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)

Kinins, which are vasodilatory, permeability-increasing, pain-producing polypeptides, are formed from inactive precursors: kininogens. Their actions make kinins a particularly powerful potential pro-inflammatory factor. However the absence of specific antagonists has so far made it impossible to ascribe them a definite role in inflammation. Two studies of experimental endotoxemia in burns patients, septicemia and septic shock have demonstrated the following facts: activation occurs of specific ( pKK ) and non-specific (plasminogen-plasmin system) kininogenases , K-HMW and K-LMW levels are significantly decreased. Kininogen consumption corresponds to increased BDK production. This would therefore appear to be one of the humoral factors responsible for haemodynamic changes. Though measurement of kininogen levels is still a painstaking process, the development of chromogenic substrates has made pKK and KK measurement simple and fast. Once they have been validated physico-pathologically in a large number of patients, such assays should take their place among the diagnostic weapons of clinical biology at the disposal of clinicians.
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PMID:[Role of the kallikrein-kininogen-kinin system in the inflammatory reaction and septic shock]. 623 19

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

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

Various parameters of fibrinolysis inhibition and the plasma concentration of fibronectin (alpha 2-surface binding glycoprotein, cold insoluble globulin) were measured in patients at risk of developing acute progressive respiratory sufficiency following trauma or sepsis - the delayed microembolism syndrome (DMS). Most parameters measuring fibrinolysis inhibition were significantly higher in the five patients with DMS than in five patients who did not develop the syndrome. Thus, the primary fibrinolysis inhibitor (alpha 2-antiplasmin) was enhanced and the alpha-form of this inhibitor, with affinity to plasminogen, showed the greatest increment and might be of major importance for the delayed elimination of fibrin from the lungs occurring in these patients. The fibronectin concentrations were not lower in patients with DMS than in those who did not develop the syndrome.
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PMID:Fibrinolysis inhibition and fibronectin in the blood in patients with the delayed microembolism syndrome. 664 94

Gram-negative septicemia presents a particular problem in the ICU. Septicemia is usually diagnosed by fever, chills, and shock. Results of blood cultures become available a few days later. Major surgery induced a marked decline in antithrombin III (AT III) and plasminogen (PLG) to a mean level of 0.60 U/ml (normal value: 0.80-1.40 U/ml) on the 2nd and 3rd postoperative days. Around the 5th postop day, these values again attained mean preoperative levels. Seventy-six surgical ICU patients were investigated preoperatively and for 10 days postoperatively to relate postop septicemia to changes in the hemostatic profile. In 15 patients with gram-negative septicemia verified by positive culture, AT III and PLG barely recovered from the postop decrease and remained significantly lower (p less than 0.05) after the 3rd postop day, compared to 61 surgical ICU patients without septicemia. The behavior of alpha 2antiplasmin (alpha 2AP) values was equal in both groups. This difference in hemostatic profile preceded the clinical manifestations of septicemia and the results of blood culture by several days. Leucocyte or platelet counts provided no reliable information on the early development of septicemia in these surgical patients. It is concluded that persistent low plasma AT III and PLG levels in the postop phase are early indicators of a developing gram-negative septicemia.
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PMID:Postoperative hemostatic profile in relation to gram-negative septicemia. 707 22

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.
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PMID:Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs. 726 67

Haemostatic parameters were studied in 12 adult patients with acute myeloid leukaemia and acute lymphoblastic leukaemia in complete remission using high-dose cytosine arabinoside regiments together with with other drugs. Increased tissue plasminogen activator (t-PA:Ag) antigen 4 hours after AraC application (p < 0.05) as well as increased levels of plasminogen activator inhibitor activity (PAI) (p < 0.05) and fibrinopeptide A (FPA) antigen (p < 0.05) were observed on day 2. All patients during bone marrow aplasia suffered from infectious complications (7 from sepsis and 5 from fever of undetermined origin). During that period of infection the increased levels of FPA on day 21 (p < 0.05), PAI on days 15 and 21 (p < 0.05) and fibrinogen on day 21 (p < 0.05) as well as decreased values of antithrombin III (p < 0.05) on day 21 and protein C on day 15 (p < 0.05) were measured. t-PA:Ag, plasminogen, alpha 2 antiplasmin and fibrin(ogen) degradation products were within normal throughout infectious complications. None of the patients experienced clinically manifest thrombotic complication. Though the results demonstrate that changes found were not clinically important (even if they were statistically significant), and that haemostasis was compensated as well as that thrombosis was not serious problem, authors recommend routine haemostasis monitoring in acute leukaemia patients, especially at diagnosis, in association with chemotherapy and during infectious complications.
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PMID:[Hemostasis in patients with acute leukemia treated with high doses of cytosine-arabinoside: the effect of chemotherapy and infectious complications on hemostasis]. 781 98

