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)

Coagulation parameters were initially monitored in 8 patients receiving whole body hyperthermia (WBH). Patients were heated by the warm water blanket technique to 41.8 degrees C (Tmax), maintained at this temperature for 2 hours, then allowed to cool. A fall in platelets was apparent by the time Tmax was achieved and continued during the 18 hours after WBH. Levels of beta-thromboglobulin (BTG) and platelet factor 4 rose by 56% and 191% by the end of treatment but returned to baseline 18 hours later. Fibrinogen, plasminogen and alpha 2-antiplasmin levels declined and FDP and fibrinopeptide A (FPA) levels increased during WBH. Factor XII and Factor VIII:C fell moderately during WBH while Factors VIII R:Ag, VIII:RC and V did not change or showed a late rise. Factor VII levels fell in 7 of 8 patients, reaching levels of 30% of normal in four. To better define the sequence of these coagulations perturbations, earlier and more frequent timepoints were studied in an additional 3 patients. This revealed that decreases in fibrinogen and plasminogen and increases in FPA and BTG occur very early (by the time the patient reaches 39 degrees C). On the other hand, a decrease in Factor VII activity was not apparent until patients had reached Tmax. WBH is therefore associated with a consumption coagulopathy. Possible mechanisms are discussed and extrapolations to the situation seen in heat stroke are suggested.
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PMID:Activation of coagulation during therapeutic whole body hyperthermia. 373 68

Effect of urinary enzyme inhibitor urinastatin (MTI) on disseminated intravascular coagulation (DIC) was investigated. The prolongation of PTT and increase in FDP in endotoxin-induced DIC in rats were restored by the intravenous infusion of MTI. The reduction in platelet counts, decrease in fibrinogen level and prolongation of PT were partially suppressed by the drug. Furthermore, in vitro addition of MTI prevented the decrease in r and k values and increase in ma and m epsilon values in the thromboelastogram of whole blood in endotoxin-induced DIC in rabbits. It is suggested that MTI might prevent DIC in vivo and in vitro through the inhibition of Factor XII activity and through the prevention of thromboplastin release caused by endotoxin.
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PMID:[Effect of urinastatin on disseminated intravascular coagulation]. 379 58

We investigated 22 severely ill patients (21 surgical, 1 medical) at the intensive care unit. Analyses of platelet count, Normotest, antithrombin III, FDP and fibrinogen were used to divide the patients into three diagnostic groups: DIC (3 positive tests), suspected DIC (2 positive tests) and No DIC. Using these criteria 9, 8 and 5 patients were referred to these diagnostic groups, respectively. Factor XII and prekallikrein did not differ significantly between the three diagnostic groups. On the other hand the capacity of the patient plasma to inhibit kallikrein was significantly lower in the DIC group. The decrease of kallikrein inhibitory capacity was correlated to the decrease of antithrombin III and alpha 2-antiplasmin. Out of the 22 patients in the study 8 patients died, 5 of these were in the DIC group. Non-surviving patients showed lower values of the protease inhibitors than survivors. It is concluded that in this type of patients and with the laboratory methods used contact phase factors do not seem to be affected in DIC. Analyses of the kallikrein inhibitory capacity, antithrombin and alpha 2-antiplasmin on the other hand seem to be of interest to measure, though the decrease of these inhibitors could be due to consumption as well as to reduced protein synthesis. Further studies are needed to prove the prognostic value of assaying these protease inhibitors.
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PMID:Analyses of factor XII, prekallikrein and kallikrein inhibitory capacity in patients with laboratory signs of DIC. 386 18

In nine patients with suspected disseminated intravascular coagulation (DIC) and five controls, the following analyses were performed on admission and 7-29 hours later: Routine coagulation studies (fibrinogen, platelet count, fibrin(ogen) degradation products, ethanol gelation, reptilase time, Factor V) providing a semiquantitative DIC score, prekallikrein (PK), Factor XII, antithrombin III (AT-III), C1(-)-inhibitor and alpha 2-macroglobulin. Significant correlations were found: PK or AT III with the DIC-score, PK with AT-III and Factor XII, AT-III with Factor XII. The changes (expressed as a percentage of normal plasma) of PK and AT-III from the first to the second evaluation were nearly identical. The two patients with rapidly fatal irreversible shock showed the highest DIC score and a pronounced decrease of PK and AT-III, whereas in reversible shock stable or increasing PK and AT-III values were found. The other variables showed an overlap between reversible and irreversible shock. DIC in these shock patients, accompanied by a decrease in PK, probably was mediated via Factor XII activation. PK and AT-III might be of prognostic value in patients with (septic) shock.
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PMID:Plasma prekallikrein, factor XII, antithrombin III, C1(-)-inhibitor and alpha 2-macroglobulin in critically ill patients with suspected disseminated intravascular coagulation (DIC). 620 13

The hypotension and disseminated intravascular coagulation (DIC) in bacteremia is thought to be mediated by the combined actions of cytokines, prostaglandins, and complement. The contact system, via the release of bradykinin and the activation of Factor XI, has been postulated to be contributing to the observed hypotension and DIC. Using a mAb to Factor XII (C6B7), we blocked the activation of the contact system in an established experimental baboon model in which Escherichia coli was infused to produce lethal bacteremia with hypotension. The untreated group (n = 5) displayed contact activation, manifested by a significant decrease in high molecular weight kininogen (HK) and a significant increase in alpha 2 macroglobulin-kallikrein complexes (alpha 2M-Kal). The C6B7-treated group (n = 5) showed an inactivation of Factor XII and the changes in HK and alpha 2M-Kal complexes were prevented. Both groups developed DIC manifested by a decrease in platelet, fibrinogen, and Factor V levels. The untreated group developed irreversible hypotension. The treated group experienced an initial hypotension that was reversed and extended the life of the animals. This study suggests that irreversible hypotension correlates with prolonged activation of the contact system, and specific antibody therapy can modulate both the pathophysiological and biochemical changes.
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PMID:The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia. In vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons. 767 10

C1-Inhibitor (Berinert, C1 INH), a 104 kDa protein, inhibits complement components (C1 esterase) as well as enzymes of the contact phase of coagulation (Factor XII, Factor XI) and kallikrein, thus regulating kinin generation. C1 INH is used for the treatment of the hereditary angioneurotic edema. This paper will give a survey about the evidence in recent literature concerning the potential efficacy of the compound on other diseases associated with shock, capillary leakage and inflammation as well. In our own experiments we evaluated whether the compound could influence acute inflammatory reactions or the severe systemic inflammatory response syndrome (SIRS) as a consequence of an experimental septic shock. To prevent the sepsis-induced DIC we co-infused the thrombin inhibitors AT III or rec. hirudin in combination with C1 INH. Coinfusion of C1-inhibitor (50-200 U/kg x h) with either rec. hirudin or AT III significantly improved survival rate compared to thrombin inhibitor alone.
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PMID:Influence of C1-inhibitor on inflammation, edema and shock. 817 80