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)

48 patients with heart failure were supported by intra-aortic balloon pumping (IABP) from 1985 to 1993. The disease included rheumatic (39 patients), congenital (7) and coronary hearts (2). The average time of supporting with IABP was 27 hours, 23 patients (48%) survied inclading 19 patients with postoperative lower cardiac output syndrome. Hemodynamics was improved. IABP increased cardiac output syndrome, and hemodynamics was improved. IABP increased cardiac output (50%), cardiac index (60%), stroke volume (50%), stroke volume index (60%) and decreased left atrial pressure or pulmonary wedge pressure. The mortality was 25 patients (52%). The death causes were as follows: arrhythmia (4), renal failure (6), lung failure (2), DIC (1), and the other (12). The main complication of IABP was lower limb ischemia particularly in surgical cut-down method to establish IABP. The analysis indicated that the temporary pacing maker with IABP could prevent some arrhythmia such as frequent premature ventricular beats. Lower limb ischemia and renal failure should receive much attention because they are easy to be confused with shock symptom when IABP.
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PMID:[Intra-aortic balloon pumping in 48 patients with heart failure]. 870 69

Coagulation activation and fibrinolysis parameters were studied in eleven cases of thrombotic microangiopathy concerning eight adult patients. In addition to routine coagulation tests, antithrombin III, von Willebrand factor (vWF), prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), D-dimer (DD), and plasminogen activator inhibitor type 1 (PAI-1) were measured in the plasma at the time of diagnosis and as soon as remission was achieved after therapy with plasma exchange and Iloprost. In the acute phase all patients showed normal aPTT, normal or slightly prolonged prothrombin time, normal or enhanced plasma levels of fibrinogen and antithrombin III, at variance with results in patients affected by disseminated intravascular coagulation. Mean F1+2, TAT, DD, vWF and PAI-1 were elevated in the acute phase, but decreased significantly in the early phase of remission. Our data provide evidence of increased thrombin generation rate which takes place in the acute phase of the disease and does not result in consumption coagulopathy, due to appropriate inhibition by antithrombin III; blood coagulation activation promptly decreased as soon as remission was achieved. Cross-linked fibrin deposition together with PAI-1 may consolidate the platelet plug, eventually resulting in microvascular occlusion and ischemia.
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PMID:Plasmatic parameters of coagulation activation in thrombotic microangiopathy. 895 55

A case of a patient developing anuric acute renal failure and a hemorrhagic syndrome resembling disseminated intravascular coagulation after contact with Lonomia caterpillars is reported. Renal histology showed only mild changes consistent with renal ischemia, although the patient never was hypotensive. The mechanisms of renal injury were obscure and might be related to transient glomerular ischemia due to microcirculation fibrin deposition or to direct venom nephrotoxicity.
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PMID:Severe acute renal failure induced by the venom of Lonomia caterpillars. 895 24

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

Tissue factor pathway of coagulation plays a dominant role during normal haemostasis. Tissue factor pathway inhibitor (TFPI), expressed primarily by the microvascular endothelium, appears to be the major physiologic inhibitor of TF-induced coagulation. TF-initiated coagulation also plays an important role in the pathophysiology of many diseases including coronary thrombosis, sepsis, disseminated intravascular coagulation, stroke, cancer, acute respiratory distress syndrome, and ischemia-reperfusion injury. Several animal studies have found a beneficial effect of anti-TF monoclonal antibodies and, recombinant TFPI in some of the above clinical conditions. rTFPI is presently being used in clinical trials in patients with sepsis and in those following microvascular surgery. This article discusses many of the animal studies addressing inhibition of TF-induced coagulation, as well as potential therapeutic uses of rTFPI in humans.
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PMID:Tissue factor pathway inhibitor: potential therapeutic applications. 919 99

The hemolytic uremic syndrome in adults is an uncommon clinical entity consisting of microangiopathic hemolytic anemia, thrombocytopenia, and renal dysfunction. A previously healthy 42-year-old man, after a 2-day prodromal phase, developed severe pain and coldness in both legs, with purpura in the face and extremities. On admission, hepatorenal dysfunction and disseminated intravascular coagulation were evident. These complicated signs and symptoms led to nonspecific supportive therapy because of delayed diagnosis. The patient's condition gradually improved except for ischemia of the legs, which progressed into symmetrical necrosis; eventually, bilateral below-knee amputation was required. This is the first reported case of the hemolytic uremic syndrome complicated by bilateral leg ischemia. A presumed cause of the ischemia was disseminated intravascular coagulation, a rare complication of the hemolytic uremic syndrome.
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PMID:The hemolytic uremic syndrome presenting as bilateral leg ischemia. 921 26

