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)

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.
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PMID:Virus infection of endothelial cells. 626 Aug 74

The importance of the blood coagulation sequence as an integral part in the pathogenesis of diseases inside as well as outside the blood vessels is becoming increasingly apparent. Mononuclear phagocytes have important functions in initiation of coagulation by producing several procoagulant substances, including thromboplastin, the potent trigger of the extrinsic pathway. Increasing evidence demonstrates the clinical importance of monocyte and macrophage thromboplastin synthesis in the pathogenesis of a variety of diseases. This review surveys the role of monocyte/macrophage thromboplastin in relation to inflammatory diseases, cancer, disseminated intravascular coagulation and diseases of the blood vessels, thrombosis and atherosclerosis.
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PMID:Clinical significance of increased thromboplastin activity on the monocyte surface--a brief review. 639 44

Clinicopathologic correlations of nonbacterial thrombotic endocarditis (NBTE) were studied with special reference to their pathogenetic role in cerebral and myocardial infarction. In 2340 cases of consecutive autopsies of the aged, NBTE was observed in 217 cases or 9.3%. The age distribution of NBTE revealed a gradual increase with advancing age. The underlying diseases of NBTE were malignant neoplasm (51.6%), infection (28.3%) and other diseases (20.1%). The incidence of NBTE in each cancer was high in cancers of the colon (16.2%), pancreas (15.2%), gall bladder or bile duct (14.1%) and lung (13.0%). The vegetations of NBTE were found on the aortic valve in 46.1%, on the mitral valve in 40.6% and on the both valves in 8.3%. The incidence of myocardial infarction and scar was 51.2% in the NBTE group, while it was 38.6% in the non-NBTE control group (p less than 0.02). This difference was marked in patients with a small infarction (10.6% vs. 5.3%) and a myocardial scar (30.4% vs. 19.0%). The grade of coronary stenosis was less in the NBTE group than in the control group (p less than 0.001), suggesting that the origin of the myocardial ischemic lesion was embolism from NBTE. The incidence of large cerebral infarction was 14.7% in NBTE and 9.2% in the control group, and that of medium sized cerebral infarction was 35.0% and 23.6% respectively. In this latter group, cortical infarction comprised 57.9% in the NBTE group and 26.6% in the control group. In large cerebral infarction, cerebral atherosclerosis was less severe in NBTE than in the control group (p less than 0.001), also suggesting an embolic mechanism. Disseminated intravascular coagulation was found in 41.9% of NBTE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonbacterial thrombotic endocarditis as a cause of cerebral and myocardial infarction. 648 38

Two cases of spontaneous atheromatous embolization associated with unusual complications are presented. One is an 85-year-old man who developed an acute abdomen and underwent a surgical resection of totally infarcted left-sided colon. Histologically, multiple acute atheromatous emboli were found occluding the serosal and pericolic mesenteric arteries causing transmural necrosis of the involved portion of bowel. The other is an 80-year-old woman who had had a coronary heart disease, hypertension, and renal insufficiency, and terminally developed a rapid deterioration of renal function and melena. Postmortem examination showed a severely, ulcerated, aortic atherosclerosis and widespread, recurrent, atheromatous emboli in many abdominal organs with the resultant severe nephrosclerosis, gastrointestinal mucosal hemorrhagic necrosis, and multiple infarcts in the pancreas and spleen. In addition, there was focal cortical necrosis of the kidneys accompanied with glomerular capillary fibrin thrombi indicating disseminated intravascular coagulation (DIC). These findings seen in the present two cases were briefly discussed in light of the previous pertinent literature.
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PMID:Atheromatous embolization. Report of two cases with unusual complications. 650 92

The role of the blood platelets in the aetiogenesis of arterial lesions has been underlined in recent years by studies of platelet elastase and above all the mitogenic factor of smooth muscle cells. A truly thrombogenic theory of atherosclerosis can now be envisaged. In the context of arterial thromboses, it is interaction between the damaged vessel wall, the lesion most often being atherosclerosis, and blood platelets which gives rise to the thrombus. In certain conditions such as diabetes abnormalities in the interaction between platelets and vessel walls may favour the development of vascular lesions and thromboses. With regard to venous thrombosis, the participation of the vessel and/or platelets is less clear. However, recently described platelet procoagulant activities could activate coagulation mechanisms. Knowledge of diseases of primary haemostasis has benefited from studies of platelet-vessel interaction. Whilst the spontaneous haemorrhagic syndrome of major thrombocytopaenia remains mysterious, platelet membrane molecular abnormalities in thrombopathies such as Bernard Soulier syndrome or thrombasthenia offer an explanation for their mechanisms. By their interaction with the vessel, platelets finally participate in mechanisms of inflammation, immunological conflicts, disseminated intravascular coagulation and metastatic dissemination.
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PMID:[Interactions between the platelets and the vessel wall. Part 2: physiopathology (author's transl)]. 746 76

