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)

Eighty-two women whose pregnancy was complicated by anemias of varying severity and twelve healthy pregnant women were examined. Blood plasma immunoglobulins A, G, and M were measured by immunochemical methods, as were the immune complexes of various levels and some parameters of the homeostasis system. The findings evidence a noticeable elevation of the concentrations of all immunoglobulins, of low-disperse immune aggregates in severe anemia of pregnancy, as well as intensive synthesis of immunoglobulin M in the fetus, low level of large immune complexes, and stimulation of some homeostasis components that results in consumption coagulopathy and chronic DIC syndrome. Correlations between some parameters of the blood coagulation and fibrinolysis systems, on the one hand, and humoral immunity characteristics, on the other, may be traced, among these correlations being reverse correlations between IgG level, activated recalcification time, fibrinogen concentration, and activated partial thromboplastin time.
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PMID:[Various factors of nonspecific resistance in pregnant women with anemia]. 195 69

High-dose interleukin-2 (IL-2) immunotherapy can cause hypotension, respiratory distress, interstitial edema, and thrombocytopenia, similar to endotoxic shock. We have observed that IL-2 has no direct effect on coagulation factors in vitro, but it has been observed to alter the coagulant properties of vascular endothelium. Accordingly, we investigated the possibility that IL-2 infusions initiate plasma fibrinolysis and disseminated intravascular coagulation (DIC). We studied the clinical course, platelet count, and coagulation profile in response to IL-2 infusion in seven patients, two with metastatic melanoma and five with metastatic renal cell carcinoma. Every patient experienced hemodynamic instability and thrombocytopenia, and one patient suffered an unusual complication, mesenteric thrombosis. No patient had appreciable changes in the prothrombin time or the partial thromboplastin time, nor did factors V or VIII decline in the two patients observed. In four patients examined, we found decreased titers of Hageman factor (factor XII), high molecular weight kininogen, prekallikrein, and plasma thromboplastin antecedent, as if these had been consumed by reactions of the intrinsic pathway of thrombin formation. Circulating D-dimer fragments were found in the plasma of every patient at some point during each infusion cycle, and we observed decreased titers of plasminogen in the four patients just mentioned, suggesting that IL-2 infusions initiated fibrinolysis. Taken together, the clotting factor derangements and related toxicity phenomena cannot be ascribed firmly to DIC. Activation of the intrinsic (contact) system of coagulation, however, may provide one link between the vascular endothelial surface alterations caused by IL-2 infusions and the development of the systemic toxicity that resembles septic shock.
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PMID:Fibrinolysis, thrombocytopenia, and coagulation abnormalities complicating high-dose interleukin-2 immunotherapy. 198 12

Antistasin (ATS) is a selective, tight-binding inhibitor of blood coagulation Factor Xa originally isolated from the salivary glands of the Mexican leech Haementeria officinalis. In order to provide sufficient quantities of ATS to further investigate the role of Factor Xa in blood coagulation, a recombinant version of ATS has been produced in an insect baculovirus host-vector system. In this study, we describe the purification and in vitro and in vivo characterization of a single recombinant antistasin (rATS) isoform. The purified protein constitutes a minor isoform relative to the more abundant ATS isoforms present in leech salivary gland extracts. In vitro, rATS inhibits purified human Factor Xa stoichiometrically, prolongs plasma-based clotting assays at nanomolar concentrations, and like native ATS, is cleaved at a single position by Factor Xa during the course of inhibition. An initial evaluation of the in vivo efficacy of rATS was addressed utilizing a rhesus monkey model of mild disseminated intravascular coagulation. rATS was shown to fully suppress thromboplastin-induced fibrinopeptide A generation in a dose-dependent fashion. The availability of rATS should provide a valuable tool for the critical evaluation of the specific role played by Factor Xa in coagulation.
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PMID:Purification and characterization of recombinant antistasin: a leech-derived inhibitor of coagulation factor Xa. 199 Sep 79

