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)

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

We studied functional protein C activity, both anticoagulant and amidolytic, as well as protein C antigen in 30 normal subjects, several members of a family with congenital protein C deficiency, 18 patients with severe preeclampsia, 27 patients with coronary heart disease, including 15 patients with myocardial infarction and 12 with angina pectoris, 20 patients on stable oral anticoagulant therapy (thrombotest values: 3-12%) and three patients with disseminated intravascular coagulation. Protein C values measured by the coagulant assay were compared to those obtained with amidolytic and immunochemical assays. In all the groups studied, the activity assays (amidolytic and coagulant) correlated significantly with each other as well as with the immunochemical assay. In patients on oral anticoagulant therapy the coagulant assay gave lower protein C values than amidolytic and immunochemical assays. A good correlation was found between immunological and amidolytic protein C assays (r=0.90, p less than 0.001), immunological and coagulant protein C assays (r=0.93, p less than 0.001), and amidolytic and coagulant protein C assays (r=0.95, p less than 0.001) in all the samples studied without including the protein C values of patients on oral anticoagulant therapy. These results allow us to recommend the functional protein C coagulant assay in patients on stable oral anticoagulant therapy because only this assay evaluates the "in vivo" protein C function in these patients.
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PMID:Assay of protein C in human plasma: comparison of amidolytic, coagulation, and immunochemical assays. 379 19

A case is described of disseminated intravascular coagulation in a premature female infant, with the unusual and predominating feature of myocardial infarction consequent upon coronary vein thrombosis.Some reference is made to the incidence of coagulation disorders in the newborn and to methods of histological diagnosis.
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PMID:Venous infarction of the myocardium in a newborn child: an unusual effect of disseminated intravascular coagulation. 412 32

Clinicopathologic correlations of nonbacterial thrombotic endocarditis (NBTE) were studied with special reference to their pathogenetic role in cerebral and myocardial infarction. In 2340 cases of consecutive autopsies of the aged, NBTE was observed in 217 cases or 9.3%. The age distribution of NBTE revealed a gradual increase with advancing age. The underlying diseases of NBTE were malignant neoplasm (51.6%), infection (28.3%) and other diseases (20.1%). The incidence of NBTE in each cancer was high in cancers of the colon (16.2%), pancreas (15.2%), gall bladder or bile duct (14.1%) and lung (13.0%). The vegetations of NBTE were found on the aortic valve in 46.1%, on the mitral valve in 40.6% and on the both valves in 8.3%. The incidence of myocardial infarction and scar was 51.2% in the NBTE group, while it was 38.6% in the non-NBTE control group (p less than 0.02). This difference was marked in patients with a small infarction (10.6% vs. 5.3%) and a myocardial scar (30.4% vs. 19.0%). The grade of coronary stenosis was less in the NBTE group than in the control group (p less than 0.001), suggesting that the origin of the myocardial ischemic lesion was embolism from NBTE. The incidence of large cerebral infarction was 14.7% in NBTE and 9.2% in the control group, and that of medium sized cerebral infarction was 35.0% and 23.6% respectively. In this latter group, cortical infarction comprised 57.9% in the NBTE group and 26.6% in the control group. In large cerebral infarction, cerebral atherosclerosis was less severe in NBTE than in the control group (p less than 0.001), also suggesting an embolic mechanism. Disseminated intravascular coagulation was found in 41.9% of NBTE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonbacterial thrombotic endocarditis as a cause of cerebral and myocardial infarction. 648 38

Three cases (one, newborn infant and two infants--one of them recently published--) who present electrocardiographic and enzymatic alterations comparative with diagnosis of ischemia and myocardial infarction are reported. Rarity of this entity in infants is stressed as most of published cases are secondary to ananomolous coronary artery. Etiology of the cases presented shows a myocardiac fibrosis with Schwachman's syndrome in one case, a coronary thrombosis secondary to a disseminated intravascular coagulation in a second case, and finally a generalized hypoplasia of coronary arteries. Hypoxia appears in these cases a factor acting in favour of myocardial ischemia. Diagnostic criteria of acute myocardial infarction are based on typical electrocardiogram and rise of isoenzymes of LDH and CPK-MB. Although rare, it is a diagnosis to be considered in cases of unknow cardiac insufficiency in newborns and infants.
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PMID:[Myocardial infarction and myocardial ischemia in newborn children and infants, not secondary to an abnormal coronary]. 666 Jun 44

