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)

The effectiveness of low-molecular weight heparin CY 216 in the prophylaxis of fatal pulmonary embolism in patients undergoing general surgery was assessed in a multicentre, double-blind, randomized, clinical trial against placebo. A total of 4,498 patients aged over 40 undergoing general surgery were enrolled in the 18 centres which took part in the trial. Patients received a single daily subcutaneous injection of 7,500 anti-Xa units I.C. of CY 216 or placebo two hours before surgery, 12 hours after the initial injection and then daily for at least seven days. A post-mortem examination had to be carried out in every patient who died. The two groups of patients were well-matched for age, sex, type of disease, site and duration of operation as well as for incidence of risk factors which could predispose to the development of thromboembolism. Twenty-six deaths were recorded and validated: eight (0.36%) in the CY 216 group and 18 (0.80%) in the placebo group (p less than 0.05). At the post-mortem examination, carried out in 23 patients (88.5%), two deaths were found to be directly due to pulmonary embolism (0.09%) in the CY 216 group and four (0.18%) in the placebo group. Pulmonary embolism contributed to death in four other placebo-treated patients. Pulmonary or extrapulmonary thromboembolism was a significantly less frequent direct cause of death (p less than 0.05) in the CY 216 group (two pulmonary embolisms) than in the placebo group (four pulmonary embolisms, one acute myocardial infarction, one disseminated intravascular coagulation, two ischemic cerebral strokes).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prophylaxis of fatal pulmonary embolism in general surgery using low-molecular weight heparin Cy 216: a multicentre, double-blind, randomized, controlled, clinical trial versus placebo (STEP). STEP-Study Group. 256 Apr 70

Plasma D-dimer was measured and compared with serum fibrinogen/fibrin degradation product levels (FDPs) in patients with disseminated intravascular coagulation (DIC) and other conditions associated with a hypercoagulable state. D-dimer (N less than 200 ng/ml) was elevated in all 43 patients with DIC, in 48 of 59 patients with liver disease, in 22 of 27 patients with acute leukaemia at presentation, in 17 of 23 patients with malignant disease, in 29 of 39 women in the third trimester of a complicated pregnancy, in 17 of 18 patients with deep venous thrombosis and in only four of 27 patients with acute myocardial infarction. There was a significant correlation between plasma D-dimer and serum FDP levels (P less than 0.01) as follows; DIC: r = 0.58, liver disease: r = 0.57, acute leukaemia: r = 0.84, malignancy: r = 0.87. The frequent elevation of D-dimer observed in liver disease, acute leukaemia, malignancy and complicated pregnancy indicates that a hypercoagulable state is a common occurrence in these conditions although in liver disease elevated levels resulting from a failure of normal clearance mechanisms cannot be excluded. The close relationship between D-dimer and FDP levels suggests that serum FDPs predominantly arise from the interaction of plasmin with crosslinked fibrin rather than with fibrinogen in the conditions in which these were compared.
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PMID:Plasma D-dimer levels and their relationship to serum fibrinogen/fibrin degradation products in hypercoagulable states. 291 30

We describe three patients who developed severe disseminated intravascular coagulation associated with large ventricular mural thrombi shortly after presenting with acute myocardial infarction. To our knowledge this association has not been reported before.
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PMID:Severe disseminated intravascular coagulation associated with massive ventricular mural thrombus following acute myocardial infarction. 325 21

An enzyme immunoassay was used for a study of the time course of the content of fibrinogen degradation products (FDP) and free hemoglobin (fHg) in the blood of patients with acute myocardial infarction (AMI) during uncomplicated hospital rehabilitation. A considerable increase in the levels of FDP in the blood serum and fHg in the blood plasma of the AMI patients were noted. These levels were particularly high on the 6-12th day of rehabilitation with further fluctuations on the 22-24th day from the beginning of disease resulting from an increase of the patients' motor activity during rehabilitation which might cause the depletion of endothelial reserves of fibrinolysis activators and an increase in thrombinemia, however changes in the content of FDP and fHg in the blood were more likely associated with DIC-syndrome inherent fluctuations in the system of hemostasis. The content of FDP and fHg in the blood of AMI patients was recommended to be used as a marker of DIC-syndrome and assessment of corrective therapy.
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PMID:[Fibrinogen and fibrin degradation products in the blood of acute myocardial infarct patients at the hospital rehabilitation stage]. 332 76

Venous and arterial coagulation and fibrinolytic activity, particularly total hemostatic potential, its plasma and platelet constituents, and functional platelet properties were examined within the first hours of acute myocardial infarction in 106 patients. Those were divided into groups with uncomplicated, recurrent and spread myocardial infarction, and with cardiogenic shock. Early signs of disseminated intravascular coagulation were registered within the first hours of the disease in the venous (more prominently) and arterial (less prominently) channels. True cardiogenic shock is associated with more apparent symptoms of the disseminated intravascular coagulation syndrome in venous and arterial blood.
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PMID:[Arteriovenous differential in the indices of hemocoagulation homeostasis in patients with acute myocardial infarct with a protracted course and cardiogenic shock]. 341 57

In a case of acute promyelocytic leukaemia presenting with an acute myocardial infarction a fibrin-platelet thrombus was demonstrated postmortem in the anterior descending branch of the left coronary artery. The possible pathogenesis of thrombus formation in the face of disseminated intravascular coagulation and thrombocytopenia is discussed.
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PMID:Acute promyelocytic leukaemia associated with acute myocardial infarction. A case report. 346 Jan 82

