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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disseminated intravascular coagulation (DIC) was induced in both normal and asplenic rhesus monkeys by intravenous challenge with Streptococcus pneumoniae. Our observations in the infected monkeys have led us to conclude that (1) pneumococcal capsular polysaccharide (PCP), immune complexes and complement may not have primary roles in the initiation of DIC; (2) intact pneumococci may be catalysts for the development of DIC; (3) the initial event in DIC may be activation of Hageman factor; and (4) evidence of activation of Hageman factor-dependent systems is present regardless of severity of infection.
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PMID:Disseminated intravascular coagulopathy during experimental pneumococcal sepsis: studies in normal and asplenic rhesus monkeys. 2 58

The classic generalized Shwartzman reaction induced in the rabbit was prevented with large doses of aspirin (250 mg/kg) when administered at the time of the first and preparing injection of endotoxin. Such a result was not observed when the drug was given at the time of the second and provoking injection of endotoxin. Our investigations on platelet and coagulation indicate that aspirin prevents disseminated intravascular coagulation through an interference with the blood coagulation and Hageman factor activation rather than by the inhibition of platelet aggregation and availability of platelet procoagulant activity.
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PMID:Prevention by aspirin of the classic generalized Shwartzman reaction. 35 56

There was no significant difference in the levels of factor XII between sick newborns and normal age-matched controls, although the levels of both groups were lower than normal older children. Detailed coagulation studies on 44 sick infants revealed 11 to have disseminated intravascular coagulation (DIC). In those with DIC, the mean Hageman factor was 20% and in those without DIC, 25% (P greater than 0.05). Rabbits given a constant infusion of lysozyme (which inhibits factor XII) showed laboratory evidence of endotoxin-induced DIC. The data suggest that neither reduced factor XII levels nor Hageman factor inhibition provided protection from DIC. The data further suggest that other coagulation pathways might be involved in order to elicit the DIC.
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PMID:Hageman factor and disseminated intravascular coagulation (DIC) in newborns and rabbits. 88 13

A secific, sensitive, and reproducible radioimmunoassay for human Hageman factor (HF, factory XII) has been developed with purified human HF and monospecific rabbit antibody. Precise measurements of HF antigen were possible for concentrations as low as 0.1% of that in normal pooled plasma. A good correlation (correlation co-efficient = 0.82) existed between the titers of HF measured by clot-promoting assays and radioimmunoassays among 42 normal adults. Confirming earlier studies, HF antigen was absent in Hageman trait plasma, but other congenital deficient plasmas, including those of individuals with Fletcher trait and Fitzgerald trait, contained normal amounts of HF antigen. HF antigen was reduced in the plasmas of patients with disseminated intravascular coagulation or advanced liver cirrhosis, but it was normal in those of patients with chronic renal failure or patients under treatment with warfarin. HF antigen was detected by this assay in plasmas of primates, but not detectable in plasmas of 11 nonprimate mammalian and one avian species.
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PMID:Radioimmunoassay of human Hageman factor (factor XII). 95 1

The therapeutic efficiency of two glucocorticoids (hydrocortisone and dexamethasone) on endotoxin-induced intravascular coagulation was investigated in the rat. Coagulation and platelet aggregation studies were performed and plaminogen was assayed. Our results indicate that pretreatment of the animals with large doses of these steroids within a few hours prior to endotoxin totally prevents the consumption in Hageman factor, measurable contact product activity, platelets, fibrinogen, plasminogen, and the loss in platelet aggregability and serotonin. In addition to this, the hypercoagulable state consecutive to endotoxin, characterized here by shortenings in the partial thromboplastin and recalcification times and by an increase in the availability of platelet procoagulant activity, was also totally prevented by the steroid pretreatment. On the other hand, it is shown that these glucocorticoids do not interfere in the normal rat with platelet aggregation (tested with thrombin,adenosine diphosphate, and collagen), but with the availability of platelet procoagulant activity. This last phenomenon, in addition to that of an interference in vivo with the mechanism of activation of Hageman factor, are believed to be responsible for prevention by glucocorticoids of endotoxin-induced disseminated intravascular coagulation.
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PMID:Prevention by glucocorticoids of disseminated intravascular coagulation induced by endotoxin: mechanisms. 109 78

