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)

Teijin and Chemo-Sero are codeveloping CTC-111 as a treatment for disseminated intravascular coagulation (DIC) due to protein C deficiency. The drug was launched for the treatment of protein C deficiency in Japan on January 31, 2001 and as of October 2001 was awaiting approval for the treatment of DIC, also in Japan [426762]. CTC-111 was evaluated in a multicenter pharmacokinetic trial in venous thrombosis patients with inherited protein C deficiency. CTC-111 was effective in six of ten patients with venous thrombosis, six of seven patients with deep vein thrombosis and two of three patients with pulmonary embolism. Treatment was safe and effective and there were no serious adverse events [350149].
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PMID:CTC-11 (Teijin). 1595 88

Tissue factor (TF) mRNA levels in leukocyte and TF antigen in plasma were examined in patients with deep vein thrombosis (DVT). Although TF mRNA levels in leukocytes were higher in patients with DVT than in healthy volunteers, they were lower in patients with DVT than in those with solid cancer and those with disseminated intravascular coagulation (DIC). On the other hand, the plasma levels of TF antigens were markedly high in patients with DVT/pulmonary embolism (PE). Analysis of the role of underlying disease of DVT showed no significant difference in TF mRNA levels and TF antigens among patients with solid cancer, post-surgical, other diseases and those free of underlying diseases. In patients with VTE, plasma levels of D-dimer, soluble fibrin, GE-XDP and plasminogen activator inhibitor-1 did not correlate with TF mRNA or TF antigen. In analysis of 18 patients with PE with and without DVT, TF mRNA levels in leukocytes correlated with the plasma levels of D-dimer. These findings suggest that TF in leukocytes is more likely to be involved in the development of thrombosis in PE than DVT.
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PMID:Elevated levels of leukocyte tissue factor mRNA in patients with venous thromboembolism. 1603 15

A thorough review of the literature and of personal files has allowed the gathering of 81 patients with rare congenital bleeding disorders and thrombotic phenomena. Sixteen of these patients had congenital afibrinogenemia, eight involved factor V deficiency, 20 factor VII defects, 33 factor XI deficiencies and only one, a factor XIII defect. Altogether 42 patients showed arterial thrombosis (myocardial infarction [MI] in 28 cases; ischemic stroke in 4; arterial occlusion in 8; 2 patients with disseminated intravascular coagulation (DIC)). Ages varied between 13 and 74. Twenty-two patients were males and 16 females. In four cases, sex was not reported. There were three fatalities: two after a MI and one because of heart failure. With regard to venous thrombosis: 9 patients had pulmonary embolism, 15 patients had deep vein thrombosis, 9 patients had both pulmonary embolism and deep vein thrombosis; 1 patient had superficial vein thrombosis, whereas, 5 cases had an unusual site venous thrombosis (two portal systems, two cerebral sinuses, one inferior vena cava) for a total of 39 cases. Age varied between 3 and 86. In this case, 20 patients were males and 17 were females. In two cases, sex was not reported. There were three fatalities: two because of pulmonary embolism and one because of inferior vena cava thrombosis. The fact that thrombosis has never been described in patients with factor II or factor X seems to underscore the central antithrombotic role that these two factors have in the coagulation system.
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PMID:Arterial and venous thrombosis in rare congenital bleeding disorders: a critical review. 1683 33

D-dimer is an indicator for in vivo fibrin formation, reflecting the formation of fibrin crosslinked by factor XIIIa. D-dimer assays are frequently used in emergency situations, such as diagnosis of venous thrombosis and pulmonary embolism, or disseminated intravascular coagulation. In these conditions, short sample turnaround times are essential. The PATHFAST D-dimer assay allows rapid quantitative measurement of D-dimer in plasma and whole blood. The study shows an excellent correlation between whole blood and plasma measurement of D-dimer both in the high range, as well as in the normal range. Intra-assay and inter-assay coefficients of variation (CV) were below 10%. The upper limit of normal (ULN = mean value measured in 100 samples from healthy blood donors + 2 x S.D.) was approximately 1 microg/ml FEU, using the assay-specific calibration. The maximal value measured in 20 replicates of calibrator 1 containing no D-dimer antigen was 0.00052 microg/ml FEU, and this 10-fold lower than the declared detection limit of 0.005 microg/ml FEU. In conclusion, the PATHFAST D-dimer assay is the first automated fully quantitative D-dimer assay, which can use plasma and whole blood as sample materials in parallel.
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PMID:Performance evaluation of a new rapid quantitative assay system for measurement of D-dimer in plasma and whole blood: PATHFAST D-dimer. 1717 10

