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)

We examined various hemostatic molecular markers in patients with disseminated intravascular coagulation(DIC), deep vein thrombosis(DVT), pulmonary embolism(PE), acute myocardial infarction(AMI), cerebral thrombosis(CT) and thrombotic thrombocytopenic purpura(TTP). Global tests were sensitive for DIC but not for pre-DIC. However, hemostatic molecular markers such as soluble fibrin were sensitive for both DIC and pre-DIC. Hemostatic molecular markers were also useful for analysis of DIC in a baboon DIC model. Activated protein C-protein C inhibitor complex and plasminogen activator inhibitor-I were useful for the diagnosis of DVT, PE, AMI or CT. These findings suggests that hemostatic molecular markers are useful for the diagnosis of various thrombotic disorders.
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PMID:[Application of hemostatic molecular markers for diagnosis of thrombosis]. 1081 Aug 74

Patients in intensive care may be at high risk of in vivo platelet activation because comorbid conditions, such as infections, septicemia, shock, disseminated intravascular coagulation, and cancer represent procoagulant states. Hyperreactivity of platelets with or without a decline of cell count may result in thromboembolic complications potentially associated with the phenomenon of heparin-induced thrombocytopenia. We analyzed the data of 10 patients highly suspected of having heparin-induced thrombocytopenia during their intensive care treatment of 29 plus or minus 22 days. In seven patients, thrombocytopenia coincided with thromboembolic complications. Six patients had additionally undergone fibrinolytic therapy before starting activated partial thromboplastin time-adapted alternative anticoagulation with r-hirudin. In three patients, the platelet count decreased without a clinical manifestation, of heparin-induced thrombocytopenia. R-Hirudin treatment monitored by activated partial thromboplastin time and prothrombin time (PT) was effective and safe. The target value for activated partial thromboplastin time was a twofold prolongation. In four of five patients with deep venous thrombosis, a partial recanalization of the lower extremity could be achieved. Three patients with pulmonary embolism associated with deep venous thrombosis in two cases and in one additional case with an acute myocardial infarction did clinically profit from fibrinolysis with recombinant tissue plasminogen activator (rtPA) and r-hirudin treatment. Two lethal events probably caused by the underlying multimorbidity could not be prevented. No recurrence of thrombosis occurred, and there were no severe bleeding complications attributed to r-hirudin treatment. Platelet counts were significantly reduced on day 9.4 plus or minus 6.4 of heparin administration in all cases (>50% decrease related to the initial values) from 224,000 plus or minus 126,000/microL to 96,000 plus or minus 61,000/microL, and increased during rhirudin treatment to mean values of 224,000 plus or minus 126,000/microL. The heparin-induced platelet activation assay (HIPAA) assay was positive in 8/10 cases, whereas the PF4 enzyme-linked immunosorbent assay showed a positive result in four of eight analyzed cases. In four cases, the assays were concordantly positive. The PF4 enzyme-linked immunosorbent assay was not performed in two cases.
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PMID:Heparin-induced thrombocytopenia: a critical risk/benefit analysis of patients in intensive care treated with R-hirudin. 1089 75

Plasma levels of activated protein C (APC)-protein C inhibitor (PCI) were significantly increased in patients with disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), acute myocardial infarction (AMI), pulmonary embolism (PE), or deep vein thrombosis (DVT) and in patients undergoing hemodialysis (HD). Plasma levels of APC-alpha(1)-antitrypsin (AT) complex were significantly increased in patients with DIC and in those with TTP. Plasma levels of PCI were significantly decreased in patients with DIC, non-DIC, or TTP and in those undergoing HD. In the pre-DIC stage, the plasma levels of APC-PCI complex were significantly increased but not those of APC-alpha(1)-AT complex. These data suggest that measurements of APC-PCI complex and APC-alpha(1)-AT complex may be useful for the diagnosis of DIC. After treatment of DIC, the plasma levels of APC-PCI complex and APC-alpha(1)-AT complex were significantly decreased, but not those of PCI. Plasma levels of thrombin-antithrombin complex (TAT), plasmin-alpha(2)-plasmin complex (PPIC), D-dimer, and soluble fibrin monomer (SFM) were markedly increased in patients with DIC or pre-DIC and were moderately increased in patients with non-DIC, TTP, AMI, PE, or DVT and in those undergoing HD. The receiving operating characteristic (ROC) analysis showed that SFM and the APC-PCT complex are useful markers for diagnosis of DIC. The specificity of plasma TAT and PPIC levels was low. The positive rate of APC-PCI complex was higher than 90% with DIC, TTP, AMI, PE, and it was higher than 60% with DVT and HD. Since the APC-PCI complex was elevated not only in patients with venous thrombosis but also in those with arterial thrombosis, components of the protein C pathway might be useful markers for the diagnosis of arterial thrombosis.
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PMID:Plasma levels of activated protein C-protein C inhibitor complex in patients with hypercoagulable states. 1093 61