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

The prognosis of septicaemia depends on the occurrence of complications such as shock and coagulation defects. The damage to haemostasis is usually explained by the action of the main coagulation and fibrinolysis enzymes, thrombin and plasmin. This paper presents data concerning the role of a third protease, granulocytic elastase. 82 patients who had been admitted to our hospital with suspected septicaemia were examined. Septicaemia was proven in 22 patients by the growth of microorganisms in blood cultures, and was clinically diagnosed in 9 patients. The plasma levels of neutrophil elastase-like protease complexed to a1antitrypsin (a1AT-ELP) were measured by zone immunoelectrophoresis assay (ZIA). The a1AT-ELP values were significantly increased in the 31 septic as compared to the 51 non-septic patients. In patients with complicated septicaemia, negative correlations of a1AT-ELP with factor XIII and the coagulation inhibitor antithrombin III were demonstrable. Among the patients with septic complications, the 3 who survived exhibited a dramatic decrease of a1AT-ELP, whereas in the other 16 patients who died the levels remained elevated. It might be of therapeutic significance that in 9 patients receiving fresh plasma and AT III-concentrate substitution for DIC the a1AT-ELP levels dropped, whereas they remained high in the other septicaemia patients. There were no correlations between a1AT-ELP and the a2antiplasmin-plasmin complexes (a2AP-P1), but strong correlations with signs of coagulation. The data suggest an interaction of coagulation and elastase release, probably involving the Hageman factor.
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PMID:Participation and interactions of neutrophil elastase in haemostatic disorders of patients with severe infections. 329 74

Since chickens are naturally deficient in several clotting factors normally present in mammalian sera, the ability of lead acetate (PbAc(2)) to sensitize 11-day-old chicks to endotoxin was compared with its ability to sensitize rats. It was found that, although the chicks could tolerate only relatively low doses of PbAc(2), even those doses would produce a greater than 200-fold sensitization to the endotoxin in rats, as compared with little sensitization in the chicks. By using larger doses of PbAc(2), known to maximally sensitize rats to endotoxin, the effect of PbAc(2) sensitization on whole-blood clotting times, platelet counts, plasma factor V and VIII activities, and the appearance of fibrin degradation products was evaluated. It was found that animals treated with lethal doses of endotoxin but no PbAc(2) showed varying degrees of consumptive coagulopathy. On the other hand, the injection of minute quantities of endotoxin into PbAc(2)-sensitized rats invariably resulted in disseminated intravascular coagulation, apparently via a complete activation of the intrinsic pathway. It is concluded that the site of PbAc(2) sensitization to endotoxin is in the blood, and most probably at the level of Hageman factor activation.
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PMID:Potentiation of endotoxin-induced consumptive coagulopathy by lead acetate administration. 461 26

Severe surgical infection is one of the most obvious clinical settings of DIC. Although many initiating triggers have been discussed, the most potent might be a bacterial endotoxin which activates Hageman factor or some components of serum complement. We examined a disorder of blood coagulation system in severe surgical infection in terms of the results of limulus test for detection of circulating endotoxin. In 59 of such patients, 10 cases (32.3%) of DIC diagnosed by MINNA 's criteria were recognized in 31 limulus positive cases, whereas only 4 cases (14.3%) in 28 limulus negative groups. Each clinical course, prognosis, or the relationship with MOF were also discussed in detail. It was emphasized that the first requirement for diagnosis of DIC should be awareness of its possibility and careful observation of platelet counts. The immediate needs for treatment of DIC are (1) a cure of underlying infection by surgical drainage and chemotherapy, and (2) inhibition of intravascular coagulation by use of heparin and/or FOY etc. Our experiments performed by a continuous drop infusion of both 0.2 mg/kg 055; B5 E. Coli endotoxin and several doses of FOY for 4 hours into rabbits showed that the most potent inhibitory effect of FOY on platelet and WBC was observed in 0.1 mg/kg/min.
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PMID:[Severe surgical infection and DIC]. 642 96

Fibrin clots have been detected at sites of inflammation, and kinins have been implicated as mediators of the vascular phenomena of acute inflammation, systemic shock, and disseminated intravascular coagulation. It is now reported that both negatively and positively charged asbestos fibers shorten the partial thromboplastin time of human plasma, indicating coagulation of the plasma. A sample containing short (less than 5 micron in length) chrysotile fibers is ineffective. Only the negatively charged amphiboles (crocidolite and amosite) are able to activate factor XII (Hageman factor). This particular effect of the amphiboles is enhanced by high molecular weight kininogen and leads to kinin formation.
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PMID:Asbestos fibers, plasma and inflammation. 664 59


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