The hemostasis profiles of 24 dogs with histologically confirmed hemangiosarcoma were prospectively evaluated. Microangiopathic hemolysis was defined as the presence of schistocytes; disseminated intravascular coagulation was defined as 1) thrombocytopenia, 2) fibrin(ogen) degradation products greater than 10 micrograms/mL, 3) prolongation of one or more coagulation times (activated partial thromboplastin time or one-stage prothrombin time) by greater than 25% of the control, 4) fragmented red blood cells (greater than or equal to 1+ based on a semiquantitative grading scale), and 5) fibrinogen less than or equal to 80 mg/dL. Three of the five criteria listed above had to be met for disseminated intravascular coagulation to be diagnosed. Fifty percent of the dogs were considered to have disseminated intravascular coagulation at presentation. Thrombocytopenia was present in 75% of the dogs and was the most common abnormality. The mean platelet count was 137,800/microL. Twenty-five percent of the dogs died as a result of the hemostatic abnormalities. Only 12% of the dogs had microangiopathic hemolysis without other evidence of disseminated intravascular coagulation. Hemostatic abnormalities are present in many dogs with hemangiosarcoma at the initial clinical presentation and represent an important clinical finding.
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PMID:Hemostatic abnormalities in dogs with hemangiosarcoma. 202 11

Most infants with hemophilia have no bleeding in the neonatal period even if birth trauma occurs. The explanation for this lack of bleeding in the first few days of life in most hemophiliacs is unknown. Maternal factors VIII and IX fail to cross the placenta and cannot, therefore, protect the neonate. There have, however, been an increasing number of reports of severe neonatal bleeding in hemophiliac neonates. Herein, a case of severe neonatal bleeding responsible for hypovolemic shock and disseminated intravascular coagulation masking the hemophilia and delaying its diagnosis is reported. Transfusion of twice the total globular mass and exchange-transfusion were required. Hemorrhagic gastric necrosis occurred, requiring subtotal gastrectomy. The diagnosis of severe hemophilia A (factor VIII = 1%) was established only at 17 days of age. At the age of five months, the child developed a dumping syndrome which improved under appropriate dietary therapy and finally resolved. Outcome was favorable and at the evaluation at two years of age the child was leading a normal life. This case underlines the difficulty of the diagnosis of hemophilia at birth. When there is no family history of bleeding, the diagnosis of hemophilia is usually missed in the neonatal period and established only later or retrospectively. Factors VIII and IX should consequently be measured in male neonates with unusual bleeding and an increased activated partial thromboplastin time, even if disseminated intravascular coagulation is present. Prompt diagnosis and initiation of specific therapy may lessen acute morbidity and prevent long-term sequelae in affected infants.
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PMID:[Disseminated intravascular coagulation masking neonatal hemophilia]. 203 86

Disseminated intravascular coagulation (DIC) or renal damage associated with septicemia was induced in rats by ligating the cecum or by injecting endotoxin. In the septicemia model, the number of E. coli and Bacteroides spp in the blood increased concomitantly with an increase of endotoxin. In this model the development of hypercoagulability with mild fibrinolysis was observed. Histopathologic findings in the kidneys, including the formation of microthrombi in the glomeruli and the vacuolization and dilatation of renal tubular cells, suggest the development of mild DIC. In the endotoxin-induced DIC model, both remarkable state of hypercoagulability and fibrinolysis were observed with fibrin thrombi in glomeruli. The administration of the platelet-activating factor antagonist, CV-6209, or of human antithrombin III, ameliorated DIC significantly by limiting the increases in prothrombin time, activated partial thromboplastin time and fibrin degradation products. These agents significantly reduced the deposition of fibrin in the glomeruli and significantly prolonged the survival time of the endotoxin injected rats. These observations suggest that the PAF antagonist CV-6209 and ATIII merit clinical evaluation in the management of DIC caused by septisemia.
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PMID:Effect of a platelet activating factor antagonist and antithrombin III on septicemia and endotoxemia in rats. 206 2