Cancer patients show an increased susceptibility to develop thromboembolic diseases, suggesting that disorders of coagulation are very common in this pathology. Tumor cells possess the capacity to interact with the hemostatic system, activating the coagulation cascade and stimulating the prothrombotic properties of other blood cell components; the same events while inducing a hypercoagulable state, also contribute to the processes of tumor growth, neoangiogenesis and metastatic formation. Multiple risk factors associated with malignant disease contribute to the hypercoagulability state: stasis induced by prolonged bed rest, vascular invasion by the tumor and iatrogenic complications including the use of central vein catheters and chemotherapy. Several tests have been developed to assess the hypercoagulable state, however their clinical significance still needs to be defined, especially in terms of their predictive value for thrombosis. Clinical manifestations vary from localized deep venous thrombosis (DVT) or pulmonary embolism, more generally associated with solid tumors, to disseminated intravascular coagulation, frequent in hematologic malignancies and metastatic cancer. Diagnosis of idiopathic DVT, in the absence of other risk factors, could indicate the presence of occult cancer, but the usefulness of an extensive work-up to detect malignancy in terms of cost to benefit ratio still has to be demonstrated. Patients with cancer and thromboembolism must be treated with anticoagulant therapy; a large number of studies have shown that either low molecular weight heparins or standard unfractionated heparin for the treatment of acute deep vein thrombosis in hospitalized patients are equally safe and effective; however, the first treatment has been reported to be associated with a lower mortality. After an episode of thrombosis the patients should be protected by a long term course of oral anticoagulation, remaining high the risk of recurrence for as long as the cancer is active.
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PMID:[Blood coagulation changes and neoplastic pathology]. 1107 43

Coagulation disorders are a common problem in neoplastic patients and many factors contribute to increase the risk of thromboembolic events in these patients. An hypercoagulable state is induced by malignant cells interacting directly with hemostatic system and activating the coagulation cascade. More sensitive tests to assess an hypercoagulable state in cancer patients have been developed; even though these tests are always altered in cancer patients, none of them possess a clinical significance in terms of predictive value for the occurence of thromboembolism and disease prognosis in the individual patient. The most frequent thromboembolic complications in cancer patients are deep vein thrombosis of the lower extremities and pulmonary embolism; therefore, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura or haemolytic uremic syndrome are special manifestations of neoplastic disease. Diagnosis of idiopathic deep vein thrombosis, in the absence of other risk factors, could indicate the presence of occult malignant disease; however, the need for an extensive work-up to detect malignancy is still controversial. Neoplastic patients showing a thromboembolic event should be treated with unfractioned heparin or, alternatively, with low molecular weight heparins. In order to prevent recurrence, the administration of heparin should be associated and followed by an oral anticoagulant drug. In recent years new approaches in anti-aggregation therapy have been studied, such as COX-inhibitors, cicaprost and ReoPro; further studies are needed to determine the usefulness of these molecules in treatment of malignancies.
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PMID:Coagulation and cancer: implications for diagnosis and management. 1117 65

