Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult respiratory distress syndrome (ARDS) is a complex pulmonary clinicopathologic condition associated with pulmonary endothelial injury and blood coagulation activation. In patients with ARDS from all causes, factor VII levels were significantly reduced. Patients with ARDS caused by sepsis had more evidence of intravascular coagulation and fibrinolysis than did patients with trauma-related ARDS by having significantly (p less than or equal to 0.05) increased prothrombin times, activated partial thromboplastin times, and fibrin degradation products, and decreased antithrombin III concentration. We sought to determine whether the proteins of the contact system of plasma proteolysis (factor XII, prekallikrein, high molecular weight kininogen, and C1 inhibitor) were also activated after acute lung injury. Patients with ARDS caused by either trauma or sepsis had significantly (p less than or equal to 0.01) reduced factor XII levels, high molecular weight kininogen functional activity, prekallikrein activity, and prekallikrein antigen levels compared with controls. In both the sepsis-related and trauma-related ARDS groups, C1 inhibitor activity was significantly reduced but C1 inhibitor antigen levels were significantly elevated from control. These findings showed that the proteins of the contact system were more extensively activated in ARDS than were the proteins that contribute to later reactions in intravascular coagulation and fibrinolysis. Activation of the contact system proteins could be the result of endothelial injury occurring as part of ARDS. Intravascular coagulation and fibrinolysis in patients with ARDS also arise from components independent from contact system activation.
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PMID:Activation of the contact system of plasma proteolysis in the adult respiratory distress syndrome. 339 29

In severe inflammatory response, various blood and tissue cells, including polymorphonuclear granulocytes, release lysosomal proteinases, extracellularly and into the circulation. Such enzymes, as well as normally intracellular oxidizing agents produced during phagocytosis, enhance the inflammatory response by degrading connective tissue structures, membrane constituents and soluble proteins by proteolysis or oxidation. We first used polymorphonuclear elastase (E) as a marker of such release reactions. The liberated proteinase competes with susceptible substrates, including alpha 1-proteinase inhibitor (alpha 1PI) and alpha 2-macroglobulin, and is eliminated finally as inactive enzyme-inhibitor complexes by the reticulo-endothelial system. Using an enzyme-linked immunosorbent assay, we determined the plasma levels of E-alpha 1PI following major abdominal surgery, multiple trauma and pancreatogenic shock. Whereas the operative trauma was followed by up to 3-fold increase of the E-alpha 1-PI, postoperative septicemia was associated with a 10 to 20 fold increase. The increase of E-alpha 1-PI and a concomitant decrease of plasma factors, such as antithrombin III, clotting factor XIII and alpha 2-macroglobulin, were correlated. Multiple trauma causes a substantial increase of E-alpha 1-PI up to 14 hours after accident. The released elastase seems to correlate with severity of injury, but assessing the relationship to consumption of plasma factors is complicated by concomitant transfusions. In acute pancreatitis, peaks, of E-alpha 1-PI coincide with a massive consumption of antithrombin III and alpha 2-macroglobulin during shock.
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PMID:Granulocyte proteinases as mediators of unspecific proteolysis in inflammation: a review. 353 55

Alterations of the kallikrein-kinin system consistent with activation and increased consumption have been reported in septic patients and it has been suggested that this activation could contribute to the development of septic shock. The aim of this work was to confirm these alterations in septic patients and to investigate the possible existence of similar changes in subjects developing cardiogenic shock secondary to myocardial infarction as a model of non septic shock. Patients with septic shock, especially in fatal cases, showed a highly significant decrease in levels of factor XII, prekallikrein, high molecular weight kininogen (HMW-kininogen), alpha 2-macroglobulin (alpha 2-M) and antithrombin III (AT-III). C1-esterase inhibitor (C1-INH) activity was increased in uncomplicated sepsis but came back to normal or was slightly decreased in septic shock. Components and inhibitors of the kallikrein-kinin system were within normal limits in patients with cardiogenic shock. Our findings support the idea of a contribution of the kallikrein-kinin system to the development of septic shock though this system does not seem to play a significant role in the pathogenesis of cardiogenic shock or seem to be altered as a consequence of it.
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PMID:Plasma kallikrein-kinin system in patients with uncomplicated sepsis and septic shock--comparison with cardiogenic shock. 367 21

