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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 relationship between factor VIII (AHF) procoagulant activity and factor VIII-related antigen were examined in patients with disseminated intravascular coagulation (DIC), pulmonary embolism (PE), and coronary artery disease with or without myocardial infarction (MI). It was found that 13 of 13 patients with DIC, 17 of 17 patients with PE, and 10 of 12 patients with MI possessed a significantly elevated factor VIII-related antigen to factor VIII activity ratio (VIII-ratio). The VIII-ratio returned to normal in each of 2 patients with DIC and 1 paitent with PE after treatment with heparin, heparin and alpha-amino-caproic acid, and heparin and coumadin respectively. In contrast, the VIII-ratio was slightly elevated only in 1 of 15 patients with coronary artery insufficiency without MI. In in vitro studies, after treatment of plasma with thrombin or plasmin, factor VIII activity was lost, whereas the amount of factor VIII-related antigen remained the same or was even increased when measured by agarose quantitative immunoelectrophoresis. These observations have led us to conclude that an elevated VIII-ratio is a very sensitive indicator of intravascular coagulation.
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PMID:In vivo and in vitro effects of thrombin and plasmin on human factor VIII (AHF). 13 71

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

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

Various hemostatic abnormalities have been reported and excess activation of coagulation factors, such as prothrombin, factor VII, factor IX, and factor XI, have been detected in thrombotic diseases states by various assay systems. We recently developed the enzyme-linked differential immunoassay for activated factor XI-alpha 1 antitrypsin complex (FXIa-alpha 1 AT) and applied it with other assays for activated factors such as thrombin-antithrombin III complex (TAT) to detect the hypercoagulable state in clinical samples. In patients with DIC, the FXIa-alpha 1 AT level in plasma increased before onset of DIC. In patients with non-insulin-dependent diabetes mellitus, FXIa-alpha 1AT and TAT levels were increased in the patient plasma. FXIa-alpha 1AT was related to the severity of urinary albumin excretion, whereas TAT was not. Plasma FXIa-alpha 1AT levels were significantly increased in patients with angiographically proven coronary artery disease, and showed a positive correlation with TAT, fibrinogen, and Lp(a). Evaluation of activated coagulation factor provides useful information on the diagnosis of thrombotic disease.
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PMID:[Activated coagulation factors in various thrombotic diseases]. 856 28

Measurement of D-dimer (fibrin degradation product) is important for determining not only the activation of fibrinolysis but also the severity of a hypercoagulable state. However, fibrin degradation products are in variable, and the reactivity to cross-linked fibrin degradation products produced during fibrin degradation differs depending on the kind of antibody used against D-dimer. In patients with disseminated intravascular coagulation or earthquake-induced mental and physical stress and in patients after percutaneous transluminal coronary angioplasty, all of which are associated with acute fibrin formation and degradation, some discrepancies between two methods of D-dimer detection, automated latex agglutination assay (LPIA) and enzyme-linked immunosorbent assay (Stago), were found. No discrepancies in persistent fibrin formation and degradation were found among the healthy elderly, patients with lacunar stroke, and patients with coronary artery disease, almost all of whom had levels under 5.0 microg/mL, as determined by both methods. Evidence of persistently increased intravascular coagulation and fibrin turnover in patients with atherosclerotic disease was found. The cleavage of cross-linked fibrin by plasmin results in a production of fibrin degradation products, mostly contained D-dimer domains. Although the clinical utility of D-dimer can be achieved by their detection with specific antibodies, measurement of D-dimer as high-molecular-weight fragments may be useful to determine whether patients will undergo further fibrin degradation. When intermediate products of the degradation process need to be assessed, D-dimer level measurement by LPIA may serve as a suitable marker for ongoing fibrinolysis.
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PMID:Fibrin D-dimer in thrombogenic disorders. 1080 90

The application of Bayesian hierarchical models to measure spatial effects in time to event data has not been widely reported. This case study aims to estimate the effect of area of residence on waiting times to coronary artery bypass graft (CABG) and to assess the role of important individual specific covariates (age, sex and disease severity). The data involved all patients with definite coronary artery disease who were referred to one cardiothoracic unit from five contiguous health authorities covering 488 electoral wards (areas). Time to event was the waiting time in months from angiography (diagnosis) to CABG (event). A number of discrete time survival models were fitted to the data. A discrete baseline hazard was estimated by fitting waiting time non-parametrically into the models. Ward was fitted as a spatial effect using a Gaussian Markov random field prior. Individual specific covariates considered were age, sex and number of diseased vessels. The recently proposed DIC criteria was used for comparing models. Results showed a marked spatial effect on time to bypass surgery after including age, sex and disease severity in the model. Notably this spatial effect was not apparent when these covariates were not included in the model. The observed small area spatial variation in time to CABG warrants further investigation.
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PMID:Measuring spatial effects in time to event data: a case study using months from angiography to coronary artery bypass graft (CABG). 1295 90

