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)

To establish the incidence of the disseminated intravascular coagulation (DIC) syndrome, 76 patients who had died from acute myocardial infarction were clinically and anatomically analysed. The studies indicated that microcirculatory thrombosis in myocardial infarction occurred in the first to early second weeks of its development and localized in minor veins of one organ and only in 21.4% of cases it involved three organs or more. The DIC-syndrome was morphologically evidenced only in 19.1% of the patients having a history of cardiogenic shock. Microcirculatory thrombosis more frequently occurred in females. Old age, persistent hypertension, diabetes mellitus were found to predispose to its development.
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PMID:[Disseminated intravascular coagulation syndrome in myocardial infarct]. 812 Nov 31

Tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) are the most important factors involved in the regulation of blood fibrinolysis. t-PA converts zymogen plasminogen to plasmin on the surface of endothelial cells to maintain blood fluidity and on the surface of the thrombus to efficiently lyse the thrombus. In circulating plasma, PAI-1 inactivates t-PA by forming an equimolar complex with t-PA to suppress the hyperfibrinolysis of the blood. Both proteins are synthesized by the vascular endothelial cells and secreted from the cells in resting state and in response to several stimuli such as thrombin, endotoxin, cytokines and growth factors. In various diseases such as DIC, thromboembolism and bacterial infection, the plasma concentrations of those two factors vary as a consequence of several stimuli, representing the altered fibrinolytic balance caused by the disease. Measurements of these factors and evaluation of the fibrinolytic balance will be important for determination of the most appropriate method of treatment. Moreover, the high plasma concentration of PAI-1 will be a prognostic marker of the disease and may be a risk factor of thrombotic events. In clinical treatment, t-PA is now widely used as a valuable fibrinolytic agent especially in myocardial infarction.
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PMID:[Tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI)]. 817 42

Symptoms of endogenic hepatic coma were observed in the course of acute hepatitis in 17 patients admitted to the I Clinic of Infectious Diseases of Silesian Medical School between 1987 and 1992. Five of them were treated with the arterialization of portal blood. At least one exchange transfusion preceded the arterialization in four cases. Recovery was obtained in 3 patients. Two patients died because of complications which occurred during the twenty-four hours after the intervention. In the first case the reason of the death was the extensive myocardial infarction, in the second one-DIC and ARDS. As it has been observed, the prothrombin rate should not be lower than 30% in these patients who are to undergo the arterialization of portal blood. This value of the prothrombin rate is provided by at least one exchange transfusion.
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PMID:[Endogenic hepatic coma in the course of acute hepatitis treated with arterialization of portal blood]. 823 45

C1-inhibitor (C1Inh), antithrombin III (ATIII), alpha 1-antitrypsin (a1AT), and alpha 2-antiplasmin (a2AP) are known inhibitors of factor XIa (FXIa). However, their precise contribution to FXIa inactivation in vivo is not known. We investigated FXIa inactivation in chimpanzees and assessed the contribution of these inhibitors to FXIa inactivation in patients with presumed FXI activation. Chimpanzees were infused with FXIa and the various FXIa-FXIa inhibitor complexes formed were measured. Most of FXIa was complexed to C1Inh (68%), followed by a2AP (13%), a1AT (10%), and ATIII (9%). Analysis of the plasma elimination kinetics revealed a half-life time of clearance (t1/2) for the FXIa-FXIa inhibitor complexes of 95 to 104 min, except for FXIa-a1AT, which had a t1/2 of 349 min. Due to this long t1/2, FXIa-a1AT complexes were predicted to show the highest levels in plasma samples from patients with activation of FXI. This was indeed shown in patients with disseminated intravascular coagulation, recent myocardial infarction or unstable angina pectoris. We conclude from this study that in vivo C1Inh is the predominant inhibitor of FXIa, but that FXIa-a1AT complexes due to their relatively long t 1/2 may be the best parameter to assess FXI activation in clinical samples.
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PMID:Inactivation of factor Xia in vivo: studies in chimpanzees and in humans. 890 95

During episodes of dental bacteremia, viridans group streptococci encounter platelets. Among these microorganisms, certain Streptococcus sanguis induce human and rabbit platelets to aggregate in vitro. In experimental rabbits, circulating streptococci induced platelets to aggregate, triggering the accumulation of platelets and fibrin into the heart valve vegetations of endocarditis. At necropsy, affected rabbit hearts showed ischemic areas. We therefore hypothesized that circulating S. sanguis might cause coronary thrombosis and signs of myocardial infarction (MI). Signs of MI were monitored in rabbits after infusion with platelet-aggregating doses of 4 to 40 x 10(9) cells of S. sanguis 133-79. Infusion resulted in dose-dependent changes in electrocardiograms, blood pressure, heart rate, and cardiac contractility. These changes were consistent with the occurrence of MI. Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro aggregation response to strain 133-79. Cultured from immunosuppressed children with septic shock and signs of disseminated intravascular coagulation, more than 60% of isolates of viridans streptococci induced platelet aggregation when tested in vitro. The data are consistent with a thrombogenic role for S. sanguis in human disease, contributing to the development of the vegetative lesion in infective endocarditis and a thrombotic mechanism to explain the additional contributed risk of periodontitis to MI.
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PMID:Effects of oral flora on platelets: possible consequences in cardiovascular disease. 891 Aug 32