Critically ill patients have been described as having blood coagulation abnormalities that predispose to bleeding and thrombosis. We have studied plasminogen activators, alpha 2-antiplasmin, X-oligomers fibrin fragments, fibronectin, antithrombin III, fibrinogen, platelets, kaolin-cephalin clotting time and prothrombin time on admission to the intensive care unit and sequentially after 24 and 48 hours in 39 adult patients: ARDS (n = 6), trauma (n = 12), sepsis (n = 8) and a miscellanea (n = 13). A decrease in plasminogen activators associated with an increase in X-oligomers, the earliest form of cross linked fibrin degradation products, indicate that fibrin deposition and the consumption of components of fibrinolysis is a widespread condition in the ICU patients. Low fibronectin levels were related to prognosis. These findings suggest that critically ill patients must be evaluated in respect to fibrinolysis and supported when necessary with prophylactic treatment.
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PMID:Changes in fibrinolysis in the intensive care patient. 367 37

Plasma proteolysis was studied in surgical patients with septicemia by means of chromogenic peptide substrate assays. Using these methods both levels of proenzyme, functional inhibition capacity and enzyme activities indicating alpha 2-macroglobulin protease complexes were determined. In fatal cases continuous low values for prekallikrein, plasminogen and antithrombin III were found until death. At autopsy a persistent septic focus was found in all but one of the fatal cases. Very low levels of prekallikrein during sepsis and reduced functional inhibition of plasma kallikrein in septic shock indicated a poor prognosis. In the survivors the parameters returned towards the normal range upon successful therapy. Furthermore, the paper demonstrates the application of a new parameter, the Proenzymes functional inhibition index (PFI-index) in patients with septicemia. The data reveal that by means of this parameter, patients at high risks can be identified at an earlier stage of the disease than previously done.
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PMID:Studies on pathological plasma proteolysis in patients with septicemia. 386 20

To evaluate the availability of the fibrinolytic system in patients suffering from acute respiratory distress syndrome, ARDS, induced by septicemia or trauma, the following parameters were analysed: fibrinogen, FG, antithrombin III, AT III, plasma prekallikrein, PPK, plasminogen, PG, alpha 2-antiplasmin, alpha 2-AP, alpha 2-macroglobulin, alpha 2-MG, urokinase-inhibitor, UK-I, streptokinase-inhibitor, SK-I, C1-inhibitor, C1-I, alpha 1-antitrypsin, alpha 1-AT, and fibrinogen-fibrin degradation products, FDP. Survivors and non-survivors of septicemia induced ARDS showed a characteristic feature: marked increase of FG and pronounced decrease of AT III and PPK in the coagulation system; concerning the fibrinolytic system a decrease of PG, alpha 2-AP and alpha 2-MG as well as an increase of inhibitors of PG-activators (PG-antiactivators) UK-I, SK-I, C1-I and alpha 1-AT; the FDP-titer was elevated. This constellation of parameters is interpreted as indicative of a marked procoagulant stimulation rendering the organism a state of hypercoagulability coinciding with a diminished availability of the fibrinolytic system, due to exhaustion of the fibrinolytic potential and increase of PG-antiactivators. In the trauma group initially the rise of FG, SK-I, C1-I and alpha 1-AT is absent independent of the outcome, but develops with progression of the disease. As ARDS is more frequently associated with septicemia, diminished availability of the fibrinolytic system simultaneously with increased procoagulant stimulation may be a particular pathophysiologic mechanism in the pathogenesis of ARDS.
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PMID:Fibrinolysis inhibition in acute respiratory distress syndrome. 386 24

