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)

Traumatology deals with two different types of shock - the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthine-xanthine oxidase system) and activation of the humoral axis - of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a "locus minoris resistentiae" for further development of endotoxemia, bacteremia, septic shock and multi-organ failure without a typical septic focus. By this "septic challenge" further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.
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PMID:[Current findings in the pathogenesis of the shock process in traumatology]. 328 34

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

A major nonrespiratory function of the mammalian lung is that of a polymorphonuclear leukocyte reservoir. Within this reservoir, granulocytes are distributed between marginating and circulating pools. Under normal conditions these cells release little, if any, toxic metabolites. Situations which facilitate chemotactic release, activation of complement, or prolonged lowering of pulmonary blood flow lead to sequestration of large numbers of polymorphonuclear leukocytes in the lungs. If these polymorphonuclear leukocytes are then stimulated to release toxic oxygen species, proteases or other metabolites, existing defense mechanisms are overwhelmed and lung injury results. Anaphylatoxins generated by complement activation, humoral factors released from platelets or macrophages, and activation of the kallikrein-kinin and coagulation systems, may exacerbate damage to the alveolar-capillary membrane. Permeability of this membrane increases, there is interstitial and then alveolar edema, with subsequent pulmonary dysfunction. While there is little doubt that this scenario holds true for some experimental models of acute lung injury, its applicability to adult respiratory distress syndrome is still controversial. Nevertheless, adult respiratory distress syndrome does arise under conditions facilitating chemotactic factor release from macrophages (e.g. hyperoxia), in situations where widespread activation of complement occurs (e.g. sepsis, trauma, microemboli), and in shock conditions where pulmonary blood flow is often lowered. Correlations exist between adult respiratory distress syndrome and activation of complement, acute neutropenia, sequestration of polymorphonuclear leukocytes and enhanced functional and metabolic activity of granulocytes. Although these findings suggest that polymorphonuclear leukocytes are an important factor in the pathogenesis of adult respiratory distress syndrome, its precise role remains to be determined.
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PMID:The role of the polymorphonuclear leukocyte in the pathogenesis of the adult respiratory distress syndrome. 383 38

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

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

Components of the plasma kallikrein-kinin system were determined in plasma samples from ten healthy subjects and eight patients with septic shock. Five of the patients died. Low levels of Hageman factor, prekallikrein, and high molecular weight kininogen, together with significantly reduced concentrations of alpha 2-macroglobulin, were observed during septic shock both in patients who died and in the survivors. The patients who died also revealed a pronounced reduction of functional kallikrein inhibition determined by a chromogenic peptide substrate assay. In the survivors, however, functional kallikrein inhibition was very well preserved during septic shock, being within the range of values found in normals. Also plasma prekallikrein and C1-esterase inhibitor levels were slightly higher in the survivors than in those who died. Our results confirm that the plasma kallikrein-kinin system becomes activated during septicemia and that consumption of components of this protease system occurs. Because both C1-esterase inhibitor concentrations and functional kallikrein inhibitory activities were higher in patients who survived septic shock than in the fatal cases, our results suggest that functional inhibition of plasma kallikrein appears to play a major role in the outcome of this condition.
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PMID:Studies on components of the plasma kallikrein-kinin system in plasma samples from normal individuals and patients with septic shock. 617 27

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

Components of the plasma proteolytic enzyme systems were studied in 15 multiple trauma patients. There were 9 survivors and 6 fatal cases. All fatal cases had sepsis and/or post traumatic adult respiratory distress syndrome. Within the first day after trauma significantly reduced values were found for plasma prekallikrein (PKK), Hageman factor (HF) and Antithrombin III (AT III). In the survivors these parameters were normalized within the first five days after the injury. In the fatal cases, however, the same parameters remained reduced or declined during the observation period. The fatal cases also revealed a high frequency of positive ethanol gelation tests (EGT), elevated serum fibrin - fibrinogen degradation products (FDP) values and persisting low platelet counts. Analyses of plasma samples from both survivors and fatal cases, fractions by Sephadex G-150 gel filtration, demonstrated alpha 2-macroglobulin - plasma kallikrein complexes. These findings demonstrate activation of the kallikrein-kinin system as a part of pathological plasma proteolysis in multiple trauma patients. Persistent reductions of PKK, HF and AT III combined with positive EGT, elevated FDP values and reduced platelet counts indicate a poor prognosis.
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PMID:Determination of components of the plasma proteolytic enzyme systems gives information of prognostic value in patients with multiple trauma. 634 78

Components of the plasma protease systems were determined by means of chromogenic peptide substrate assays during the early stage of septicemia in 21 patients of whom 11 died. The proenzyme functional inhibition index, calculated from the measured values for plasma prekallikrein, functional kallikrein inhibition, plasminogen and functional antiplasmin and antithrombin III activities, were markedly reduced in both groups, but significantly lower in the fatal cases than in the survivors from the first day of septicemia and throughout the observation period. Fatal septicemia thus appear to be associated with a more extensive proteolytic activity in plasma than nonfatal septicemia and can be readily disclosed by calculation of the proenzyme functional inhibition index.
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PMID:Evaluation of severity and prognosis in early stages of septicemia by means of chromogenic peptide substrate assays. 637 97

Plasma prekallikrein and functional kallikrein inhibition were studied in 18 surgical patients with complicating septicemia using chromogenic peptide substrate assays. Nine patients died and nine survived. In all 18 patients plasma prekallikrein values were reduced markedly when septicemia was diagnosed. During treatment gradually increasing values were found in the survivors, whereas values remained low in the fatal cases. Significantly reduced functional plasma kallikrein inhibition was associated with the development of fatal septic shock. The findings show that determination of these components of the plasma kallikrein-kinin system gives valuable information of prognostic value in patients with septicemia. Furthermore, the chromogenic peptide substrate assays used are fast and easy to perform and therefore suitable for intensive care medicine.
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PMID:Plasma kallikrein-kinin system in septicemia. 654 98


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