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)

Thrombocytopenia without other hemostatic changes is the most common coagulopathy associated with sepsis. We studied pneumococcus (PNC)-induced hemostatic changes, including thrombocytopenia, in rabbits. Nonviable PNC or saline solution was injected into rabbits preinfused with chromium 51-labeled platelets or iodine 125-fibrinogen. Blood was serially obtained for determination of platelet counts, 51Cr activity or 125I activity, and fibrinogen and fibrin degradation products. Lung, liver, and spleen tissues were counted for 51Cr or 125I activities per gram of wet tissue. PNC-challenged animals displayed profound thrombocytopenia from 0.5 to 48 hours with the mean nadir (-80% relative to the baseline) at 3 hours and a significantly (P less than 0.025) shortened 51Cr-platelet survival of 1.45 +/- 0.71 days vs. 2.72 +/- 1.09 days for saline-injected controls. Circulating fibrinogen level increased, whereas 125I-fibrinogen survival was unchanged (2.6 +/- 0.5 days in PNC-challenged vs. 2.8 +/- 1.0 days in saline-injected). No increased tissue deposition of either 51Cr-labeled platelets or 125I-fibrinogen was found. Rabbits infused with either serum, plasma, or saline solution after each was incubated with PNC all developed significant thrombocytopenia of less than 1 hour duration with maximal mean decreases relative to the baseline of -76% (P less than 0.001), -65% (P less than 0.0005), and -84% (P less than 0.0005), respectively. Inactivation of serum or plasma complement before PNC incubation or heat treatment after PNC incubation in serum or saline solution did not alter the thrombocytopenia. The thrombocytopenia-promoting activity was also trypsin resistant, did not require the presence of serum, plasma, or PNC capsular polysaccharide for its in vitro generation, and had a mol wt of 100,000 to 300,000. Therefore, PNC-induced thrombocytopenia, in the absence of other hemostatic changes, may be explained on the basis of the direct action of a PNC-derived substance(s) on circulating platelets.
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PMID:Pneumococcus-induced thrombocytopenia in rabbits. 403 31

In 119 children, predominantly newborns and babies with sepsis, alpha 2-Antiplasmin was determined by the use of the chromogenic substrate S-2251. In healthy newborns, the inhibitor level averaged 65 per cent of the adult level. Already in the initial phase of sepsis, enhanced alpha 2-antiplasmin values were observed. During the further course, they increased markedly. Thus, alpha 2-antiplasmin proved to be an acute phase reactant together with fibrinogen, factors II and X, and alpha 1-antitrypsin measured as trypsin inhibitor capacity. The correlation analysis in all subgroups showed moderately tight binding to fibrin. In patients with shock or in those who decreased, lower levels were measured. The overproduction is assumed to be caused by disseminated intravascular coagulation processes. In other diseases such as respiratory distress, alpha 2-antiplasmin was reduced. In case of disseminated intravascular coagulation that was not caused by sepsis consumption of components dominated. In the probability paper, distribution of the values of the subgroups was found to differ markedly. Thus, the inhibitor proved to be of diagnostic value.
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PMID:[Alpha 2-antiplasmin in childhood]. 617 99

A nephelometric method is described for determination of plasminogen and two types of plasmin inhibitors in human plasma having different affinity toward plasmin. This method is based on the kinetic analysis of effects of whole plasma and plasmin inhibitor fraction obtained from plasma on the activity of exogenously added plasminogen which was determined by measuring the decrease of light scattering of fibrin suspension. With this method we have determined the activity of plasminogen and two types of inhibitors in the plasma of normal subjects and patients with high fibrinogen degradation product values. They include patients with various malignant tumors with DIC, chronic renal failure, sepsis, vascular diseases, and liver cirrhosis with hepatoma.
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PMID:Nephelometric determination of plasminogen and plasmin inhibitors in human plasma using fibrin suspension as a substrate. 622 10

Experience with angio-access in patients with chronic end-stage renal failure undergoing haemodialysis, including those with arteriovenous fistulas constructed within the past 3 years, is reviewed. In patients in group 1, 137 fistulas were constructed; the patency rate at 2 years was 66% and at 4 years 47%. Complications were due to thrombosis, aneurysm and poor operative technique. In group 2 fistulas were constructed from synthetic material in 33 patients; the patency rate at 2 years was 44% and at 4 years 36%. Complications were due to thrombosis and sepsis. No correlation was found between raised fibrinogen levels and fistula or graft failures. Dialysis needles of different gauges were compared; the 16-gauge Terumo needle was found to cause no hemolysis and was adequate for use in dialysis.
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PMID:Vascular access for haemodialysis--experience at Johannesburg Hospital. 623 27

