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)

Therapeutic defibrination by Arwin was induced in a group of nine patients suffering from unstable angina combined with hyperfibrinogenaemia and in a further six patients who developed hyperfibrinogenaemia accompanied by angina pectoris after thrombolytic therapy with streptokinase for recent myocardial infarction. In patients of the former group with unstable angina a mean pretreatment plasma fibrinogen concentration of 4.9 g/1 was lowered to 1.4 g/l over a period of four weeks, whilst in the latter group, the plasma fibrinogen was lowered from 5.7 g/l to 2.0 g/l over 10 days. In all cases a remarkable improvement in the severe anginal symptoms was achieved already at fibrinogen levels within the lower range of normal. This improvement outlasted the period of therapy in most patients. Two patients died following acute myocardial infarction; one of the patients with unstable angina died 15 months after Arwin therapy and the second patient discontinued therapy after one week and died three weeks later.
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PMID:[Therapeutic defibrination by arwin in unstable angina pectoris combined with hyperfibrinogenaemia (author's transl)]. 71 35

In patients with angina pectoris and acute myocardial infarction different signs of disseminated intravascular coagulation were found, their intensity depending on the severity of the clinical course. In myocardial infarction with a complicated course and, especially, in shock signs of disseminated intravascular microthrombus formation were revealed, its criteria including, according to the author's data, reduced platelets count, factor V activity, shortening of platelets life and period of labelled fibrinogen circulation, appearance of large quantities of the fibrin-monomer complex.
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PMID:[Disseminated intravascular coagulation in myocardial infarct]. 102 34

Thrombomodulin (TM) is an endothelial cell membrane glycoprotein which neutralizes thrombin clotting activity and accelerates thrombin-catalyzed activation of plasma protein C. Its role is considered to be very important to prevent thrombosis. Recently, TM has been found in circulating blood and the roles and the functions have been investigated. In this study, we evaluated the reliance and the clinical usefulness of a TM-measuring-kit by enzyme immunoassay (MGC-01-001: Mitsubishi Gas chemical company). Intraassay reproducibility test, dilution linearity test and in vitro recovery test was obtained satisfactory results. A correlation between plasma and serum on TM levels of healthy individuals was very good and the difference between them was not significant. Normal value of plasma TM levels was instituted 15.73 +/- 6.98 ng/ml by measuring 52 healthy adults. The difference between male and female was not significant. Plasma TM levels did not change significantly after venous occlusion test and on circadian fluctuation. Plasma TM levels in patients with occlusion test and on circadian fluctuation. Plasma TM levels in patients with disseminated intravascular coagulation (DIC) was 40.15 +/- 22.68 ng/ml (mean +/- SD, n = 14). It is significantly higher than the levels in healthy adults. However, the levels in patients with angina pectoris, acute myocardial infarction and aortic aneurysm were not significantly different from those of healthy adults. These findings suggest that the precision of this TM-measuring-kit is satisfactory and the measurement of plasma TM can be useful to diagnose of DIC.
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PMID:[Evaluation of an enzyme immunoassay for plasma thrombomodulin]. 165 17

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 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

We measured various coagulable factors and molecular markers in plasma and serum in the disease group including DIC, DIC suspect, thrombosis, acute myocardial infarction, angina pectoris, sepsis, malignant tumor and type II diabetes and the healthy subject group, and surmised the intravascular coagulative-fibrinolytic activity in each disease group compared with the healthy group. Additionally we selected parameters useful for early detection of the pre-thrombotic state and hypercoagulable state. As a result, of the parameters for the coagulative system, those considered useful were the assay of soluble fibrin monomer complexes using the synthetic substrate (FM.Oita), assay of soluble fibrin monomer complexes using HPLC(SFMC.Oita) and thrombin-anti-thrombin III complex (TAT) in this order. Of the parameters for the fibrinolytic system, those considered useful were FDP assay using ELISA (FDP.Oita) and plasmin-alpha 2 plasmin inhibitor complex (PIC). This FDP.Oita had a considerably high detection sensitivity compared with the FDP assay (Diayatron Co.) using the latex photometric immunoassay which has been commercially available. When measurement was made with plasma and serum in the subject disease group as the sample by the high sensitivity assays mentioned above, it was made clear that both the coagulative activity and fibrinolytic activity are increased, albeit with some differences in intensity, in all the disease groups compared with the healthy group. In order for the hypercoagulable state and pre-thrombotic state to be detected, it is important to know the balance between the coagulative activity and fibrinolytic activity. According to the results of the present experiment, a significant directly proportional correlation was recognized between FM.Oita and FDP.Oita and between TAT and FDP.Oita. Therefore, examination of these ratios will be a more detailed indicator of coagulative-fibrinolytic activity than the TAT/PIC ratio, PAI-1/TPA ratio and ATIII/alpha 2 PI ratio hitherto in use. If useful molecular markers such as FM.Oita are measured over time in various cases and these data are compiled and analyzed statistically, it will not be long before the criteria for the hypercoagulable state and pre-thrombotic state are established.
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PMID:[Molecular marker for detecting hypercoagulable state]. 810 79