The proband, a 43-year-old woman, suffered from right transverse sinus thrombosis during oral contraceptive treatment. A month after stopping the drug, her plasma activities of antithrombin III, protein C, protein S, heparin cofactor II, plasminogen and plasminogen activator inhibitor were normal, but her plasma histidine-rich glycoprotein (HRG) level was only 21% of the normal level of 109.5 +/- 51.5% (mean +/- 2 SD). The HRG concentrations in her plasma determined on four different occasions over 6 months were similar. She showed no clinical signs of liver insufficiency or sepsis. Low levels of plasma HRG (20% to 35% of normal) were also found in her aunt, uncle and two daughters. These results suggest that congenital HRG deficiency is inheritary in this family.
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PMID:Congenital histidine-rich glycoprotein deficiency. 823 32

The vascular endothelium plays a central role in the regulation of extrinsic fibrinolysis and thus maintains vascular patency through clot dissolution. Plasminogen activation provides an important source of localized proteolytic activity not only during fibrinolysis but also during a variety of other physiological and pathological processes. Numerous studies have indicated that human endothelial cells can directly synthesize and secrete plasminogen activators (PA) and inhibitors of these activators. PAs specifically hydrolyse a single arginine-valine bond in plasminogen, an abundant and widely distributed plasma zymogen, to form the broad spectrum serine protease, plasmin. Tissue type-PA (t-PA) and urokinase type PA (u-PA) forms of PA have been described in endothelial cells, although t-PA production and secretion is elevated most frequently. The tPA form of PA functions predominantly in endothelial cell mediated fibrinolysis, while uPA is involved in tissue remodeling. During inflammatory reactions activated mononuclear phagocytes produce a variety of cytokines which may influence the phenotype of the endothelium through a process termed "endothelial cell activation". Tumor necrosis factor alpha (TNF alpha), a mononuclear cytokine, is a distinct polypeptide of Mr 17,000 and has been implicated as a mediator of gram negative induced sepsis as well as angiogenesis. TNF alpha is known to interact with specific endothelial cell receptors and to alter endothelial coagulant and anticoagulant properties implying that cytokines may be potent modulators of hemostasis. Recent observations have indicated that TNF alpha and lymphotoxin (TNF beta) can promote the expression, synthesis and secretion of urokinase plasminogen activator (uPA) in human endothelial cells. The upregulation of uPA results in an alteration in the fibrinolytic capacity of endothelial cells and allows cells the selective ability to degrade and invade underlying subendothelial extracellular matrix (ECM). Endothelial cells treated with TNF alpha also display, in an in vitro angiogenic assay, the ability to invade Matrigel and reorganize into tube-like structures, unlike control cultures. The effects of TNF alpha on the PA proteolytic system of endothelial cells, the biological significance of this event and potential in vivo consequences will be discussed. In addition, the influence of cytokine regulatory control systems will be described, since it is becoming increasingly clear that cytokines do not act in isolation. The vascular endothelium serves as a widely distributed anatomical interface between the blood and tissue with diverse capabilities, performing distinctive biologic functions at different sites and within specific organs.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytokine regulation of endothelial cell extracellular proteolysis. 835 23

Various assays have been developed for quantitation of soluble fibrin or fibrin monomer in clinical plasma samples, since this parameter directly reflects in vivo thrombin action on fibrinogen. Using plasma samples from healthy blood donors, patients with cerebral ischemic insult, patients with septicemia, and patients with venous thrombosis, we compared two immunologic tests using monoclonal antibodies against fibrin-specific neo-epitopes, and two functional tests based on the cofactor activity of soluble fibrin complexes in tPA-induced plasminogen activation. Test A (Enzymun-Test FM) showed the best discriminating power among normal range and pathological samples. Test B (Fibrinostika soluble fibrin) clearly separated normal range from pathological samples, but failed to discriminate among samples from patients with low grade coagulation activation in septicemia, and massive activation in venous thrombosis. Functional test C (Fibrin monomer test Behring) displayed good discriminating power between normal and pathological range samples, and correlated with test A (r = 0.61), whereas assay D (Coa-Set Fibrin monomer) showed little discriminating power at values below 10 micrograms/ml and little correlation with other assays. Standardization of assays will require further characterization of analytes detected.
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PMID:Comparison of immunological and functional assays for measurement of soluble fibrin. 858 5


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