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)

Increased fibrinolytic activity and consumption coagulopathy are common consequences of liver transplantation and are a major cause of morbidity and death. In the present investigation the effects of hepatic ischemia on the coagulation mechanism were studied in the stump-tail monkey. The results suggest that, although fibrinolytic activity is induced by both major intraabdominal operations as well as one hour of hepatic ischemia, consumption coagulopathy, presumably due to intravascular clotting, is enhanced by the revascularization of the ischemic liver, possibly because of clotting within the liver itself. Release of a plasminogen activator from the liver due to hepatic ischemia alone is not demonstrated by these studies. It is believed that the first phase of intravascular coagulation after liver transplantation is due to release of tissue activators from vascular endothelium, which may be minimized by the action of ganglionic blocking agents. The severity of fibrinolysis in this stage is aggravated by the "liverless state," in which no clearance of plasminogen activators occurs. The degree of liver injury directly affects the ability of the liver to control hypercoagulability in the second phase. Thrombus formation which we believe occurs during this phase may be minimized by use of continuous controlled heparinization.
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PMID:Effects of hepatic ischemia on coagulation in primates. Application to liver transplantation. 1048 79

Recently, basic and clinical advances have provided insights into the molecular events that link inflammation with blood coagulation and thrombosis. At least in cell culture, the inflammatory cytokines, especially tumour necrosis factor alpha (TNF) and interleukin 1-beta (IL-1), are major mediators that can elicit changes in cell phenotype. With respect to coagulation, one of the clot-promoting and one of the inhibitory pathways seem especially prone to modulation by these cytokines. Whenever Tissue Factor contacts the blood, coagulation is initiated rapidly. These cytokines can elicit Tissue Factor production on endothelium and monocytes. Thus, the cytokines elaborate Tissue Factor formation intravascularly. This contrasts with the normal situation in which Tissue Factor is located exclusively in the extravascular space, largely on fibroblasts, where it is expressed constitutively. Furthermore, cytokines, especially interleukin 6 (IL-6), can stimulate new platelet formation, and the new platelets responding to IL-6 have increased sensitivity to thrombin activation and increased procoagulant activity. Regulating the clotting process are a large number of anticoagulant and fibrinolytic mechanisms. The three major anticoagulant mechanisms appear to involve antithrombin-heparin, Tissue Factor pathway inhibitor (TFPI) and the Protein C pathway. Of these, the Protein C pathway appears to be the primary target for cytokine action. The Protein C pathway is initiated when thrombin binds to thrombomodulin (TM). TM is expressed constitutively on endothelium. In tissue culture, TNF, IL-1 or endotoxin lead to a slow loss of TM and endothelial cell Protein C receptor (EPCR) from the cell surface. In addition, Protein S levels decrease in patients with disseminated intravascular coagulation (DIC). Taken together, these results suggest that cytokines should elicit massive thrombotic responses when administered systemically. At near toxic levels, TNF fails to elicit an overt DIC or thrombotic response in patients, although sensitive markers of coagulation do detect changes in coagulation in response to TNF. In baboons, very high levels of TNF also fail to elicit fibrinogen or platelet consumption. However, if the Protein C pathway is blocked, these cytokines can elicit either DIC or deep-vein thrombosis, depending on the conditions. Thrombus formation is potently potentiated by impeding flow and/or by catheterization. DIC is facilitated by providing membrane surfaces, possibly mimicking complement mediated platelet activation/damage that occurs in shock. Thus, available evidence suggests important roles for inflammatory cytokines in DIC and thrombosis, but they seem insufficient by themselves to elicit overt thrombotic responses without secondary stimuli. Current data suggest that anti-inflammatory drugs are a viable candidate to blocking DIC or thrombosis without impairing the haemostatic balance.
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PMID:Possible involvement of cytokines in diffuse intravascular coagulation and thrombosis. 1085 74

