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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Case of hematological disorders associated with acute myocardial infarction had been found in five of forty five autopsy cases which had hematological disorders during the past seven years. The five cases of hematological disorders consisted of two cases of myelodysplastic syndrome, a case of aplastic anemia, a case of primary myelofibrosis in blast transformation, and a case of acute myelogenous leukemia. All the patients were over 60 years old. Four patients had coronary artery stenosis and extensive myocardial infarction. Fibrinogen degradation products were elevated in four patients. DIC was recognized in two and suspected in two others. In all cases, platelet counts markedly decreased to less than 2.5 x 10(10)/L. Since no chest pain was noted by any patient, it was difficult to diagnose acute myocardial infarction without autopsy, except in one case. It is important to recognize the possibility of severe cardiac dysfunction due to myocardial infarction in thrombocytopenia, especially in the aged with DIC.
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PMID:[Five cases of hematological disorders associated with acute myocardial infarction in thrombocytopenia]. 160 11

Pulmonary and myocardial damage are frequently cited as manifestations of disseminated intravascular coagulation (DIC), but rarely as causes. Three elderly cases of severe DIC due to pulmonary and myocardial infarction are reported. All three patients died. Necropsy showed extensive pulmonary emboli in each case with large pulmonary infarcts in cases 1 and 2 and a ventricular aneurysm containing thrombus in cases 2 and 3. Early diagnosis and treatment of pulmonary embolism requires a high degree of clinical suspicion but may prevent progression to the irreversible stage of severe DIC.
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PMID:Pulmonary infarction, myocardial infarction, and acute disseminated intravascular coagulation. 179 Dec 8

A clinicopathological analysis of myocardial infarction with an onset of stroke-like symptoms was carried out on 30 autopsy cases at the Tokyo Metropolitan Geriatric Hospital. The cases were classified into four groups according to the types of brain lesions, I: embolism (n = 17), II: thrombosis (n = 9), III: bleeding (n = 2), and IV: no remarkable focal lesion (n = 2). Classification was made based on clinical findings, and pathological features. The characteristic clinical findings were conciousness disturbance, no elevation of blood pressure at the onset of stroke, hemiplegia and shock. However, the typical anginal chest pain was found in only 17% of cases. The underlying diseases and complications were hypertension, atrial fibrillation (Af), disseminated intravascular coagulation (DIC), renal failure, malignant neoplasma, and diabetes mellitus. The incidences of Af, DIC, mural thrombus, non-bacterial thrombotic endocarditis (NBTE) were significantly higher in the group with cerebral embolism than in the group with cerebral thrombosis. The coronary stenotic index was also smaller in the group with cerebral embolism. Therefore, the major etiology of cardio-cerebral apoplexy was a simultaneous embolism to the brain and heart due to Af, NBTE or, DIC.
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PMID:[Myocardial infarction beginning with cerebral symptoms in 30 cases of cardio-cerebral apoplexy]. 204 62

A case of disseminated intravascular coagulation (DIC) and fatal myocardial infarction in a haemophilia B patient is described. DIC occurred after 4 days of therapy with unactivated prothrombin complex concentrates during the post-operative period. Therapy with fresh frozen plasma, heparin and antithrombin III concentrates was started without efficacy; after autopsy myocardial infarction was evident.
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PMID:Disseminated intravascular coagulation and myocardial infarction in a haemophilia B patient during therapy with prothrombin complex concentrates. 210 59

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

Broad spectrum assays which measure a range of fibrinogen/fibrin derivatives (FDPs) in serum have become an established means of identifying activation of blood coagulation and/or fibrinolysis, such as occurs in disseminated intravascular coagulation (DIC). There is considerable interest in the application of these assays to the diagnosis of other hypercoagulable states, such as recurrent deep venous thrombosis and myocardial infarction. In recent years, more sensitive and specific FDP assays (e.g. for fragment E, fragment E neoantigen, D-dimer, fragment D neoantigen, fibrinopeptide A and fibrin fragment beta 15-42) have been devised, some of which allow measurement in plasma of FDPs without interference from fibrinogen or certain of its derivatives. It was predicted that these assays would both avoid the possibility of artifacts introduced as a consequence of serum preparation and improve detection of hypercoagulable states. In the light of these expectations we have reviewed data published on the use of assays to detect clinical hypercoagulability, giving prominence to assays of crosslinked fibrin derivatives and nothing particularly certain studies that have compared the performance of different assays on the same samples. The accumulating evidence indicates that all of the assays are adequate for detection of DIC. The same cannot be said for other hypercoagulable states. Here much variation is evident between different studies of similar patients in the ability of a particular marker to discriminate between a normal control group and patients determined to be hypercoagulable by an independent method. This variability would seem to be a function of patient group heterogeneity and selection, as assays that detect different antigenic determinants produce results on the same plasma samples that are well correlated. It appears that the precise antigenic determinant does not critically affect detection of hypercoagulability. Additionally, some studies have indicated that use of serum need not introduce artifacts. Despite there being no other obvious advantage, the convenience of some of the plasma assays may well encourage their widespread use. Assays have also been developed for measuring activation fragments of coagulation proteins (e.g. prothrombin fragment F1 + 2 and protein C activation peptide) and for proteinase inhibitor complexes (e.g. thrombin-antithrombin complex) generated during activation of coagulation. The latter assays have been useful in providing a biochemical definition of a 'prethrombotic state'.
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PMID:Assessment of hypercoagulable states by measurement of activation fragments and peptides. 218 46