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Multiple extremity gangrene developed in five patients as a complication of dopamine therapy. The clinical conditions were (1) penetrating chest trauma requiring pneumonectomy with postoperative sepsis, (2) cardiac arrest with aspiration pneumonia, (3) lymphoma with sepsis, (4) Klebsiella pneumonia, and (5) myocardial infarction. The development of acrocyanosis leading to gangrene occurred at dopamine dosages of 5.1 to 10.2 micrograms/kg/min. The alpha-adrenergic vasoconstriction effects of dopamine would not be expected from the doses employed in these patients. Thus, other factors beside pure alpha vasoconstriction are responsible for tissue necrosis after the use of dopamine. We believe that the embolic complications of disseminated intravascular coagulation and hypovolemia are serious risk factors in the development of dopamine gangrene. Peripheral vasoconstriction from dopamine, even at low doses, may set the stage for thrombotic complications of disseminated intravascular coagulation and lead to tissue damage. In laboratory models of disseminated intravascular coagulation, an alpha-adrenergic drug is required to produce peripheral ischemic tissue damage. Treatment of tissue ischemia related to dopamine depends on early recognition of acrocyanosis. Phentolamine, an alpha blocker, has been recommended for treating dopamine ischemia, either through local instillation into ischemic tissues or intravenous infusion. We recommend a high index of suspicion for, and early treatment of, underlying consumptive coagulopathy in all patients requiring dopamine.
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PMID:Dopamine gangrene. Association with disseminated intravascular coagulation. 730 16

The incidence and pathologic features of cardiac lesions in 184 autopsied aged patients with disseminated intravascular coagulation (DIC) were reported. Coronary thrombosis was noted in 31 (16.8%), fresh myocardial necrosis in 60 (32.6%) and massive myocardial hemorrhage in 49 (26.6%) of these patients. Fresh myocardial infarction was present in 16 (8.7%) patients, 13 of whom manifested coronary thrombosis. The site of thrombi deposition was closely related to preexisting stenotic lesions of the coronary arteries. Only 3 of 16 patients with disseminated intravascular coagulation and acute myocardial infarction had typical cardiac symptoms. In most patients, the electrocardiographic changes were equivocal or not diagnostic for the diagnosis of acute myocardial infarction. We suggest the possibility that coronary thrombi in disseminated intravascular coagulation may gradually increase in extent and severity, leading to confluent areas of myocardial necrosis. The possibility of death due to heart failure, arrhythmia or cardiac rupture, points to the importance of recognizing the frequent cardiac involvement in aged patients with disseminated intravascular coagulation.
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PMID:Disseminated intravascular coagulation in the aged complicated by acute myocardial infarction. 733 11

Important discoveries of the last twenty years indicate that blood platelets play an important role in the etiopathogenesis of many serious diseases. These include atherosclerosis with its acute vascular complications like myocardial infarction and many forms of disseminated intravascular coagulation. Their role is not limited here to platelet participation in thrombus formation. This is why we are constantly searching for a method which will allow to detect platelet activation in vivo before any important damage to vital organs and tissues will take place. Despite the implementation of sophisticated modern laboratory techniques reliable assessment of such activation poses still a clinical and laboratory problem.
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PMID:[Laboratory methods of estimating blood platelet activation]. 799 72

We have evaluated plasma F1+2 values by enzyme immunoassay (Enzygnost F1+2; Behringwerke) in 80 healthy blood donors in various ages and compared to that from patients with DIC, thrombosis and oral anticoagulant therapy. The reference range of F1+2 from 35 donors with 20 to 29 age-group, was found 0.82 +/- 0.39 nM, whereas the range from 20 donors with 30 to 39 age-group showed higher F1+2 levels with 1.46 +/- 0.56nM (p < 0.001). F1+2 values from 15 donors with 40 to 49 age-group revealed similar with 30 to 39 age-group, while the range from 10 donors with 50 to 59 age-group was found much higher F1+2 levels with 2.16 +/- 0.80nM (p < 0.001). In patients with DIC, F1+2 levels were significantly higher than those in all healthy subjects (p < 0.01). In patients under stable oral anticoagulant therapy, F1+2 values were significantly lower than in healthy donors with any age-group (p < 0.001). On the contrary, in patients with thrombosis including 9 AMI and 4 DVT, the determination of F1+2 values appeared controversial. They were significantly higher than those in 20 age-group donors (p < 0.001), however, when compared with those in all healthy donors, it showed no statistical significance. These results suggest that evaluation of reference range of plasma F1+2 values is very important from the viewpoint of aging. In addition, F1+2 determination is clinically useful for monitoring of DIC and anticoagulant therapy.
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PMID:[Evaluation of plasma prothrombin fragment 1+2 in healthy donors and thrombotic diseases]. 810 84


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