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)

Disturbances of blood coagulation were studied in 32 consecutive patients with typhoid fever on their admission to hospital. Estimations of prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation products (FDPs), factors VII, VIII and XII, alpha I antitrypsin, plasminogen, CI esterase inhibitor, and platelet counts were performed as well as liver function tests and blood counts. Five patients had laboratory evidence of disseminated intravascular coagulation (DIC) and two had a generalised bleeding disorder which in the other three was inapparent. The platelet count in the group as a whole was low (P less than 0.05) and the FDPs in most cases were mildly elevated. The pre-kallikrein values were depressed in three of the five with DIC, whereas factor XII was not reduced. These results indicate that bleeding disorders in typhoid fever are uncommon. The depression of pre-kallikrein indicates that the DIC is probably triggered by activation of the intrinsic coagulation pathway. Most patients had lymphopenia and monocytopenia but only two had neutropenia.
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PMID:Disturbances of blood coagulation associated with Salmonella typhi infections. 335 16

A study of 93 patients with liver cirrhosis showed that the most important blood coagulation disorder in this pathology resulting in hypocoagulation, was not decreased synthesis and deficit of the prothrombin complex factors but disturbance of the final stage determined by afibrinogenemia. Considerable depression of XIIa-kallikrein-dependent fibrinolysis and marked increment of an antiplasmin level in the plasma were noted. Positive paracoagulation tests were revealed in 57% of the patients, and as other signs typical of the lingering DIC-syndrome were absent, they were interpreted as the "hypercoagulation syndrome" or "pre-DIC syndrome". The problem of possible relationship of development of both thromboses and hemorrhages with acquired afibrinogenemia in liver cirrhosis was discussed.
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PMID:[Role of dysfibrinogenemia and disorders of fibrinolysis in the pathogenesis of hemostatic pathology in liver cirrhosis]. 357 61

Coagulation, fibrinolytic, kallikrein, and complement systems were studied in 20 patients with multiple trauma. Three of four patients with a trauma score less than 10 on hospital arrival died, compared to one of 16 with a score over 10. Five patients developed disseminated intravascular coagulation. Signs of activated cascade systems were evident in most patients on hospital arrival. Changes were not related to trauma score, but patients with an arterial pressure below 110 mm Hg had significantly lower levels of antithrombin III and alpha 2-antiplasmin than those with higher BP. This study confirms that the cascade systems are activated very soon after multiple trauma.
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PMID:Early activation of humoral proteolytic systems in patients with multiple trauma. 376 1

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 vitro effects of S-2441, H-D-Pro-Phe-Arg-NH-Heptyl, include potent anti-bradykinin activity and broad-spectrum inhibition of serine proteases involved in the coagulation cascade. In this study, rats infused with 7.8 X 10(8) viable Escherichia coli were treated either with saline (group A) or with intravenous (0.1 mg) and intraperitoneal (0.4 mg) doses of S-2441 (group B). Survival rates for groups A and B were 68% and 98%, at 12 hours (P less than 0.001), and 37% and 73% at 24 hours (P less than 0.001), respectively. Hematologic studies revealed that S-2441 significantly inhibited E. coli-induced prolongation of prothrombin time and partial thromboplastin time as well as a rapid decrease in the values of factor X, anti-thrombin III, and fibrinogen. In addition, S-2441 attenuated E. coli-induced hypoglycemia and a marked reduction of serum complement level. Ultrastructural evaluation of the liver demonstrated that S-2441 prevented the development of extensive sinusosoidal microthrombosis and hepatocellular necrosis. The results indicate that S-2441 affords protection in lethal gram-negative bacteremia owing in part to attenuation of disseminated intravascular coagulation and complement-mediated reactions. The findings are consistent with the concept that S-2441 and related oligopeptides modulate serine protease-mediated responses involving inhibition of active enzymes with competitive antagonism of pharmcologically active products formed during the activation of coagulation, fibrinolytic, kallikrein, and complement systems.
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PMID:Efficacy of S-2441, a synthetic oligopeptide, in a rat model for gram-negative bacteremia. 388 74

Plasma fibronectin (Fn), a glucoprotein of suggested importance in host defence during infections also seems to be involved in blood coagulation and to be consumed during clot formation. Low Fn concentrations have been found in patients with DIC, but also in patients with infections without signs of overt DIC. In a randomized trial of Fn supplementation 28 patients with moderately severe infections, hospitalized in the Department for Infectious Diseases, were scheduled to receive either cryoprecipitate from 30 donors (n = 14) or 250-300 ml of stored plasma (n = 14). To elucidate the relationship between Fn plasma levels, Fn-rich cryoprecipitate infusion, and possible low-grade DIC in these patients, we measured platelet count, prothrombin complex (NT), fibrinogen, F V, F VIIIR:Ag, F VIII:C, F XII, plasminogen (Plg), antiplasmin (AP), antithrombin III (AT), kallikrein-inhibiting activity (KI) and spontaneous proteolytic activity (SPA). Compared to healthy controls, high initial values (p less than .001) were found for fibrinogen, F VIIIR:Ag, F VIII:C and SPA. Most values for platelets, F V, Plg, AP and KI were within the reference range. Low levels (p less than .001) were found for Fn, NT, F XII, AT and for the ratio F VIII:C/F CIIIR:Ag. A significant correlation was found between F XII, Plg and AT. Fn correlated poorly to the other variables. Cryoprecipitate infusion normalized the Fn concentration, but had no influence on other measured variables. Thus, although no patient had clinically overt DIC, and all survived, we observed a distinct pattern indicating activation of the coagulation system. Fn levels were low, but were not specifically related to this activation.
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PMID:Fibronectin and other DIC-related variables in patients with moderately severe infections receiving cryoprecipitate. 393 19

