Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some traditional coagulation assays and several new molecular markers of hemostatic activation were measured in 37 patients with spinal cord injury (SCI). Twenty one of the patients (57%) developed deep vein thrombosis (DVT). The radiofibrinogen uptake test (RFUT) was used to diagnose DVT. Thirty eight percent of quadriplegic and 88% of paraplegic patients developed DVT (p < 0.005). No significant differences were found in platelet counts, mean platelet volumes, fibrinogen levels, von Willebrand factor (Ag) levels, platelet factor 4 and beta thromboglobulin concentrations between the groups with and without DVT. Fibrinopeptide A, thrombin/antithrombin III (TAT) complexes and plasma D-dimer levels were significantly higher in the patients with thrombosis. Most patients with DVT had elevated TAT complex levels up to three days before the RFUT became positive. D-dimer levels were highest after the diagnosis had been made.
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PMID:Thrombosis in spinal cord injury. 129 Jan 64

Thromboembolism is a major cause of morbidity and mortality in patients with spinal cord injury. The prevalence of DVT approaches 100%, and 1 to 2% will die of PE. Following injury, there is hypercoagulability as reflected by an increase in von Willebrand factor activity and antigen, and increased platelet reactivity to collagen. Thrombosis usually occurs 1 to 3 weeks after injury, with a peak between days 7 and 9. Intermittent calf compression boots reduce the frequency of thrombosis to 40%, and the addition of aspirin, 300 mg twice daily, and dipyridamole, 75 mg thrice daily, decrease this further to 25%. In an attempt to provide more effective prophylaxis, a further trial was conducted using heparin. Twenty-nine patients were randomized to receive 5000 U subcutaneously every 12 hours and compared with an equal number of patients treated with doses of heparin adjusted to prolong the APTT to 1.5 times control values; the mean dose was 13,200 U every 12 hours. Thromboembolism occurred in 9 (31%) of those on the fixed dose (6 DVT and 3 PE) and only 2 (7%) on the adjusted dose (p less than 0.05); however, 7 (24%) of the patients receiving the higher doses of heparin had bleeding compared with none of those on the fixed dose (p less than 0.02). Most recently, we have compared the safety and effectiveness of a low molecular weight heparin (Logiparin, Novo) with standard heparin. The former was given once daily in a dose of 3500 anti-Xa units, and the latter was 5000 U every 8 hours, both given subcutaneously.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of thromboembolism after spinal cord injury. 180 5

Aa a plasma marker of an endothelial abnormality, the serum activity of angiotensin-converting enzyme (ACE) was investigated at rest and after stimulation either by local venostasis or infusion of an analogue of lysine-vasopressin (desmopressin acetate). Desmopressin acetate did not induce any significant change in ACE, in contrast to the effect of venostasis. Searching for an endothelial abnormality implicated in the genesis of deep vein thrombosis, we used the local venostasis test in patients affected by recurrent deep vein thrombosis. Patients, divided in three groups (group I, documented history of recurrent deep vein thrombosis; group II, only one deep vein thrombosis or recurrent superficial venous thrombosis; group III, history of arterial thromboembolism), and controls were screened for basal and stimulated levels of serum ACE, together with fibrinolytic activity and von Willebrand factor level. Two types of abnormalities of serum ACE activity were found: low basal level in group I, and low response to venostasis in groups I and III; group II did not differ from controls. Measures of fibrinolytic and ACE activities are not redundant because the two types of ACE abnormalities were not individually encountered in the same patients and were independent from abnormalities of the fibrinolytic system. These findings suggest that an endothelial lesion could participate in the pathogenesis of some forms of recurrent deep vein thrombosis and support interest in the measurement of serum ACE to discriminate some patients at high risk of deep vein thrombosis.
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PMID:Serum angiotensin-converting enzyme: an endothelial cell marker. Application to thromboembolic pathology. 284 37