Although D-dimer has gained widespread clinical use as a parameter for detection of in vivo fibrin formation, the issue of standardization of D-dimer assays remains to be resolved. The FACT study was performed to generate basic data for development of calibrators and standard preparations. A set of 86 samples, including plasma samples from patients with DIC, DVT. and other clinical conditions, serial dilutions of pooled plasma samples, and plasma samples containing fibrinogen- and fibrin derivatives, were distributed to 12 manufacturers of D-dimer assays. D-dimer assays differ concerning specificity for crosslinked fibrin, and preference for either high molecular weight fibrin complexes, or low molecular weight fibrin degradation products. Terminal plasmin digests of fibrin clots for calibration produce aberrant results in some assays, especially those with preference for high molecular weight crosslinked fibrin derivatives. The best conformity is achieved by the use of pooled plasma samples from patients with high levels of D-dimer antigen in plasma. In vitro preparations containing a comparable composition of fibrin derivatives to clinical plasma samples may also serve as reference material.
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PMID:The Fibrin Assay Comparison Trial (FACT): evaluation of 23 quantitative D-dimer assays as basis for the development of D-dimer calibrators. FACT study group. 1134 4

Alterations in hemostasis are common in patients with cancer admitted to the ICU. Depending on the underlying disease and specific hemostatic abnormality, the patient with cancer may develop bleeding, thrombosis, or both, such as DIC. Bleeding complications usually result from abnormalities in platelets or deficiency of coagulation factors and require specific blood or coagulation factor replacement. Similarly, critically ill patients with cancer are predisposed to thrombotic complications such as DVT, PE, and central vein thrombosis, the last as a result of the widespread use of long-term indwelling catheter devices. Advances in diagnostic imaging and the availability of newer and more potent anticoagulant agents have facilitated the care of these patients greatly. Ultimately, it is hoped that a thorough understanding of the various disturbances in hemostasis, innovative treatment approaches, and implementation of preventive strategies in patients with cancer will lead to decreased morbidity and improved survival rates of critically ill patients with cancer in the ICU.
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PMID:Bleeding and thrombotic complications in critically ill patients with cancer. 1152 50

The development of deep venous thrombosis and the ensuing secondary complications of pulmonary embolism, disseminated intravascular coagulation, and stroke may be produced in high altitude climbers as a result of acclimatization to altitude. To prevent these serious disorders, investigation for predisposing risk factors and consideration of anticoagulative therapy should be considered.
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PMID:Prophylaxis of climbers for prevention of embolic accidents. 1160 72

Clinical hematologists are frequently consulted for the care of hospitalized patients with complicated coagulopathies. This chapter provides an update on the scientific and clinical advances noted in disseminated intravascular coagulation (DIC) and discusses the challenges in hemostasis consultation. In Section I, Dr. Marcel Levi reviews advances in our understanding of the pathogenic mechanisms of DIC. Novel therapeutic strategies that have been developed and evaluated in patients with DIC are discussed, as are the clinical trials performed in patients with sepsis. In Section II, Dr. Lawrence Leung provides an overview of the challenging problems in thrombosis encountered in the inpatient setting. Patients with deep vein thrombosis that is refractory to conventional anticoagulation and those with extensive mesenteric thrombosis as well as the evaluation of a positive PF4/heparin ELISA in a post-operative setting are discussed. Novel treatments for recurrent catheter thrombosis in dialysis patients is addressed as well. In Section III, Dr. Julie Hambleton reviews the hemostatic complications of solid organ transplantation. Coagulopathy associated with liver transplantation, contribution of underlying thrombophilia to graft thrombosis, drug-induced microangiopathy, and the indication for postoperative prophylaxis are emphasized. Dr. Hambleton reviews the clinical trials evaluating hemostatic agents in patients undergoing liver transplantation.
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PMID:Coagulation: consultative hemostasis. 1244 31

Heparin-induced thrombocytopenia (HIT) is a severe adverse effect of heparin therapy. Although most cases occur in patients receiving unfractionated heparin, HIT can arise in venous thrombosis prophylaxis with a low-molecular-weight heparin (LMWH). We report an uncommon case of HIT in a postoperative orthopedic patient associated with LMWH (nadroparin), complicated by deep venous thrombosis, pulmonary embolism, and disseminated intravascular coagulation, treated successfully with recombinant hirudin and immunoglobulin therapy.
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PMID:Heparin-induced thrombocytopenia with pulmonary embolism and disseminated intravascular coagulation associated with low-molecular-weight heparin. 1254 86


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