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)

Fatal multiple organ failure after severe infection may be related to an early activation of protease cascade systems. This study aimed to relate changes in coagulation, fibrinolysis, and kallikrein to shock and outcome. Of 53 patients with severe infection, 30 did not develop shock, 12 survived septic shock, and 11 died from organ failure after septic shock. No patient had overt disseminated intravascular coagulation. We measured 17 components of the coagulation/fibrinolysis/kallikrein pathways on admission and on the next 2 days. High values for fibrinogen, factor VIII:C, von Willebrand factor antigen, and D-dimer were seen in all patients; factor XII, prekallikrein, factor VII, antithrombin, protein C, and fibronectin were low. The patients thus appeared to be hypercoagulable. These disturbances were more pronounced in septic shock survivors, who also had low plasminogen and antiplasmin, indicating ongoing fibrinolysis. Nonsurvivors of sepsis were distinguished mainly by high plasminogen activator inhibitor values; this suggests an impaired functional fibrinolysis in fatal sepsis, with possible therapeutic implications. Cryoprecipitate infusion increased the fibronectin concentration, but did not influence the other factors studied.
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PMID:Coagulation, fibrinolysis, and kallikrein systems in sepsis: relation to outcome. 250 62

Effects of non-lethal Sarcocystis miescheriana infections on the blood coagulation system were investigated. Nine pigs were inoculated orally with 2 X 10(5) sporocysts (Group A) and nine pigs (Group B) served as non-infected controls. Blood samples were taken from the vena jugularis externa every 2 or 3 days until 19 days post-infection (dpi). The following parameters were investigated: partial thromboplastin time (PTT), prothrombin time (PT), thrombin time (TT), thrombin coagulase time (TCT), fibrinogen (FIB), factor (F) VIII, F XI, F XII, antithrombin III (AT III), alpha 2 macroglobulin (alpha 2 MG), alpha 2 antiplasmin (alpha 2 AP), pre-kallikrein (PK), and the number of circulating thrombocytes. All infected pigs suffered from acute sarcocystiosis between 12 and 19 dpi. Clinical illness was most severe from 14 to 17 dpi. At this time, PTT and FIB increased, and TT and TCT decreased slightly. The activities of the clotting factors increased at 17 and 19 dpi. However, only F VIII activity was significantly higher in the infected pigs than in the controls at 17 and 19 dpi. PK was significantly lower in the infected pigs at 12, 14, and 17 dpi. Thrombocyte counts were reduced with the onset of the acute phase of illness and some pigs had marked thrombocytopenia. These results indicate low-grade disseminated intravascular coagulation (DIC) in the course of mild S. miescheriana infections in pigs.
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PMID:Hemostatic alterations in pigs fed sublethal doses of Sarcocystis miescheriana. 251 58

DIC in patients affected by cirrhosis, accompanied by portal hypertension and splenomegaly, has been suspected in the past. The main aim of this study is to ascertain the incidence of this phenomenon. We carried out coagulation and fibrinolytic tests in 113 cirrhotic patients and 20 healthy control persons. We found chronic consumption coagulopathy at analysis level in 28 cases (24.8%) with a decrease of fibrinogen, factor V, kallikrein, platelets, prothrombin complex activity, increase of PDF, partial thromboplastic time and euglobulin lysis. 25 cases had active cirrhosis, with ascites, variceal bleeding and/or hepatic encephalopathy; 3 were non-active cirrhosis. Only 7 patients had clinical DIC. We observed that coagulation disorders increased with more active cirrhosis.
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PMID:[The incidence of consumption coagulopathy in liver cirrhosis]. 256 20

We studied contact factors and kinin-kallikrein in normal non-pregnant and pregnant women, FXII deficient toxemia and DIC. The results obtained are as follows: 1. The levels of plasma prekallikrein, high molecular weight kininogen, kallikrein inhibitor, and C-1 INA were gradually decreased at delivery, and the levels of kallikrein like activity and bradykinin were increased during pregnancy and at the time of parturition. These facts indicate that kinin kallikrein systems played important role in uterine contraction. 2. The levels of contact factors (FXII and FXI) were lower at delivery than those of term. 3. In rat uterus, specific binding of bradykinin was observed by the method of radio receptor assay in the pelet of 10,000 X g fetal membranes, and its activity was 38%. 4. A synthetic kallikrein inhibitor (OS-291, MS) and bradykinin antagonist inhibited completely spontaneous uterine contraction of Wistar rats during delivery. 5. In the case of FXII deficiency, the levels of plasma prekallikrein, high molecular weight kininogen were normal, but at delivery, these levels were lower than those of term. The levels of kallikrein like activity which was half of normal parturition level was increased at parturition. 6. In cases of DIC (17) and severe toxemia (22), plasma prekallikrein levels were lower than the normal controls. The decrease was due to consumption of plasma prekallikrein to kallikrein activation.
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PMID:[Physiopathology of kinin forming system in reproduction]. 259 38

The inhibitory effect of gabexate mesylate, which is used therapeutically in the treatment of pancreatitis and disseminated intravascular coagulation, and as a regional anticoagulant agent for hemodialysis, has been measured on bovine factor Xa, bovine alpha-thrombin, human Lys77-plasmin, human urinary kallikrein, human urokinase, porcine pancreatic beta-kallikrein-B, and bovine beta-trypsin catalyzed hydrolysis of p-nitrophenyl esters of N-alpha-carbobenzoxy-L-arginine and N-alpha-carbobenzoxy-L-lysine. On the basis of enzyme:gabexate mesylate affinities, the serine proteases can be arranged as follows: human urinary kallikrein approximately porcine pancreatic beta-kallikrein-B much less than bovine beta-trypsin approximately bovine factor Xa approximately human Lys77-plasmin approximately human urokinase approximately bovine alpha-thrombin. The mode of binding of gabexate mesylate to the serine proteases conforms to the active-reactive site geometries observed in their complexes with natural and synthetic inhibitors. Differences in gabexate mesylate affinities for these proteases reflect structural differences at their primary specificity subsite, which have been investigated by comparative analysis of amino acid sequences and by computer-graphics techniques.
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PMID:Gabexate mesylate inhibition of serine proteases: thermodynamic and computer-graphics analysis. 310 78

Components of the kallikrein-kinin system of the blood and some hemostatic indices were studied in parallel in 32 patients with diffuse toxic goiter. A decrease in the levels of prekallikrein, kininogen, the activity of kallikrein and kininase inhibitors in the blood plasma of the examinees resulted in raised activity of the kallikrein-kinin system in decompensated thyrotoxicosis. Hemostatic changes were characterized by signs of chronic disseminated intravascular coagulation. It was shown that kinin formation and blood coagulation were correlated. A certain parallelism in the increment of the activity of the kinin system and disorders of hemocoagulation was noted with an increase in a degree of severity of thyrotoxicosis. A tendency to improved indices was also noted after thyrostatic therapy.
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PMID:[Several aspects of the pathogenesis of disturbances of hemostasis in patients with diffuse toxic goiter]. 321 79

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


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