Several studies have shown that thrombosis and inflammation play an important role in the pathogenesis of Ischaemic Heart Disease (IHD). In particular, Tissue Factor (TF) is responsible for the thrombogenicity of the atherosclerotic plaque and plays a key role in triggering thrombin generation. The aim of this study was to evaluate the TF/Tissue Factor Pathway Inhibitor (TFPI) system in patients with IHD. We have studied 55 patients with IHD and not on heparin [18 with unstable angina (UA), 24 with effort angina (EA) and 13 with previous myocardial infarction (MI)] and 48 sex- and age-matched healthy volunteers, by measuring plasma levels of TF, TFPI, Prothrombin Fragment 1-2 (F1+2), and Thrombin Antithrombin Complexes (TAT). TF plasma levels in IHD patients (median 215.4 pg/ml; range 72.6 to 834.3 pg/ml) were significantly (p<0.001) higher than those found in control subjects (median 142.5 pg/ml; range 28.0-255.3 pg/ml). Similarly, TFPI plasma levels in IHD patients were significantly higher (median 129.0 ng/ml; range 30.3-316.8 ng/ml; p<0.001) than those found in control subjects (median 60.4 ng/ml; range 20.8-151.3 ng/ml). UA patients showed higher amounts of TF and TFPI plasma levels (TF median 255.6 pg/ml; range 148.8-834.3 pg/ml; TFPI median 137.7 ng/ml; range 38.3-316.8 ng/ml) than patients with EA (TF median 182.0 pg/ml; range 72.6-380.0 pg/ml; TFPI median 115.2 ng/ml; range 47.0-196.8 ng/ml) and MI (TF median 213.9 pg/ml; range 125.0 to 341.9 pg/ml; TFPI median 130.5 ng/ml; range 94.0-207.8 ng/ml). Similar levels of TF and TFPI were found in patients with mono- or bivasal coronary lesions. A positive correlation was observed between TF and TFPI plasma levels (r = 0.57, p<0.001). Excess thrombin formation in patients with IHD was documented by TAT (median 5.2 microg/l; range 1.7-21.0 microg/l) and F1+2 levels (median 1.4 nmol/l; range 0.6 to 6.2 nmol/l) both significantly higher (p<0.001) than those found in control subjects (TAT median 2.3 microg/l; range 1.4-4.2 microg/l; F1+2 median 0.7 nmol/l; range 0.3-1.3 nmol/l). As in other conditions associated with cell-mediated clotting activation (cancer and DIC), also in IHD high levels of circulating TF are present. Endothelial cells and monocytes are the possible common source of TF and TFPI. The blood clotting activation observed in these patients may be related to elevated TF circulating levels not sufficiently inhibited by the elevated TFPI plasma levels present.
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PMID:Elevated tissue factor and tissue factor pathway inhibitor circulating levels in ischaemic heart disease patients. 953 Oct 29

A 73-year-old man who had been receiving treatment for hypertension and angina pectoris was admitted to hospital following a transient ischemic attack. He was diagnosed as having chronic disseminated intravascular coagulation (DIC) complicated by a thoracoabdominal aortic aneurysm, and was treated with heparin sodium and a protease inhibitor. Although the DIC was controlled, the patient had to remain hospitalized in order to receive the medication by continuous infusion. Therefore, the heparin sodium and protease inhibitor were replaced by camostat mesilate, a drug suitable for oral administration and widely used for treatment of chronic pancreatitis. The drug proved effective for the chronic DIC, thus allowing the patient to receive regular treatment on an outpatient basis, and improving his quality of life.
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PMID:[Effective use of camostat mesilate for chronic disseminated intravascular coagulation complicated by thoracoabdominal aortic aneurysm]. 1123 31