Tissue thromboplastin generation in monocytes was studied during various stages of Escherichia coli endotoxinaemia in pigs. The pigs were monitored in halothane anaesthesia and mechanically ventilated. Blood was sampled from the superior caval vein before and during endotoxin infusion and up to 6 hours after its start. Monnuclear leukocytes were harvested with Lymphoprep separation and monocyte counts were made, using TRITC-labelled sheep erythrocytes, acridine orange and a fluorescence microscope. Thromboplastin was quantified in a two-stage assay by incubating the test sample together with purified factor X, factor VII and Ca++. The generated factor Xa was thereafter assayed. There was statistically significant increase of tissue thromboplastin activity in monocytes after endotoxin infusion. Maximum level was reached at the end of the infusion and was maintained throughout the observation period. Decrease occurred in platelets, leukocytes, antithrombin III, fibrinogen and clotting factors V, VII and VIII, and clotting time was prolonged. These findings indicated significant disseminated intravascular coagulation. The endotoxin-stimulated monocytes with their elevated tissue thrombo-plastin activity thus may play an important part in development of the DIC which so often follows septicemia.
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PMID:Tissue thromboplastin generation in circulating mononuclear phagocytes and development of coagulation disorders during E. coli endotoxinaemia in pigs. 392 66

The plasma concentration of beta-thromboglobulin was serially measured in nine patients with septicemia, ten patients with pneumonia and five thrombo- and granulocytopenic patients with acute leukemia. Six patients with septicemia out of the eight studied on days 1-3 and all eight patients studied 7-14 days after onset had an abnormal high beta-thromboglobulin level. One patient with pneumonia out of six studied on days 1-3 and six out of nine studied on 7-14 days after onset had an abnormal high value. A rising trend in plasma beta-thromboglobulin with the highest mean levels at one to two weeks after onset was common to both groups. Positive ethanol gelation, increased level of fibrin/fibrinogen degradation products, decreased antithrombin III, increased FVIII complex and disproportionate ratio of FVIII:C to FVIIIR:Ag were common in both groups in the early stages of the disease. All the five patients with leukemia had a lower than normal beta-thromboglobulin level throughout the study but showed in the coagulation parameters changes similar to those observed in the other groups. Judging from the commonness of abnormal beta-thromboglobulin values in the two first patient groups, low grade platelet activation is a normal response in severe infection.
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PMID:Plasma beta-thromboglobulin in severe infection. 618 May 2

In the present study treatment of sepsis in 18 surgical patients, 9 survivors and 9 fatal cases, were evaluated by determining components of the plasma proteolytic enzyme systems using chromogenic peptide substrate assays. During persistent sepsis, continuous low values for prekallikrein, plasminogen and antithrombin III were found until death. At autopsy a septic focus was found in all but one of the fatal cases. Very low levels of prekallikrein during sepsis and reduced functional inhibition of plasma kallikrein in septic shock indicated a poor prognosis. In the survivors all parameters returned towards normal range upon successful therapy. Plasminogen and antithrombin III were most rapidly normalized. It is concluded that determination of components of the plasma protease systems using chromogenic peptide substrate assays, gives valuable information about course and prognosis in surgical sepsis, and that they are suitable for practical clinical use.
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PMID:Treatment of sepsis in the surgical patient evaluated by means of chromogenic peptide substrate assays. 618 46

Values of mean antiproteases were studied in 60 children with meningococcal sepsis. At illness onset, increased levels of alpha-1 antiquimotrypsin (p less than 0.001) and decreased of alpha-2 macroglobulin (p less than 0.001) were found. Moreover, patients who were complicated with a disseminated intravascular coagulation (DIC) also showed a decrease of antithrombin III (p less than 0.001) and inter alpha-1 trypsin inhibitor (p less than 0.001). There was not relationship between antiproteases levels and mortality. In 33 cases the measures were repeated 24 hours later, but no homogeneous results were found, in spite of alpha-2 macroglobulin fall in patients complicated with DIC (p less than 0.05). Phenotypic variants of alpha-1 antitrypsin were studied in 47 cases by isoelectric focusing. Results did not provide evidence that "abnormal phenotypes" (no-Pi MM) could facilitate meningococcal sepsis or DIC, but an increased number of "abnormal phenotypes" (5/9) were found in dead patients (p less than 0.025).
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PMID:[Pi phenotypes of alpha-1-antitrypsin and antiproteases in meningococcal sepsis]. 619 15


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