Time course of parameters characterizing vascular platelet and coagulation hemostasis was studied in 83 patients with colorectal cancer before, during, and for 7 days after surgery. Before the intervention the disorders in regulation of the blood aggregate state present as chronic disseminated intravascular coagulation (DIC) syndrome. The intervention induces the development of subacute DIC syndrome. During the postoperative period disorders in hemostasis system manifest by chronic hypercompensated DIC syndrome. Thrombotic complications during the postoperative period were prevented by fraxiparin 2 h before the intervention and then during 5 days of the postoperative period in a daily dose of 7500 units anti-Ca (about 100 units/kg) and verapamil starting from day 1 after surgery in a dose of 0.2-0.3 mg/kg for 3 days.
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PMID:[Complex prevention of thrombotic complications in patients with colorectal cancer during different stages of surgical treatment]. 1175 3

Systemic bleeding due to consumption coagulopathy and thrombocytopenia due to activation of procoagulants is the leading manifestation and cause of death in Russell's viper systemic envenoming. Thrombotic occlusion of the blood vessels is rare in cases of snakebite. In this report, two adult patients with Russell's viper systemic envenoming presented multiple cerebral infarctions, digital gangrenes and ischaemic organs in addition to typical clinical manifestations of bleeding diathesis and renal involvement. Our findings in these two special cases suggest that the venom-induced coagulopathy and endothelium damage, predisposed by toxin-induced vasoconstriction, might be the possible mechanism of multiple thrombotic vascular occlusions in systemic envenoming of Formosan Russell's viper.
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PMID:Multiple thrombotic occlusions of vessels after Russell's viper envenoming. 1242 9

Thrombosis in congenital factor (F) VII deficiency was investigated through extensive phenotypic and molecular-genetic studies. Patients with a history of thrombosis among 514 entries in the FVII Deficiency Study Group database were evaluated. Thrombotic events were arterial in one case, disseminated intravascular coagulation in another and venous in seven. Gene mutations were characterized in eight patients: three were homozygous, three compound heterozygous and two heterozygous. FXa and IIa generation assays were consistent with the genetic lesions. One patient was heterozygous for the FV Leiden and one for the FIIG20210A mutation. In seven patients, surgical interventions and/or replacement therapies had a close temporal relationship with thrombosis, while in the remaining, events were apparently spontaneous. Thromboses were not associated with any specific age, phenotype, mutation zygosity or thrombophilic abnormalities. In particular, severe FVII deficiency did not seem to offer protection from strong thrombosis risk factors such as surgery and replacement therapy.
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PMID:Thrombosis in inherited factor VII deficiency. 1452 98

Acute hemorragic and thrombotic complications in cancer are often life threatening. Hemorragic disease are frequent (10%) and sometimes revealed the cancer. In more than 50% thrombocytopenia is involved. Bleeding is related to a vessel wound in 30% of the hemorragic complications either by a tumoral diffusion or by the tumor itself. In less than 10%, the bleeding is linked to disseminated intravascular coagulation. Very rarely coagulation factor deficit is found. Thrombotic manifestations are also frequent (15% of cancer patients). Venous system are usually involved. Clinicians must be aware of these complications to favor the best treatment early as possible to prevent fatal complications.
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PMID:[Acute thrombotic and hemorragic complications in cancer]. 1500 72

The pathomorphology of intoxication of alcohol surrogates is described. A high frequency rate of DIC-syndrome is shown for the condition. A majority of thrombi accumulates at places with the highest concentrations of toxic substances as well as at those places, through which poisoning substances are brought out of the body, i.e. in the liver (since toxic substances are introduced perorally) and kidneys. Thrombi were detected in all internals, including the brain, in lethal intoxication. The immediate toxic effect from methanol and from higher spirits can matter in the genesis of changes, including acute swelling and chromatolysis with subsequent cell death. Exclusively cerebral or coagulopathic-cerebral types of thanatogenesis were registered in studied case of intoxication.
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PMID:[The forensic medical diagnosis of intoxication of alcohol surrogates by morphological findings]. 1552 82