The plasma kallikrein-kinin system (KKS) participates in the pathogenesis of inflammatory reactions involved in cellular injury, coagulation, fibrinolysis, kinin formation, complement activation, cytokine secretion and release of proteases. It has been shown that KKS activation in the systemic inflammatory response syndrome results in decrease of its component plasma proteins. Similar changes have been documented in diabetes, sepsis, children with vasculitis, allograft rejection, disseminated intravascular coagulation, patients with recurrent pregnancy losses, hereditary angioedema, adult respiratory distress syndrome and coronary artery disease. Direct involvement of the KKS in the pathogenesis of experimental acute arthritis and acute and chronic enterocolitis has been documented by previous studies from our laboratory using experimental animal models. It has been found that in HK deficient Lewis rats, experimental IBD was much less severe. We showed a genetic difference in kininogen structure between resistant Buffalo and susceptible Lewis rats, which results in accelerated cleavage of HK and it is responsible for the susceptibility to the inflammatory process in the Lewis rats. It has been demostrated that therapy with a specific plasma kallikrein inhibitor (P8720) modulated the experimental enterocolitis, arthritis and systemic inflammation. Furthermore, it has been shown that a bradykinin 2 receptor (B2R) antagonist attenuates the inflammatory changes in the same animal model. We have showed that a monoclonal antibody targeting HK decreases angiogenesis and arrests tumor growth in a syngeneic animal model. In summary, these results indicate that the plasma KKS plays a central role in the pathogenesis of chronic intestinal inflammation, arthritis and angiogenesis.
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PMID:[High molecular weight kininogen in inflammation and angiogenesis: a review of its properties and therapeutic applications]. 1670 6

A 73-year-old man underwent a facial skin biopsy, after which he experienced persistent, severe bleeding over a 4-day period that could not be staunched by suturing or cauterization. Patient history suggested a bleeding diathesis. A condition of chronic disseminated intravascular coagulation (DIC) that decompensated into an acute state of DIC subsequent to the biopsy was diagnosed based on laboratory findings. Physical examination followed by imaging revealed a large abdominal aortic aneurysm as the likely underlying etiology. The patient achieved stability with blood component replacement therapy and an initial round of heparin that was substituted with enoxaparin. Following cardiac catheterization, where triple vessel coronary artery disease was diagnosed, surgical correction of the abdominal aortic aneurysm and coronary artery bypass grafting were deemed to be too high risk. The patient was treated medically for his abdominal aortic aneurysm, coronary artery disease, and acute and chronic DIC. Within a year, the patient succumbed to a brainstem stroke. In patients with acute or chronic DIC, a thorough examination is recommended to exclude rare causes and to improve overall general management.
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PMID:The secret behind profuse bleeding following a routine skin biopsy. 1739 55

Electrophoretic analysis of protein variation at the coagulation F13B locus has previously revealed three alleles, with alleles 1, 2, and 3 each being at high frequency in European, African, and Asian populations, respectively. To determine if this unusual pattern of interpopulation differentiation reflects local natural selection or neutral genetic drift, we re-sequenced 4.6 kb of the gene, encompassing all exons, splice junctions, and 1.4 kb of the promoter, in African, European, and Asian samples. These analyses revealed three major lineages, which correspond to the common protein alleles and differ from each other at a non-synonymous substitution in exon 3 and a novel splice acceptor in intron K. There is previous evidence that these lineages are not functionally equivalent; we therefore carried out case-control analyses and confirmed that variability at F13B modulates susceptibility and/or survivorship in coronary artery disease (P<0.05) and type II diabetes within the coronary artery disease cohort (P<0.01). Tajima's D and Fu and Li's tests did not indicate significant departures from neutral expectations. However, publicly available data from SeattleSNPs and HapMap do indicate highly unusual levels of population differentiation (P=0.003) and an excess of allele-specific, extended haplotype homozygosity within the African population (P=0.0125). Possible causes of this putative signal of selection include hematophagous organisms, infection by pathogens that cause disseminated intravascular coagulation, and metabolic or dietary factors.
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PMID:Natural selection and the molecular basis of electrophoretic variation at the coagulation F13B locus. 1871 11

The case report describes an interesting and unusual finding of acute coronary artery thrombosis in a patient presenting with septic shock without any clinical and laboratory evidence of disseminated intravascular coagulation (DIC). The patient presented with leucocytosis and refractory hypotension requiring pressor support and found to have anterior and inferior ST-elevation in 12-lead electrocardiogram. Coronary angiogram revealed acute thrombotic occlusions in the proximal right coronary artery and the proximal left anterior descending coronary artery. There was no occlusive atherosclerotic coronary artery disease. The patient underwent mechanical thrombectomy. Haemodynamic parameters obtained from right heart catheterisation confirmed sepsis as the aetiology of hypotension. The patient was treated successfully with broad spectrum antibiotics, pressors and intravenous fluid.Acute myocardial infarctions as a complication secondary to disseminated intravascular coagulation in patients with sepsis and septic shock have been described in the literature. To our knowledge, this is the first reported case of acute coronary artery thrombosis in patient with septic shock without DIC and without any underlying occlusive coronary artery disease.
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PMID:Acute coronary thrombosis in a patient with septic shock without any evidence of disseminated intravascular coagulation. 2185 77


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