Measurements were made of levels of D-dimer in plasma and serum, thrombin-antithrombin complex (TAT) in plasma and fibrinogen/fibrin fragment E antigen (FgE) in serum in a normal healthy control group and in patients with a range of disorders associated with hypercoagulability. Levels were determined in 31 normal healthy controls, 30 patients with disseminated intravascular coagulation (DIC), 21 patients with deep venous thrombosis (DVT), 27 patients with myocardial infarction (MI), 26 patients with acute leukaemia and 56 patients with liver disease. Considering all subjects, significant correlations were established between the results of all assays. Notably high correlations (r greater than 0.9) were established between plasma and serum levels of D-dimer, between plasma levels of D-dimer and serum levels of FgE, and between serum levels of D-dimer and FgE. All assays showed very high discrimination (sensitivity) between the normal control group and patients with DIC (97-100%), but there were marked differences between the assays in sensitivity for DVT and MI. In general, the FgE assay was more sensitive than the D-dimer assay, whilst both the FgE and D-dimer assays were more sensitive than the TAT assay. The same trends were apparent in the capability of the assays to discriminate between the normal control group and patients with acute leukaemia and liver disease: disorders with an unknown prevalence of activation of coagulation/fibrinolysis. Our results indicated that measurements of fibrinogen/fibrin degradation products (FDPs) in serum were almost unaffected by artefacts. The data further suggested that the broad-spectrum FgE assay was better than the more specific D-dimer assay in detecting clinical hypercoagulability. Our study showed that, in the clinical conditions examined, FDPs were more effective markers of hypercoagulability than TAT.
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PMID:A comparative evaluation of assays for markers of activated coagulation and/or fibrinolysis: thrombin-antithrombin complex, D-dimer and fibrinogen/fibrin fragment E antigen. 218 90

The authors observed 53 cases of diabetic ketoacidosis treated with low doses of insulin. Mean age of the patients was 41 +/- 17 years, duration of diabetes mellitus 7.5 +/- 6.4 years. Ketoacidosis was due to: infections in 36%, other diseases in 7%, and cessation of insulin therapy in 25% of cases. Ketoacidosis was a first sign of diabetes mellitus in 19% of cases while causative factor was not detected in 13% of cases. At the admission to hospital mean blood pH was 7.02 +/- 0.15, mean bicarbonate concentration 6.17 +/- 3.45 mM/l, and glycaemia 40.6 +/- 16.8 mM/l. Therapy of ketoacidosis was complicated by hypopotassemia in 1 patient and transient hypoglycaemia in another patient. Five patients (9.6%) died. Infections, myocardial infarction, acute pancreatitis, pulmonary edema, and disseminated intravascular coagulation were the causes of deaths.
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PMID:[Analysis of the cause of death in diabetic ketoacidosis based on 5 years of personal observation]. 251 62

The thrombocytic link of hemocoagulation hemostasis was studied in patients (young, middle-aged, old) during the first week of myocardial infarction. It was found that the middle-aged showed the syndrome of disseminated intravascular coagulation in the pathogenesis of which thrombocytes are involved. In each age group this syndrome exhibits certain characteristic features. This should be considered in therapeutic and prophylactic measures.
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PMID:[The thrombocyte link in the hemostasis of patients with acute myocardial infarct]. 275 Jan 3

A 40-year-old woman was admitted to our hospital because of left hemiplegia. She was affected with myocardial infarction and cerebral infarction. Echocardiogram revealed that the aortic and mitral valves had thick and uneven echoes suggesting vegetations. Judging from the finding that repeated blood cultures were negative, we had considered in her lifetime that myocardial and cerebral infarctions were due to embolization associated with nonbacterial thrombotic endocarditis (NBTE). At autopsy, histological diagnosis was made as ovarian cancer with disseminated intravascular coagulation. From the clinical course and the histological findings, we diagnosed this patient as NBTE.
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PMID:Cerebral and myocardial infarction induced by nonbacterial thrombotic endocarditis in a patient with ovarian cancer: report of a case. 305 70


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