Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to further elucidate the pathophysiological significance of plasma proteolysis during septicemia, surgical patients with septicemia were studied by means of chromogenic peptide substrate assays. 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 proenzyme functional inhibition index (PFI-index) in patients with septicemia. The data reveal that by means of this parameter patients at high risk can be identified at an early stage of the disease.
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PMID:Uncontrolled plasma proteolysis: a major threat to the septicemic patient. 302 78

74 patients treated in the intensive care unit for postoperative sepsis were prospectively documented. The severity of sepsis was monitored by a scoring system. Additionally, daily measurements of antithrombin III (AT-III) levels, thrombocytes and endotoxin plasma concentrations were performed. The sepsis score only discriminated between surviving and non-surviving patients. The sensitivity in predicting death due to sepsis was 94%, the specificity 80% in case that a sepsis score of 19 was achieved. In contrast, thrombocytes, endotoxin plasma concentrations and AT-III levels were not able to predict the final outcome, but could be correlated to the severity of sepsis. Since high score levels can also be caused by multiple organ failure due to other reasons, the septic condition of the patients should be defined in the future by the combination of this scoring system with the endotoxin or AT-III measurement.
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PMID:[Follow-up of infected patients in an intensive care unit using the "infection score," endotoxin and AT III determination]. 337 97

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

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

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

In 284 children with sepsis coagulation analyses were carried out. In sepsis in the postnatal period number of thrombocytes, plasminogen, antithrombin III, alpha 2-macroglobulin and factor V were initially decreased on an average, but fibrinogen, alpha 2-antiplasmin, the factors II and X as well as the trypsin inhibitor capacity were increased. The initially on an average reduced parameters often still considerably decreased, in order to increase after this to the norm of age within one to two weeks. The thrombocytopenia longest persists, often to the third week. The components initially found increased on an average in most cases rapidly increase and beyond the norm of age. They behave as acute phase proteins. In sepsis beyond the neonatal period the quality of the acute phase protein is in numerous components still more distinct than in the postnatal period. Several parameters also showed a completely other dynamics: the thrombocytopenia is of lesser size and shorter duration and is very often changed by a thrombocytosis. Here alpha 2-macroglobulin also has the quality of an acute phase protein. From the dynamics observed is concluded that disseminated intravascular coagulation processes frequently accompany the initial phase of the sepsis. They cause an eminent over-production of coagulation components which is limited by their production capacity and partly compensates the defects. The diversity of the constellation is explained by different sizes of consumption and compensation. The parameters in their dynamics have diagnostic valency. As far as the difference from fibrinogen level and number of thrombocytes is concerned it could already proved by simple means.
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PMID:[Effect on hemostasis and thrombogenesis by septic processes especially in childhood]. 646 15

An acute depletion of plasma fibronectin or FN has been observed in critically ill, surgical, or trauma patients, but there is little information on the relationships between FN levels and the final outcome in such cases, and on the simultaneous behaviour of other serum proteins. The daily values of FN, antithrombin III, IgG, C3, prealbumin, and transferrin were monitored in 98 intensive care patients after major elective surgery or trauma. According to their clinical course, they were divided retrospectively into three groups. Group A (33 patients) had sepsis. Group B (31 patients) had nonseptic complications, and group C (34 patients) had no complications in the ICU. The individual, nadir levels of FN, AT III, prealbumin, and transferrin were lower (p less than 0.01) in the septic group A than in B and C. Within the septic group, the nadir levels of AT III, but not those of FN, were lower (p less than 0.01) in the 14 nonsurvivors than in the 19 survivors. The FN and AT III levels had returned at least temporarily to the normal range in the six ultimate fatalities from sepsis who survived for more than two weeks. In the septic group, transferrin showed the highest percentages of actually subnormal levels and differed from FN in this respect with p less than 0.05. Furthermore, all six proteins showed a significant overall pattern (p less than 0.01) of parallel variations. The results confirm other reports on the behavior of fibronectin in septic patients as a group, but it was not informative as to the individual outcome, and its reduction might be viewed as part of a general plasma protein depletion associated with acute septic disease. This pattern is probably attributable to a combination of intravascular consumption and an overall excess of protein catabolism over synthesis.
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PMID:Plasma fibronectin and associated variables in surgical intensive care patients. 683 Mar 38


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