The lower temperatures utilized during profound hypothermic circulatory arrest (PHCA) surgery may exacerbate the hypothermia associated platelet and clotting factor dysfunction observed in conventional cardiopulmonary bypass (CPB) procedures. Hypothermia has been shown to impair the activity of the enzymes involved in the platelet activation pathways and to reduce the enzymatic activity of clotting factors upon coagulation activation. The resulting retardation of the generation of fibrin/platelet clot compounded by the presence of heparin may contribute significantly to a bleeding tendency. Excessive fibrinolytic activity may disrupt surgical wound thrombi and exacerbate haemorrhage. There is good evidence that the fibrinolytic activity, mediated predominantly by tissue plasminogen activator (tPA), is a secondary response to thrombin generated by coagulation activation, which is ongoing during CPB despite full heparinization. The effects of hypothermia on the fibrinolytic response remain to be clarified and the extent to which the lower temperatures and blood stasis associated with PHCA moderate this response is unknown. Despite impairment of coagulation activation by hypothermia there appears to be a shift in the hemostatic balance towards thrombosis presumably as a consequence of endothelial cell injury by both hypothermia and stasis induced ischemia. There is evidence that widespread microvascular thrombus deposition may occur as a consequence of stasis in patients undergoing PHCA and that this might result in vascular occlusion and end organ damage. Although it is not uncommon to find laboratory evidence of disseminated intravascular coagulation (DIC) in patients presenting with aortic aneurysm rupture or dissection, the incidence of clinically overt DIC resulting in bleeding is low. The underlying hemostatic disturbance however may contribute to the surgery-associated bleeding diathesis.
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PMID:Hematological consequences of profound hypothermic circulatory arrest and aortic dissection. 927 46

A total of 140 pathoanatomic conclusions and files collected by the author are analyzed. Morphological signs of the DIC syndrome were detected in 55% of patients who died. In 42% of lethal outcomes this syndrome was the final direct cause of death after such conditions as terminal stage of cancer, sepsis, extensive myocardial infarction, mechanical jaundice, uremia, bacteremia, etc. In 13% of autopsies fatal intravascular coagulation was a complication of the intervention or hemorrhage which was arrested before death. The DIC syndrome is diagnosed during autopsy due to a complex of peculiar changes in the viscera which are called "shock" in such cases. The signs of a shock liver are as follows: a characteristic red net pattern of the sliced surface and histological phenomena related to blocking of the sinusoidal bloodflow and lobular ischemia: abnormal hepatocyte complexes, fragmentation of liver bulks, and necrosis of the central lobules.
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PMID:[Morphological diagnosis of DIC syndrome. Shock liver]. 951 Dec 43

Antithrombin III (AT III) supplementation has proven to be effective in the treatment of disseminated intravascular coagulation. Administration of AT III is also useful for prevention of organ failure in animals challenged with endotoxin or bacteria and it increases the survival rate of such animals. Since inhibition of coagulation abnormalities failed to prevent organ failure in animals given bacteria, AT III may exert a therapeutic effect independent of its anticoagulant effect. This therapeutic mechanism of AT III has been explored using an animal model of septicemia. AT III prevented pulmonary vascular injury by inhibiting leukocyte activation in rats given endotoxin. This effect is mediated by the promotion of endothelial release of prostacyclin which inhibits leukocyte activation. Interaction of AT III with heparin-like glycosaminoglycans (GAGs) on the endothelial cell surface appears to be important for this effect. Heparin inhibits these therapeutic effects of AT III by preventing AT III from interacting with the cell surface heparin-like GAGs. This activity of AT III may explain why AT III prevents organ failure as well as coagulation abnormalities in patients with sepsis. This antiinflammatory activity of AT III may be useful for the treatment of organ failure such as in ischemia/reperfusion-induced organ dysfunction, in which activated leukocytes play a critical role.
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PMID:The anti-inflammatory properties of antithrombin III: new therapeutic implications. 951 77

Pneumonia is the most common serious complication of varicella infection in adults. A variety of thrombotic complications including purpura fulminans and disseminated intravascular coagulation have been reported in children with varicella but not in adults. Two men with varicella pneumonia who had profound lower extremity ischemia caused by thrombosis of the profunda femoris and tibial arteries are reported. Both patients had free protein S deficiency and vascular thrombosis in association with varicella pneumonia without overt evidence of disseminated intravascular coagulation or purpura fulminans. Antiphospholipid immunoglobulin G and immunoglobulin M antibodies were present in one, whereas the other had evidence of the lupus anticoagulant. The proposed pathogenesis and management options including intraarterial thrombolytic therapy with urokinase and the need for long-term anticoagulation are discussed.
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PMID:Spontaneous tibial artery thrombosis associated with varicella pneumonia and free protein S deficiency. 954 47


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