Thrombotic microangiopathies (TMAs) are characterized by thrombocytopenia, microangiopathic hemolytic anemia, and organ failure (mostly renal dysfunction). TMA includes thrombotic thrombocytopenic purpura (TTP) with predominant neurological signs and hemolytic uremic syndrome (HUS) with predominant renal dysfunction, but they are often indistinguishable each other with the clinical signs alone. Recent availability of von Willebrand factor-cleaving protease or ADAMTS13 activity has defined that TTP is a syndrome frequently associated with a deficient ADAMTS13 activity with or without its inhibitors (autoantibodies), whereas HUS has almost the normal activity. Here, we present two cases of TMA, who were initially diagnosed as "multiple sclerosis" because of the fluctuated neurological signs. Case 1 was a 54-year-old male and case 2 was a 30-year-old female. During their clinical course, they accompanied thrombocytopenia, to which the etiology left undetermined in case 1, but case 2 was suspected DIC because she had such past history. Prophylactic infusion of platelet concentrates to both cases dramatically aggravated their clinical signs. Case 1 was diagnosed to be intravascular lymphoma complicated with acquired TTP, after showing a deficient ADAMTS13 activity. Case 2 was unable to assay ADAMTS13 activity, but later the autopsy revealed the presence of multiple hyaline membrane thrombosis in many organs, together with a lack of demyelinating lesions, solely confirming a diagnosis of TMA.
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PMID:[Thrombotic microangiopathy]. 1743 15

Hereditary haemorrhagic telangiectasia (HHT) causes chronic nasal and gastrointestinal haemorrhage. Prothrombotic agents are commonly used for severe haemorrhage. Thrombotic risks have not been defined. In order to identify prothrombotic variables in HHT patients, and assess their potential functional significance, a pilot ELISA-based study comparing plasma proteins in healthy individuals with HHT to age/sex-matched non-HHT controls was validated in a full study of 309 consecutive HHT-affected individuals. In the pilot study, factor VIII (FVIII) and von Willebrand factor antigen concentrations were elevated in the HHT group compared to non-HHT controls (p<0.0013, Mann-Whitney). Service laboratory measurements confirmed high FVIII:Ag in 125 HHT-affected individuals with no recent ill-health, intervention or venous thromboemboli. FVIII:Ag levels increased with age. Logistic regression also suggested an age-independent association with HHT-associated pulmonary arteriovenous malformations (AVMs). No association was demonstrated between FVIII:Ag and acute phase response, disseminated intravascular coagulation, ABO group, pulmonary artery pressure, or markers of HHT haemorrhage. Elevated FVIII:Ag were associated with shortened activated partial thromboplastin times (APTTs), and VTE:VTE affected 20/309 (6.5%) HHT-affected individuals, at median age 61(36-71) years. Four VTE occurred in factorV Leiden heterozygotes in the months following PAVM-associated brain abscess. The strongest association with VTE was with log-transformed FVIII:Ag measured 10-132 months from VTE (odds ratio 2.41, 95% confidence intervals 1.254, 4.612, p=0.008). Age made no additional contribution to VTE risk once adjusted for FVIII:Ag. In conclusion, HHT-related elevation of FVIII:Ag levels may influence thrombotic risk in HHT. Individualised risk-benefit considerations may be helpful in HHT management.
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PMID:Elevated factor VIII in hereditary haemorrhagic telangiectasia (HHT): association with venous thromboembolism. 1861 56

The association between thrombosis and cancer has been extensively studied since first pointed out by Trousseau in 1895. It is, however, not commonly appreciated that the incidence of thrombosis in malignant hematologic disorders is as high or even higher than in solid tumors. Thrombotic complications in acute leukemia are often overlooked because bleeding complications generally dominate the clinical picture. Yet, the patient is at risk for both. While there are many thrombogenic factors shared by both solid tumors and leukemia, many additional prothrombotic features are present in leukemia. The prothrombotic factors include hyperleukocytosis, increased expression of tissue factor and its activation in leukemic cells, and the prothrombotic adverse effects of therapeutic agents and vascular access catheters. In addition, comorbid conditions including hereditary thrombophilia, infection, endothelial cell activation by cytokines, antiphospholipid syndrome and acquired activated protein C resistance are major contributory factors. Factors that increase the bleeding risk include thrombocytopenia, disseminated intravascular coagulation, and excessive fibrinolysis, which is enhanced by increased expression of Annexin II by leukemic cells. Therapeutic approaches to both bleeding and thrombotic conditions require special considerations of these factors.
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PMID:Double hazard of thrombophilia and bleeding in leukemia. 1802 23


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