Important discoveries of the last twenty years indicate that blood platelets play an important role in the etiopathogenesis of many serious diseases. These include atherosclerosis with its acute vascular complications like myocardial infarction and many forms of disseminated intravascular coagulation. Their role is not limited here to platelet participation in thrombus formation. This is why we are constantly searching for a method which will allow to detect platelet activation in vivo before any important damage to vital organs and tissues will take place. Despite the implementation of sophisticated modern laboratory techniques reliable assessment of such activation poses still a clinical and laboratory problem.
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PMID:[Laboratory methods of estimating blood platelet activation]. 799 72

The authors compared the course of the postoperative period in patients with obliterating diseases of the vessels in the lower extremities and concomitant diabetes mellitus who were on conventional drugs and on a new home-made drug dimephosphon. It has been established that the use of dimephosphon in a complex postoperative therapy improves the results of surgical treatment of patients with obliterating atherosclerosis of the vessels in the lower extremities and concomitant diabetes mellitus. The results are due to dimephosphon-induced activation of fibrinolysis, platelet hemostasis normalization, arrest of latent disseminated intravascular coagulation syndrome, immunocorrecting drug effect and its positive impact on hormonal homeostasis.
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PMID:[Use of dimephosphon in patients with obliterating diseases of the vessels of lower limbs during the postoperative period]. 808 Jan 30

Endothelium damage is associated with thrombotic risk in a variety of diseases including atherosclerosis, gram negative sepsis, viral infections and neoplastic disease. Therefore, it appears necessary to find a mean for the clinical investigation for such a damage. Among the markers of these cells, thrombomodulin which is a membrane glycoprotein, seems to be of great interest for this purpose. Actually, thrombomodulin is also found in plasma, following an endothelial lesion. Plasma levels of thrombomodulin are increased in a certain number of pathologies associated with endothelium lesion: atheromatous arterial disease, disseminated intravascular coagulation syndrome and also in systemic lupus erythematosus where the levels of plasma thrombomodulin are related to the severity of the pathology. Moreover, previous in vitro studies confirm the fact that the release of thrombomodulin from the endothelial cell membrane occurs during the course of injury by activated leukocytes or hydrogen peroxide. So, one can suppose a prospective interest in the measurement of plasma thrombomodulin as a diagnostic tool for the approach of endothelium damage.
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PMID:Plasma thrombomodulin: new approach of endothelium damage. 820 13

There is compelling experimental evidence that tissue factor pathway inhibitor (TFPI) exerts important role(s) as a natural anticoagulant. Immunodepletion of TFPI lowers the treshold by which tissue factor (TF) can induce disseminated intravascular coagulation. Conversely, infusion of recombinant TFPI protects against thrombosis and disseminated intravascular coagulation in numerous experimental models. Since TFPI mutants associated with thrombosis have not yet been identified, a definite role of TFPI in coagulation is yet to be assigned. Current research on TFPI is mainly focused on the cell biology of TFPI, on the contribution of TFPI to the anticoagulant action of heparins, and on the role of lipoprotein-associated TFPI. TFPI is produced constitutively in endothelial cells, and is to a great extent bound to its surface. The binding molecule(s) have not yet been characterized, but TFPI is rapidly released by heparin and other negatively charged ions. In other cell lines degradation of TFPI is mediated by the low density lipoprotein receptor-related protein, which may be important for its clearance. In plasma, TFPI contributes strongly to the postheparin anticoagulant effect seen in dilute prothrombin time assays. The effect is probably mediated by redistribution of TFPI. Moreover, in the presence of heparin, antithrombin and TFPI cooperate to inhibit activation of coagulation. Antithrombin abrogates activation of factor VII bound to TF, whereas TFPI inhibits factor VIIa/TF complexes formed. The role of lipoprotein associated TFPI is still essentially unknown, but may play an important role in atherosclerosis.
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PMID:Tissue factor pathway inhibitor (TFPI)--an update. 897 19

Intravascular activation of leukocytes has been shown to be involved in a wide range of different and apparently unrelated clinical situations, such as systemic inflammatory response syndrome, ischemia/reperfusion, disseminated intravascular coagulation, atherosclerosis... All of them involve to different degrees many steps of the inflammation process, with leukocyte accumulation and release of toxic species. Haemostasis, leukocyte functions and their cross-talk are summarized in this paper, as well as the most popular methods used for studying leukocyte functions in vascular pathologies. The strengths and present limitations of flow cytometry are analyzed in comparison with the biochemical and functional approaches.
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PMID:Flow cytometry assessment of leukocyte functions in vascular pathologies. 903 Sep 64


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