The development of postoperative deep vein thrombosis (DVT) was studied in 45 patients subjected to major abdominal surgery, 17 of whom showed signs of DVT as defined by 125I-fibrinogen test. The preoperative levels of von Willebrand factor (F VIII RAg) and platelets were higher in these 17 patients than in those remaining free from DVT. A contributing factor in DVT development thus may be more active primary haemostasis. Preoperative F XII levels were similar in the two groups, but the post-operative drop in F XII was more pronounced in the DVT group. An inhibitor of plasminogen activation behaved similarly in both groups. C1-inhibitor, the main inhibitor of the F XII-dependent clotting and fibrinolytic pathways, showed a typical acute-phase response postoperatively, without intergroup difference. The study suggested that F XII-dependent pathways play a role in the genesis of venous thrombi, at least in the postoperative period, though whether the postoperative F XII drop was due to a role in clotting or to fibrinolysis activation remains unclear.
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PMID:Relationship between factor XII, von Willebrand factor and postoperative deep vein thrombosis. 309 Aug 10

In nine patients with non-malignant diseases undergoing major upper abdominal surgery, the mechanism of the postoperative fibrinolytic shut-down was investigated because of its potential significance for postoperative deep vein thrombosis by employing new and specific methods for assessing and stimulating the fibrinolytic system. The shut-down was found to result from an impairment of the balance between tissue-type plasminogen activator, t-PA, and its recently discovered fast-acting inhibitor. In this balance, the t-PA antigen concentrations both in resting conditions and after stimulation evoked by desamino-D-arginine vasopressin (DDAVP) were found to be unchanged by surgery. However, there was a significant postoperative increase in t-PA inhibitor levels. The release of t-PA under the stimulus of DDAVP infusion overcame the postoperative shut-down of t-PA activity. However, DDAVP infusion was associated with potentially unfavourable increases in the Factor VIII/von Willebrand factor complex. The discovery of increased t-PA inhibitor in the postoperative period opens new possibilities for a rational approach to reduce or abolish the postoperative fibrinolytic shut-down.
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PMID:Fibrinolytic shut-down after surgery: impairment of the balance between tissue-type plasminogen activator and its specific inhibitor. 393

Hypervascularity, focal necrosis, persistent cerebral edema, and rapid cellular proliferation are key histopathologic features of glioblastoma multiforme (GBM), the most common and malignant of human brain tumors. By immunoperoxidase and immunofluorescence, we definitively have demonstrated the presence of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFr) in five out of five human glioma cell lines (U-251MG, U-105MG, D-65MG, D-54MG, and CH-235MG) and in eight human GBM tumor surgical specimens. In vitro experiments with glioma cell lines revealed a consistent and reliable relation between EGFr activation and VEGF production; namely, EGF (1-20 ng/ml) stimulation of glioma cells resulted in a 25-125% increase in secretion of bioactive VEGF. Conditioned media (CM) prepared from EGF-stimulated glioma cell lines produced significant increases in cytosolic free intracellular concentrations of Ca2+ ([Ca2+]i) in human umbilical vein endothelial cells (HUVECs). Neither EGF alone or CM from glioma cultures prepared in the absence of EGF induced [Ca2+]i increases in HUVECs. Preincubation of glioma CM with A4.6.1, a monoclonal antibody to VEGF, completely abolished VEGF-mediated [Ca2+]i transients in HUVECs. Likewise, induction by glioma-derived CM of von Willebrand factor release from HUVECs was completely blocked by A4.6.1 pretreatment. These observations provide a key link in understanding the basic cellular pathophysiology of GBM tumor angiogenesis, increased vascular permeability, and cellular proliferation. Specifically, EGF activation of EGFr expressed on glioma cells leads to enhanced secretion of VEGF by glioma cells. VEGF released by glioma cells in situ most likely accounts for pathognomonic histopathologic and clinical features of GBM tumors in patients, including striking tumor angiogenesis, increased cerebral edema and hypercoagulability manifesting as focal tumor necrosis, deep vein thrombosis, or pulmonary embolism.
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PMID:Epidermal growth factor stimulates vascular endothelial growth factor production by human malignant glioma cells: a model of glioblastoma multiforme pathophysiology. 768 Feb 47