D-dimers are fibrin degradation products which are released during local or systemic activation of coagulation. D-dimer testing is widely used for the work-up of patients suspected of deep vein thrombosis or pulmonary embolism. Interpretation of D-dimer levels must take into account the sensitivity and specificity of the assay. The specificity is usually low, and increased D-dimer levels are encountered in many non-thrombotic situations. The sensitivity varies among the different testing methods and is maximal with ELISA assays. Highly sensitive assays allow exclusion of venous thromboembolism when D-dimer levels are normal, without further imaging. However, this diagnostic strategy may only be used safely when the clinical probability of thromboembolism is low to moderate. When combined with other tests of coagulation, D-dimer testing is also useful in the diagnosis of disseminated intravascular coagulation.
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PMID:[Clinical use of D-dimer testing]. 1734 27

Elevated plasma homocysteine levels are associated with an increased risk of deep vein thrombosis. Herein we report a case of familial hyperhomocysteinemia-related cerebral venous sinus thrombosis and pulmonary embolism in a 21-year-old man who presented with severe headache over bilateral frontal areas. Neurological examination revealed no evidence of focal neurological deficit. Chest CT showed pulmonary thromboembolism in bilateral basal lung fields and brain MRI disclosed right transverse and sigmoid venous sinus thrombosis. Routine immunological tests, coagulation factors and occult tumor screening were normal, as were vitamin B12 and folate levels. The DIC profile was negative, The only risk factor we were able to identify was an elevated serum homocysteine level, namely 46.23 microM/L. Hyperhomocysteinemia was also noted in the patient's asymptomatic elder brother (68.0 microM/L) and, to a lesser extent, in his parents (father 12.5 microM/L; mother 11.7 microM/L). In conclusion, the cause of cerebral venous thrombosis and pulmonary embolism in this young patient was most likely related to familial hyperhomocysteinemia, with the thromboembolic events precipitated by a preceding systemic infection. After anticoagulation therapy; the patient recovered completely without any residual neurological deficit.
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PMID:Familial hyperhomocysteinemia-related cerebral venous sinus thrombosis and pulmonary embolism: a case report. 1768 34

The D-dimer levels are considered to be useful for the diagnosis of thrombosis, and they can be clinically used as a negative predictive value (NPV). However, evidence for the efficacy of diagnosing thrombosis based on the D-dimer levels is still not well established. The present study was designed to evaluate the cut-off values of D-dimer levels as a negative predictor for thrombosis. The plasma concentrations of D-dimer were measured in inpatients suspected of having thrombosis, and then the findings were evaluated to assess the correlation with the diagnosis of thrombosis. In healthy volunteers, the median value of VIDAS-D-dimer was 0.12 microg/ml, and the 95% confidence interval was from 0.05 to 0.38 microg/ml. However, the plasma D-dimer levels were significantly higher in patients with thrombosis than in those without thrombosis; there was no significant difference in D-dimer levels among various thromboses such as pulmonary embolism (PE), deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC). The NPV for venous thromboembolism was 100% in patients with 0.5 microg/ml VIDAS-D-dimer and 1.2 microg/ml LPIA-D-dimer levels. Elevated D-dimer levels might indicate a high risk of thrombosis, especially DVT/PE, and they are thus considered to be useful as a negative predictor for thrombosis.
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PMID:Negative predictive value of D-dimer for diagnosis of venous thromboembolism. 1828 26