Several new drugs for the management of thromboembolic disorders have recently become available. Low-molecular-weight heparins are being evaluated for the prophylaxis of medical and surgical deep venous thrombosis and pulmonary embolism; for the treatment of pre-existing thrombosis; and for cases of coronary syndrome (unstable angina, myocardial infarction), thrombotic and ischemic stroke, interventional cardiology, pregnancy, cancer, and transplantation-associated thrombosis. A chemically synthesized heparin pentasaccharide, which has purely anti-factor Xa activity and does not induce thrombocytopenia, is also in clinical trial. Thrombin inhibitors, such as hirudin and argatroban, are a practical anticoagulant substitute where heparin cannot be used. They are also useful for the management of coronary syndrome and as adjunct therapy. The antiplatelet agent ticlopidine and its analogue, clopidogrel, which does not produce blood dyscrasia, are effective for the secondary prevention of thrombotic stroke and the management of combined arterial thrombotic syndromes. Glycoprotein-targeting antibodies, synthetic derivatives, and peptides (some of which are orally bioavailable) have added a new dimension to the management of arterial thrombosis and high-risk patients having angioplasty. Plasma-derived agents, such as antithrombin III, are available for the management of thrombophilia and disseminated intravascular coagulation. Compression devices and the foot pump, alone and in combination with pharmacologic agents, have been used successfully. Combination therapy using various agents in different proportions have also been found useful. Although there is much enthusiasm in this quickly developing area and clinical trials are demonstrating the antithrombotic efficacy of the new drugs, safety considerations require additional clinical validation. Long-term outcomes and costs also need to be addressed objectively.
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PMID:Current status on new anticoagulant and antithrombotic drugs and devices. 926 11

The number of liver resection in Poland has recently increased. Most frequent indications are benign tumors of the liver, metastatic changes and primary hepatic carcinoma. The aim of work is to discuss incidence of complications which appeared after liver resections at our Department. Among 56 patients aged 19-76, 32 anatomical and 24 nonanatomical resections of hepatic tissue were performed. In the early postoperation period, 8 patients had peritoneal fluid collections and 3 laparotomies with drainage were necessary, while in 5 cases fluid was aspirated under usg guidance. The outflow of bile and blood contents from subhepatic space was prolonged to 9 days in 3 patients, gastric or duodenal 3 stress ulcerations complicated with bleeding were observed as well as transitory hemobilia in 3 and jaundice in 6 cases. Early hemorrhage from excision line of hepatic tissue was observed in 2 patients which needed additional surgical intervention. Atelectasis and inflammatory changes of the right lung appeared in majority of patients operated on. The postoperative mortality of 16% (9 patients of total 56) was mainly dependent on hepatorenal or cardiorespiratory failure, however myocardial infarction and DIC syndrome were also noticed. In spite of progress of surgical technique and intensive perioperative care, resection procedures of the liver are still accompanied with large percentage of serious complications.
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PMID:[Complications after surgical resection of liver parenchyma]. 942 88

A total of 140 pathoanatomic conclusions and files collected by the author are analyzed. Morphological signs of the DIC syndrome were detected in 55% of patients who died. In 42% of lethal outcomes this syndrome was the final direct cause of death after such conditions as terminal stage of cancer, sepsis, extensive myocardial infarction, mechanical jaundice, uremia, bacteremia, etc. In 13% of autopsies fatal intravascular coagulation was a complication of the intervention or hemorrhage which was arrested before death. The DIC syndrome is diagnosed during autopsy due to a complex of peculiar changes in the viscera which are called "shock" in such cases. The signs of a shock liver are as follows: a characteristic red net pattern of the sliced surface and histological phenomena related to blocking of the sinusoidal bloodflow and lobular ischemia: abnormal hepatocyte complexes, fragmentation of liver bulks, and necrosis of the central lobules.
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PMID:[Morphological diagnosis of DIC syndrome. Shock liver]. 951 Dec 43

During fiscal years 91-95, 6260 patients underwent 6269 abdominal aortic aneurysm (AAA) repairs in Veterans Affairs Medical Centers. Those > or =80 years old comprised 3.7% (n = 231) of the patients. A total of 5833 patients underwent repair of nonruptured AAA: mortality was 4.1% (228/5627) in those <80 and 8.25% (17/206) in those > or =80 years old (p < 0.009). Logistic regression analysis indicated age > or =80 was independently associated with higher mortality (odds ratio 1.834:1, 95% bounds 1.117-3.012). Octogenarian status (defined as > or =80 years of age), however, had a less important association with in-hospital death than did surgical complications of the heart or genitourinary tract, postoperative hemorrhage, septicemia, respiratory insufficiency, myocardial infarction (MI), acute renal failure, surgical complications of the central nervous system (CNS), aneurysm rupture, postoperative shock, or disseminated intravascular coagulation (DIC), in ascending order of importance. Only 5.9% (n = 25) of the 427 patients undergoing repair of ruptured AAA were > or =80 years old. In those > or =80 undergoing repair of ruptured aneurysms, mortality was 48% which did not differ from the 45% mortality in those <80 (NS). The likelihood that one would be operated for rupture was statistically greater (1.66:1) for those > or =80 years (p < 0.025). Length of stay (LOS) for those > or =80 undergoing AAA repair was longer being 22.3 +/- 14.8 days versus 18.3 +/- 13.2 days for younger patients (p < 0.001). Mortality and LOS after AAA repair were statistically greater for those > or =80 years of age. Severity of illness, however, was also greater for octogenarians. Patient Management Category (PMC) software defined illness severity was 4.06 +/- 1.22 in octogenarians versus 3.84 +/- 1.13 for those younger (p < 0.005). Though age > or =80 was independently associated with increased mortality, selected elderly patients could benefit from AAA repair.
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PMID:Outcomes after abdominal aortic aneurysm repair in those > or =80 years of age: recent Veterans Affairs experience. 951 26

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


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