To clarify whether activated platelets play an important role in the occurrence and exacerbation of disseminated intravascular coagulation (DIC), we investigated the effects of 4 anti-platelet drugs, a PGI2 analog (CS-570), a thromboxane synthetase inhibitor (dazoxiben), a thromboxane receptor antagonist (BM-13177), and ticlopidine, in an experimental DIC model in rats. Experimental DIC was induced by a continuous infusion of lipopolysaccharide (LPS derived from E. coli, 055 B5, 25 mg/kg/hr) for 4 hrs. In the time-course determination of the coagulation parameters and prostanoids, an abrupt increase in TxB2 (a stable metabolite of TxA2) and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was followed by a decrease in platelet count, a prolongation of blood coagulation time, and an increase in fibrinogen/fibrin degradation products (FDP). Four hours after the start of LPS infusion, the rats were considered to be in the state of DIC. The effects of the anti-platelet drugs were investigated 4 hrs after the start of LPS infusion. CS-570 and ticlopidine ameliorated DIC in a dose-dependent manner. CS-570 (10 micrograms/kg/min) improved DIC in the platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fbg), and FDP, without affecting TxB2 and 6-keto-PGF1 alpha formation. Ticlopidine (200 mg/kg, i.p.) prevented the exacerbation of DIC in such item parameters as platelet count, APTT, and FDP. Both dazoxiben and BM-13177 (30 mg/kg, i.p.) ameliorated DIC in following parameters as platelet count, APTT and FDP. Dazoxiben, but not BM-13177, significantly inhibited the increase in TxB2 concentration at 4 hr. These observations suggest that drugs which inhibit platelet activation by a TxA2-dependent route are effective in improving DIC induced by LPS, and that drugs which inhibit multiple platelet-activating routes improve DIC in more item parameters than drugs which inhibit only the TxA2-dependent activating route. Consequently, it is concluded that activated platelets might play an important role in the occurrence and exacerbation of DIC induced by LPS, and that one of the roles of TxA2 in DIC is to activate platelets.
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PMID:Role of activated platelets in endotoxin-induced DIC in rats. 208 Apr 92

Thrombohemorrhagic risk is one of the main limiting factors in extracorporeal circulation. We describe here our experience in managing some life-threatening hematological complications in 58 patients with acute respiratory failure treated with long-term extracorporeal assistance. These patients were studied by clinical and laboratory means to assess questions related to heparin monitoring, coagulation complications and bleeding incidence. We found that two clotting tests, activated partial thromboplastin time (APTT) and activated clotting time (ACT) can be easily used to assess the safety of anticoagulant treatment (therapeutic ranges: APTT from 55 to 95 sec and ACT from 170 to 220 sec). A certain degree of coagulation activation, despite heparin, was indicated by the constant finding of thrombin-antithrombin complexes, while fibrinolytic activation, measured as plasminogen activator activity, was confined to the time of bypass connection and was of no clinical consequence. Platelet function was always impaired without relation to the platelet loss. Disseminated intravascular coagulation (DIC) (13 episodes) and severe bleeding (11 episodes) were major complications. DIC was corrected with a good outcome for 8 of 13 patients, while severe bleeding was correlated with a poor outcome in 8 of the 11 patients, probably because of the severity of the underlying disease.
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PMID:Physiopathology and management of coagulation during long-term extracorporeal respiratory assistance. 211 73

Forty-eight patients with hepatic malignancy (47 with hepatocellular carcinoma, one with metastatic colon carcinoma), who underwent transcatheter arterial embolization (TAE) for treatment of hepatic neoplasms, were investigated to determine the effects of TAE on coagulation and fibrinolysis. TAE was followed by a significant decrease in the platelet count (P less than .001); a prolongation of prothrombin time (P less than .001); an early increase in levels of fibrinopeptide A (P less than .01), fibrinopeptide B beta-15-42 (P less than .001), and fibrin(ogen) degradation products (P less than .001); and a delayed increase in the fibrinogen level (P less than .001), without a significant prolongation of the activated partial thromboplastin time. In the three patients who developed disseminated intravascular coagulation (DIC) after TAE, a reduction of both the platelet count and fibrinogen level occurred significantly earlier and in a more severe form than in the other patients without DIC; this reduction preceded the onset of the characteristic symptoms of DIC. Data suggested that close monitoring of platelet count and fibrinogen level is important for early detection of DIC following TAE.
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PMID:Hepatic neoplasms: effects of transcatheter arterial embolization on coagulation and fibrinolysis. 215 36

Rheologic properties of red blood cells and hemostasis were studied in patients with acquired autoimmune hemolytic anemia who received antilymphocytic globulin (ALG). Hypocoagulation changes attended by elevation of red blood cell aggregation activity were detected in the patients already at their admission to the hospital. After administration of ALG, growth of these shifts, characteristic of disseminated intravascular blood coagulation (DIC) syndrome, was noted. It was shown that erythrocytic thromboplastin and antiheparin factor action on blood coagulation, mainly at the expense of the young cell fraction, was responsible for disorders in hemostasis. Nevertheless, despite the presence of DIC syndrome, in the group of patients, who received ALG, no clinical signs of this state were recorded, that could be explained by the protective effect of red blood cell intensified capacity for aggregation leading to the improvement of blood coagulation parameters.
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PMID:[Rheological properties of erythrocytes and hemostasis in patients with acquired autoimmune hemolytic anemia treated with anti- lymphocyte globulin]. 221 Mar 16


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