The parkinsonism-hyperpyrexia syndrome (PHS) is a rare but potentially fatal complication seen in Parkinson's disease (PD) patients, most commonly following reduction or cessation of antiparkinson medications. Clinically it resembles neuroleptic malignant syndrome with rigidity, pyrexia, and reduced conscious level. There may be features of autonomic instability, and serum creatine kinase (CK) may be elevated. Complications of PHS include acute renal failure, aspiration pneumonia, deep venous thrombosis/pulmonary embolism, and disseminated intravascular coagulation (DIC). Management consists of dopaminergic drug replacement, supportive measures, and treatment of complications. The prognosis is improved with early recognition and management. Mortality of up to 4% has been reported, but an additional one-third of patients have permanent sequelae. Patients and physicians should be warned against sudden reduction in antiparkinson medications. PHS should always be considered in a patient with parkinsonism who presents with an acute deterioration in symptoms.
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PMID:The parkinsonism-hyperpyrexia syndrome. 1871 8

It is well known that solid cancers are associated with thromboembolic complications, but recent studies have shown that the incidence of thrombosis may be as high (or even higher) in patients with malignant haematological disorders. However, this may be obscured by the significant morbidity and mortality due to other complications of haematological malignancies, such as bleeding and infections. The vast majority of patients with haematological neoplasias also have clinically silent haemostatic abnormalities, but some may show clinical manifestations, including venous thromboembolism, pulmonary embolism, disseminated intravascular coagulation and life-threatening thrombohaemorrhagic syndrome in acute leukaemias. The pathogenesis of thromboembolic disease in haematological malignancies is complex and multifactorial: tumour cell-derived procoagulant, fibrinolytic or proteolytic factors and inflammatory cytokines affect clotting activation, and chemotherapy and anti-angiogenic drugs increase thrombotic risk in patients with lymphoma, acute leukaemia and multiple myeloma. Infectious complications are another important factor: endotoxins from gram-negative bacteria induce the release of tissue factor (TF), Tumor Necrosis Factor (TNF) and interleukin-1b (IL-1b), and gram-positive organisms can release bacterial mucopolysaccharides that directly activate factor XII. Leukaemic patients may be affected by other prothrombotic factors, including hyperleukocytosis, increased TF expression and activation, and the prothrombotic properties of therapeutic agents such as all-trans retinoic acid and L-asparaginase, which can induce thrombosis involving multiple organs. The very high risk of haemorrhaging in these patients warrants prospective randomised trials evaluating optimal anti-thrombotic prophylaxis and treatment.
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PMID:Thromboembolic complications in malignant haematological disorders. 1948

An immune-mediated, severe, acquired prothrombotic disorder, heparin-induced thrombocytopenia type II (HIT II) occurs in 0.5-5% of patients exposed to unfractionated heparin longer than 5-7 days. Arterial and venous thromboses are induced by HIT II in about 35-50% of patients. Typical death rate for HIT is about 29%, while 21% of HIT patients result in amputation of a limb. The trend towards the occurrence of HIT due to the administration of low molecular weight heparins (LMWH) taking ever conspicuous place in the standard venous thromboembolism (VTE) prophylaxis has been more frequently observed recently. It is considered that LMWH may cause HIT II in about 0.25-1%. The need for further modification of HIPA assays with LMWH has been imposed in the HIT laboratory diagnostics, heretofore overburdened with complexity. There are several constantly opposing problems arising in HIT laboratory diagnostics, one of which is that in a certain number of patients immunologic assays detect nonpathogenic antibodies (mainly IgM or IgA heparin-PF4 antibodies) while, on the other hand, the occurrence of HIT pathogenetically mediated by minor antigens (neutrophil-activating peptide 2 or interleukin 8) may be neglected in certain cases. The following factors play an important role in the interpretation of each laboratory HIT assays performed: 1. correlation with HIT clinical probability test, the best known of which is 4T'score, 2. the interpretation of the laboratory findings dependent on the time of the thrombocytopenia onset, as well as 3. the sensitivity and specificity of each test respectively. The HIT diagnostics in the presence of other comorbid states which may also induce thrombocytopenia, more precisely known as pseudo HIT (cancer, sepsis, disseminated intravascular coagulation, pulmonary embolism, antiphospholipid syndrome, etc), represents a specific clinical problem.
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PMID:Obstacles in the diagnostics and therapy of heparin-induced thrombocytopenia. 2022 87


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