Increased fibrinopeptide A (FPA) levels have been reported in various non-thrombotic disorders, including cancer, acute myocardial infarction, liver cirrhosis and collagen vascular diseases. To investigate the significance of these findings, the present study combined the radioimmunoassay of FPA with that of fibrinogen/fibrin degradation fragment E (FgE) in the aforementioned disorders and compared the results with those observed in healthy subjects as well as in patients with thromboembolism and overt disseminated intravascular coagulation (DIC). Mean FPA and FgE in malignancy were 6.3 and 305 ng/ml, in myocardial infarction 5.6 and 98 ng/ml, in liver cirrhosis 2.7 and 132 ng/ml and in collagen vascular diseases 5.6 and 142 ng/ml. All these values were significantly higher than in healthy controls (mean FPA 1.6 ng/ml, mean FgE 49 ng/ml) but significantly lower than in thromboembolism (mean FPA 10.7 ng/ml, mean FgE 639 ng/ml). and DIC (mean FPA 22.0 ng/ml, mean FgE 1041 ng/ml). The overall correlation between FPA and FgE was highly significant. However, different disorders showed peculiar patterns in FPA, FgE and fibrinogen levels. In malignancy, a definite increase of FPA, FgE and plasma fibrinogen levels was observed. This finding probably indicates a compensated state of (intra- or extravascular) fibrin formation and lysis. Acute myocardial infarction was characterized by a high FPA to FgE ratio, which is interpreted to reflect acute thrombin generation and fibrin formation. FPA in cirrhosis was only marginally elevated with most single values within the normal range, indicating that intravascular coagulation was infrequent and unimportant in quantitative terms.
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PMID:Relationship between fibrinopeptide A and fibrinogen/fibrin fragment E in thromboembolism, DIC and various non-thromboembolic diseases. 367 28

Eighteen patients whose mean age was 61 years were referred to us with acute aortic occlusion from 1977 to 1985. Ten patients had cardiac emboli (group I) and eight had aortoiliac occlusive disease (group II). Fourteen of these patients had paresis or paralysis. Diagnosis was prompt but the time lapse from onset of symptoms to revascularization averaged 18 hours (group I, 10.3 hours; group II, 26.1 hours). All 10 patients in group I had embolectomy alone; of the eight patients in group II, two had transfemoral thrombectomy and six had bypass procedures. The perioperative mortality rate was 40% in group I and 62.5% in group II. Complications developed in 12 patients (nine died); renal failure occurred in 11, compartment syndrome in nine, adult respiratory disease syndrome in three, acute myocardial infarction in three, disseminated intravascular coagulation in two, and paraplegia in one. No amputations were required in the nine survivors and limb function was restored in eight of these patients. Acute aortic occlusion sets in motion a chain of events that threatens life and limb. Prompt diagnosis and revascularization by the simplest operation are required to decrease morbidity and mortality.
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PMID:Acute aortic occlusion--a multifaceted catastrophe. 374 30

A significant correlation was found between heightened plasma viscosity and increased red blood cell aggregation and the severity of coronary artery disease. At low shear rates and exhausted vasomotion these rheological factors can cause a reversible loss of fluidity. The reduced fluidity may induce a limitation in microcirculatory flow due to the viscus resistance. Rheological treatments aim at restoration of impaired perfusion by decreasing plasma viscosity and thus diminishing red blood cell aggregation. Further therapeutic measures tend to improve red blood cell deformability. Because of limited coronary reserve in coronary artery disease hemodilution therapy is contraindicated except the cases with polyglobulia. Thrombolytic therapy in acute myocardial infarction causes a significant reduction of plasma viscosity and red cell aggregation for at least 72 hours. This improvement in blood fluidity may beneficially influence the reperfusion of ischemic areas. A therapy with orally active hemorheological drugs (pentoxifylline and buflomedil) can be discussed as an additive treatment in severe angina pectoris refractory to specific medical therapy, since these drugs increase fluidity and inhibit platelet aggregation. The defibrination may cause thrombotic and bleeding complications in the early phase of treatment. Coronary small vessel disease represents a rare type of coronary heart disease. This disease is defined by normal epicardial coronaries and reduced coronary artery reserve. In disorders of coronary microcirculation with abnormal rheology (Waldenstrom's macroglobulinemia) rheological treatment is a rational and causal therapy.
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PMID:[Hemorheologic therapy applications in coronary heart disease]. 382 69

A new method is described for identifying low concentrations of circulating derivatives of fibrinogen and fibrin, even when present in heterogeneous mixtures. This technique is applicable to plasma and serum and uses electrophoresis in 2% agarose in the presence of sodium dodecyl sulfate (SDS) followed by immunological identification of separated derivatives, using radiolabeled antifibrinogen antiserum and autoradiography. Unique electrophoretic patterns distinguish plasmic derivatives of crosslinked fibrin from those of fibrinogen and also identify crosslinked fibrin polymers produced by the combined action of thrombin and factor XIII on fibrinogen. The assay is sensitive to a concentration of 0.1 micrograms/mL of fibrinogen in serum or plasma. Fibrin polymers, plasmic degradation products of fibrinogen, and plasmic degradation products of crosslinked fibrin were detected in the plasma or serum of a patient with disseminated intravascular coagulation. Plasmic derivatives of both fibrinogen and crosslinked fibrin appeared in serum in the course of fibrinolytic therapy for pulmonary embolism, whereas during acute myocardial infarction a marked increase in the proportion of fibrin polymers in plasma was found in comparison with normal controls. Thus, the procedure can distinguish between the simultaneous processes of fibrin polymer formation, fibrinogenolysis, and fibrinolysis, and is sufficiently sensitive to detect relevant quantities of derivatives in pathologic conditions.
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PMID:Specific identification of fibrin polymers, fibrinogen degradation products, and crosslinked fibrin degradation products in plasma and serum with a new sensitive technique. 397 Oct 42


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