Desmopressin acetate (1-deamino-8-D-arginine vasopressin [DDAVP]) improves hemostasis in hemophilia A and von Willebrand's disease and in some platelet disorders. In complex cardiac operations, excluding simple coronary artery bypass graft procedures, we found that desmopressin reduced blood loss by 40% and the need for transfusion by 34%. Conflicting reports followed. Future trials should emphasize patients with excessive bleeding. A possible post-desmopressin prothrombotic state was studied after hip replacement surgery. The incidence of deep vein thrombosis associated with warfarin sodium therapy was the same as that associated with desmopressin plus warfarin therapy. No desmopressin-induced thrombotic tendency was detected. A trend toward reduced blood loss with desmopressin was not significant. During cardiac catheterization, the plasma von Willebrand factor level was correlated with hemodynamic variables, including pulmonary vascular resistance, pulmonary arterial pressure, and (inversely) with cardiac index. von Willebrand factor concentration was highest in mitral stenosis. The relationship of these factors to the response to desmopressin remains to be defined.
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PMID:Adventures in hemostasis. Desmopressin in cardiac surgery. 843 Nov 22

We investigated hemostatic abnormalities in 37 patients with deep vein thrombosis (DVT) and pulmonary embolism (PE) (PE patients) and in 40 patients with DVT without PE (DVT patients). Plasma fibrinogen, thrombin-antithrombin complex (TAT), plasmin-plasmin inhibitor complex, fibrin-D-dimer, activated protein C (APC)-protein C inhibitor (PCI) complex, von Willebrand factor (vWf), tissue plasminogen activator (t-PA), PA inhibitor-I (PAI-1), and thrombomodulin levels in both PE and DVT patients were significantly increased compared with normal volunteers. Plasma APC-PCI complex, PAI-1, and vWf levels in PE patients were significantly higher than those in DVT patients without PE. These findings indicate that PE patients are more hypercoagulable and hypofibrinolytic than DVT patients. Plasma TAT, APC-PCI complex, PAI-1, and vWf levels were the most sensitive indicators for PE. In these patients, increases in TAT and APC-PCI complex suggest DVT and increased PAI-1 and vWf suggest the risk of onset of PE.
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PMID:Hemostatic abnormalities in patients with pulmonary embolism compared with that in deep vein thrombosis. 856 33

Platelet membrane glycoprotein Ibalpha (GPIbalpha) is a major receptor for von Willebrand factor and thrombin, which plays a key role in the initial development of thrombi. Two polymorphisms (HPA-2 and VNTR) that affect phenotype have been described in GPIbalpha. The relevance of these polymorphisms to thrombotic disease was investigated by genotypic identification in three case-control studies: 104 case patients with acute cerebrovascular disease (CVD), 101 case patients with acute coronary heart disease (CHD), 95 patients with deep venous thrombosis (DVT), and one control age-, sex-, and race-matched for each case patient. Results show that the C/B genotype of the VNTR and the HPA-2b polymorphisms of GPIbalpha are strongly associated with increased risk of coronary heart disease and cerebral vascular disease but not with deep vein thrombosis. These two polymorphisms of GPIbalpha may represent newly identified risk factors for arterial thrombotic disease, but not for venous thrombosis.
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PMID:Polymorphisms of platelet membrane glycoprotein Ib associated with arterial thrombotic disease. 976 62

The mechanism of arterial thrombosis, including coronary thrombosis, is different from that of thrombosis which occurs at sites of blood stasis such as deep venous thrombosis. Considering the onset of arterial thrombus formation, soluble coagulant factors may not play important roles for its onset since they are diluted by the effect of blood flow and cannot reach high enough concentrations to form insoluble fibrin. Platelets, which can stick to damaged vascular lumen even in the presence of shearing effects of blood flow, may play a crucial role in the onset of arterial thrombus formation. Thus, the mechanism of platelet thrombus formation should be assessed in the presence of blood flow. However, current dogma that fibrinogen binding to activated GP IIb/IIIa is the final common pathway for platelet thrombus formation was developed by using the function assay system of aggregometer, in which the effects of blood flow were not seriously considered. We are proposing in this review that plasma ligand protein of von Willebrand factor (vWF) and its interactions with platelet GP lb and GP IIb/IIa, which become apparent only in assays systems under influence of high shear rates of flow condition such as flowchambers or coneplate viscometers, are the key events leading to the onset of arterial thrombosis. A better understanding of the vWF-mediated mechanism of platelet thrombus formation is important for the development of better clinical tools to prevent ischemic heart disease as well as for a complete understanding of the mechanism of coronary thrombosis.
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PMID:Coronary thrombosis. Effects of blood flow on the mechanism of thrombus formation. 992 90


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