recurrent heparin-induced thrombosis and disseminated intravascular coagulation (DIC) occurred. Replacing the heparin with a different brand of the same drug resulted in reversal of the DIC and in clinical improvement. If severe heparin-induced thrombosis occurs in a patient in whom anticoagulation with other drugs is contraindicated, substituting one brand of heparin for another could be of value.
 ...
PMID:Heparin-induced thrombocytopenia and recurrent thrombosis in pregnancy. A case report. 378 42

A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.
 ...
PMID:Defibrination during warfarin therapy in a man with protein C deficiency. 383 6


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