In a controlled study of fibronectin supplementation in sepsis, 11 ICU patients in septic shock were scheduled to receive either cryoprecipitate from 20-40 donors (n = 6) or 250-300 ml of stored plasma (n = 5) (two infusions over 24 h). We wanted to: compare some "conventional" DIC variables in the ICU (platelet count, prothrombin complex = NT, FDP) to additional variables: Fibronectin (Fn), fibrinogen (Fg), F V, FVIII R:Ag, F VIII:C activity, F XII, plasminogen (Plg), antiplasmin (AP), antithrombin (AT), kallikrein inhibiting activity (KI) and spontaneous proteolytic activity (SPA): study the effects of cryoprecipitate or plasma infusion on three variables. Samples were taken before the first infusion, and 24 and 48 h after. At onset, high levels (p less than .001 when compared to blood donors) of Fg, VIIIR:Ag and VIII:C were seen. KI levels were within the normal range. F V was low (p less than .05). Fn, NT, XII, Plg, AP and AT were markedly low (p less than .001). SPA showed great variation. When compared to 28 patients with severe infections, but not in septic shock, the ICU group had higher VIIIR:Ag (p less than .05) and VIII:C (p less than .01), and lower XII, Plg, AP and AT (p less than .001). FDP was elevated in all ICU patients. Five patients were thrombocytopenic, and in these a pattern with low levels of Plg and AT was observed. Fn did not correlate well to the other variables measured. These results indicate a marked activation of coagulation and fibrinolysis in these severely ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibronectin and other DIC-related variables in septic ICU patients receiving cryoprecipitate. 393 20

It has been shown that the development in animals of disseminated intravascular coagulation (DIC) caused by long-term intravenous infusion of thrombin was accompanied by appreciable activation of the kallikrein-kinin system, being characteristic of acute pathological processes. In the initial stages of the process development, prekallikrein and kallikrein inhibitor were observed to be secreted from the lungs to arterial blood. Further development of DIC led to the depletion of the reserves of the kinin system. Pretreatment with a single low dose of acetylsalicylic acid considerably reduced the total animals' lethality and postponed blood kinin system activation determined by the development of DIC.
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PMID:[Activation of the blood kallikrein-kinin system in disseminated intravascular coagulation in rats. The significance of the pulmonary component and an attempt at correction with aspirin]. 633 54

Levels of prekallikrein and HMW kininogen that had increased during pregnancy decreased with start of labor. The role of the kinin-forming system with oxytocin in the mechanism of labor was suggested from the results of decreased prekallikrein and HMW kininogen, appearance of a free kallikrein-like enzyme during labor, and from the case of arrested labor in which both prekallikrein and HMW kininogen were markedly decreased. Prekallikrein was markedly decreased in patients with acute obstetrical DIC and severe toxemia of pregnancy. The excessive activation of prekallikrein in DIC seemed to be of help for understanding such clinical signs as shock, abnormal labor, and increased permeability in obstetrical DIC.
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PMID:The kinin-forming enzyme system in pregnancy and obstetrical DIC. 642 Dec 72

In a search for new variables, for the diagnosis of disseminated intravascular coagulation (DIC) and for guidelines of therapy in such conditions, 22 severely ill patients were studied. The diagnosis of DIC was based on determinations of platelet counts, prothrombin complex (Normotest), antithrombin (AT), fibrinogen degradation products and fibrinogen. Nine patients were diagnosed as having DIC, eight patients were referred to a suspected DIC group and five to a group of no DIC. The laboratory findings were found to agree with the clinical status. In addition several new parameters were investigated: factor XII, prekallikrein, Simplastin A--another prothrombin complex factor method, factor X, plasminogen (PLG), antiplasmin (AP) and kallikrein inhibitors (KI). Platelet counts, prothrombin complex and antithrombin were mostly pathological in DIC-patients. Of the alternative tests prothrombin complex, fibrinopeptide A and the kallikrein inhibitor as well as the two tests for fibrinolysis (PLG and AP) were significantly altered in DIC-patients. The inhibitor capacity (AT, APV and KI) was lower in patients who died than in survivors and decreased still further in those of the non-survivors who had DIC. Thus the inhibitors can be used as predictors of outcome and hopefully for guiding therapy. To establish the diagnosis of DIC we suggest measurement of platelet count, prothrombin complex, plasminogen as well as of the inhibitors.
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PMID:Blood coagulation and fibrinolytic factors and their inhibitors in critically ill patients. 655 31


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