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)

The authors report a case of a 70-year-old man, with repeating episodes of systemic subdermal hematoma due to consumption coagulopathy associated with abdominal aortic aneurysm and the bilateral femoral arterial aneurysms. Prior to the first operation for abdominal aortic repair, anticoagulation therapy was applied to treat thrombocytopenia and hypofibrinogenemia. Five years following the first surgery, the same treatment was required before resection of the femoral lesions. Consumption coagulopathy is seen in approximately 1-4% population of aortic aneurysms, however, repeated appearance of symptomatic coagulopathy is rarely reported. Anticoagulation therapy was effective to normalize the coagulation and fibrinolytic system and followed by uneventful surgical resection of the aneurysms.
J Cardiovasc Surg (Torino) 2001 Apr
PMID:Consumption coagulopathy associated with aneurysms of the abdominal aorta and the bilateral femoral arteries. Report of a case. 1129 44

Active infective endocarditis is associated with high operative mortality and morbidity. The outcome may be improved by operating at the optimal time using the most appropriate surgical procedure. We describe a 15-year-old man with active infective endocarditis of the mitral valve associated with an annular abscess. Disseminated intravascular coagulation was associated with progressive decrease in the platelet count. The abscess was debrided, the mitral annulus was patch-reconstructed using bovine pericardium treated with glutaraldehyde, then the mitral valve was replaced. The patient was discharged from intensive care unit 3 days after operation with clinical and blood examination improvement. The patient is being observed carefully by periodic follow-up echocardiography, and there is no evidence of PVD, PVE or calcification of the patch during 14 months of follow-up period. Patch reconstruction of the annulus using bovine pericardium treated with glutaraldehyde reinforced the annulus and prevented local reinfection of the prosthesis in this patient.
Ann Thorac Cardiovasc Surg 2001 Feb
PMID:Patch reconstruction of the mitral annulus for active infective endocarditis with annular abscess. 1134 68

Although hemolytic anemia and thrombosis, which can be serious or even lethal, are often encountered in daily common practice, their pathogenesis has remained obscure, partially because of the absence of appropriate models. Here we present a unique chemically induced rat model of hemolytic anemia and disseminated thrombosis in which the organs developing infarction are comparable to those seen in humans. We exposed male and female Fischer F344 rats to two, three, or four daily doses of 2-butoxyethanol (BE) at 250 mg/kg body weight and examined for hemolysis and histopathological evidence of disseminated thrombosis on d 2, 3, 4, and 29. Time-course BErelated erythrocytic changes were statistically significant in both sexes. Evidence of thrombosis and infarction was seen mainly in females dosed more than once with widespread thrombotic crisis after two or three dosing, likely explicable by the more significant morphological changes in erythrocytes and hemolysis observed in this gender. We documented thrombosis and infarction in the heart, brain, lungs, eyes, and bones. Our model with its list of target organs similar to that observed in human diseases characterized by hemolysis and thrombosis [for example, thalassemia, sickle cell disease (SCD), paroxysmal nocturnal hemoglobinuria (PNF), disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), and hemolytic uremic syndrome (HUS)] suggests that it can be an excellent tool to study the pathogenesis of such complications.
Cardiovasc Toxicol 2002
PMID:A chemically induced rat model of hemolysis with disseminated thrombosis. 1266 64

The extrinsic hypercoagulation often resulting from sepsis could contribute to disseminated intravascular coagulation and cardiovascular complications. The effective prevention and intervention remained largely complex and unclear. In a cell model of human leukemia THP-1 monocytes following bacterial endotoxin (LPS) exposure, we show the novel anticoagulant ability of polyamino acid (polyAA) to suppress the extrinsic hypercoagulation. LPS-induced monocytic tissue factor (mTF) procoagulation was readily offset by poly-L-lysine (PLK), poly-L-arginine (PLR), or poly-L-ornithine (POR) included in single-stage clotting assays. IC50 was estimated at 0.35, 0.30, or 0.58 microM for PLR, POR, or PLK, respectively, whereas, poly-L-asparatic acid (PLD) remained ineffective. In a separate approach, inclusion of cationic polyAA in human plasma significantly prolonged prothrombin time, confirming the depressed extrinsic coagulation. In chromogenic assays dissecting the extrinsic pathway, we further determined the inhibitory site(s). PLK, PLR, or POR significantly inhibited LPS-induced FVII activation, which was consistent with the diminished FVIIa formation shown on Western blotting analysis. In contrast, polyAA did not show any additional effect on either FVIIa/FXa amidolytic activities or mTF/FVIIa-catalyzed FX activation. Nor did polyAA show any effect on FVII activation directly catalyzed by FXa. Taken together, PLK, PLR, or POR preferentially inhibited mTF-dependent FVII activation, accounting for their novel anticoagulant activities. PolyAA might present the specific antagonists to arrest the extrinsic hypercoagulation following inflammation.
J Cardiovasc Pharmacol 2003 Oct
PMID:Novel anticoagulant activity of polyamino acid offsets bacterial endotoxin-induced extrinsic hypercoagulation: downregulation of monocytic tissue factor-dependent FVII activation. 1450 32

Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Pro-inflammatory cytokines play a central role in the differential effects on the coagulation and fibrinolysis pathways. Vice-versa, activation of the coagulation system may importantly affect inflammatory responses by direct and indirect mechanisms. Apart from the general coagulation response to inflammation associated with severe infection, specific infections may cause distinct features, such as hemorrhagic fever or thrombotic microangiopathy. The relevance of the cross-talk between inflammation and coagulation is underlined by the promising results in the treatment of severe systemic infection with modulators of coagulation and inflammation.
Cardiovasc Res 2003 Oct 15
PMID:Infection and inflammation and the coagulation system. 1452 4

An 87-year-old woman who had undergone a stent-graft repair of a descending aortic aneurysm had additional stent-graft implantation for endoleak. The postoperative course was eventful reflecting her preexisting multiple organ disorder, and despite intensive treatment over a span of 2 months, she died of disseminated intravascular coagulation due to intestinal ischemia. Autopsy revealed a thrombus originating from the frayed distal edge of the graft. Although the relation between intestinal ischemia and the thrombus remains to be proven, this is considered a vital finding.
Jpn J Thorac Cardiovasc Surg 2004 Feb
PMID:Thrombus originating from frayed distal edge of an aortic stent-graft. 1499 82

This unusual report shows the association between thoracic aortic mural thrombus formation and the hypercoagulable state without concomitant disseminated intravascular coagulation. The patient's hypercoagulability was reflected by laboratory results that included elevated Factor VIII and fibrinogen levels, along with a decreased level of antithrombin III. The underlying cause was probably acute peritonitis, a condition associated with coagulopathy.
Cardiovasc Dis 1981 Dec
PMID:Thoracic aortic thrombi and hypercoagulability. 1521 74

Gram-negative sepsis is associated with disseminated intravascular coagulation (DIC) due to endothelial damage, which is induced by inflammatory mediators released from phagocytes activated by lipopolysaccharide (LPS). DIC is a systemic hemorrhagic syndrome, which results from the consumption of coagulation factors for the formation of multiple thrombi in the systemic microvessels; it is associated with multiple organ failure. Therefore, not only the systemic activation of coagulation but also the inflammatory response has been perceived as the therapeutic target for DIC in sepsis. We gave attention that protein C inhibitor (PCI) acts as an inhibitor of both plasma kallikrein and thrombin, which are known to act not only as procoagulant proteases but also as chemotactic factors toward phagocytes. Then, we hypothesized that PCI possibly acts as an anti-DIC agent rather than an inhibitor of the protein C anticoagulant pathway under the pathophysiology of DIC, accompanied by the decrease in the thrombomodulin expression on endothelial cells. Our studies have suggested that PCI purified from human urine (uPCI) improves the pathophysiology of DIC through the inhibition of activities of plasma kallikrein and thrombin, and the activities of PCI are regulated by N-glycans. This review introduces the anti-DIC action of PCI and about the modification of N-glycosylation site(s) of PCI to heighten the value of PCI as an anti-DIC agent.
Curr Med Chem Cardiovasc Hematol Agents 2004 Jan
PMID:Protein C inhibitor as an anti-disseminated intravascular coagulation agent--mechanism and modification. 1532 Aug 3

The acronym DIC is commonly interpreted as "death is coming." This pessimistic view emphasizes the deficiency of available treatment options following diagnosis of disseminated intravascular coagulation. Clinically, DIC manifests as a systemic hemorrhagic disorder associated with widespread activation and eventual exhaustion of the coagulation system, although events underlying DIC also involve effectors of inflammation. DIC can be associated with diverse conditions including sepsis and major trauma and, when identified, signifies a significant worsening in prognosis and expected mortality. Although recent clinical studies have shown that activated protein C reduces mortality in patients with severe sepsis, there is a need for further investigation and a better understanding of the underlying mechanisms.
Timely Top Med Cardiovasc Dis 2004 Aug 01
PMID:Alternative treatments for disseminated intravascular coagulation. 1554 51

Since Haissaguerre and his colleagues demonstrated the importance of the pulmonary veins in the generation of atrial fibrillation (AF) in 1998, a variety of different ablative interventions have been performed to eliminate AF. Various complications related to catheterization, ablation itself including pulmonary vein stenosis, pericardial effusion, stroke, and atrioesophageal fistula have been reported. Disseminated intravascular coagulation (DIC) is a systemic syndrome characterized by enhanced activation of coagulation with some intravascular fibrin formation and deposition. This is the first report, to our knowledge, of a patient whose condition was complicated by DIC after segmental ostial isolation of pulmonary veins for persistent AF. The patient has completely recovered from the DIC by hemodialysis, administration of blood constituents for 15 days.
J Cardiovasc Electrophysiol 2005 Sep
PMID:Disseminated intravascular coagulation as a complication of radiofrequency catheter ablation of atrial fibrillation. 1617 24


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