A 17-year-old male with previously undiagnosed congenital Factor IX deficiency (13%) presented with gastrointestinal bleeding and a hepatic mass. Prolonged thrombin and Reptilase times, which partially corrected with CaCl2 and a discrepancy between thrombin-clottable and immunoreactive plasma fibrinogen, suggested a dysfibrinogenemia. Laparotomy disclosed metastatic hepatoma. Adequate hemostasis was obtained with clotting factor replacement, but wound healing was delayed. Patient fibrinogen purified with 2.1 M glycine migrated normally on immunoelectrophoresis and 7.5% polyacrylamide-SDS gel electrophoresis. However, fibrin monomers prepared from purified patient fibrinogen displayed impaired aggregation at high and low ionic strengths when compared with fibrin monomers from normal and control Factor IX deficient subjects. Aggregation of normal monomers was delayed when mixed 1:1 with patient monomers. Fibrinopeptide release was normal, and total sialic acid content was similar to that of normal and control fibrinogens. Chemotherapy, consisting of 5-FU given via intra-arterial hepatic infusion, was accompanied by significant transient clinical improvement which coincided with correction of thrombin clotting times and fibrin monomer aggregation. Reappearance of fibrinogen dysfunction occurred with clinical deterioration prior to death from metastatic hepatoma and sepsis. This case is the first to corroborate the postulated tumor marker role of dysfibrinogenemia in a patient with hepatoma by documenting a direct relationship with response to chemotherapy.
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PMID:Acquired dysfibrinogenemia in a hemophiliac with hepatoma: resolution of fibrinogen dysfunction following chemotherapy. 626 56

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

The pathologic changes in septic shock, a disease state involving several hemodynamic and metabolic parameters, are not completely understood. Because research on animals can provide information vital to treating disease in humans, and because of the increasing constraints on clinical trials with humans, a clinically relevant animal sepsis model has been developed using adult male Sprague-Dawley rats. Sepsis was induced in large numbers of rats by IP injections of discrete quantities of live E coli organisms. The following elements were measured at specific times: MAP, CO, CVP, WBC, platelets, hemoglobin, hematocrit, PT, PTT, fibrinogen, clotting factors, glucose, blood gases, Ca++, Mg++, and TSP. The study shows that the model is easily replicated and relatively inexpensive, and that it can be used for detailed study in rats of several of the pathophysiological states characteristic of sepsis in humans.
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PMID:Rat intraperitoneal sepsis--a clinically relevant model. 635 75

Fibronectin (FN) is a glycoprotein (disulfite-bonded dimer of 200 to 220 Kd submits) found in a soluble form in blood (concentration 250--500 microg/ml), it can be removed from it by cryoprecipitation and affinity chromatography on gelatin or heparin-agarose. It is also found in an insoluble fibrillar form as a component of connective tissue matrix like collagen, proteoglycans... FN fundamentally forms molecular complexes with collagen, fibrinogen or fibrin, heparin, activated factor XIII, bacteria, cellular membranes..., these various proteins binding with now well known functional "domains" on subunits. Thus FN mediates adhesion of cells to cells as well to biomaterials or tissue, cell migration and chemotactic activity, tissue stromal organization... The transformed cultured cells in presence of oncogen virus loose ability to secrete FN which contribute to their invasive tendency. FN also interacts with hemostatic and fibrinolytic systems, as component of the subendothelium (secreted, like Willbrand factor, by endothelial cells) and of platelet alpha-granules released by stimulated platelets. FN could then provoke platelet spreading on the subendothelium surface after collagen-platelet adhesion, triggered by Willebrand factor, has happened. FN is a part of the fibrinous clot. It participates in anchorage of the clot to subendothelium and mediates its colonisation by fibroblasts, first step to wound reparation. Lastly FN probably has an important role in organism defence. It acts as a non-immunological opsonin, promoting phagocytosis by RES macrophages of bacteria, cellular or fibrin fragments, immune complexes... present in blood. Plasmatic FN concentration is strongly decreased in several ill patients following major trauma, extensive burns, shock, sepsis, with or not evidence of DIVC, of respiratory distress... SABA and various other authors have obtained good results after injections of FN (as cryoprecipitates or concentrated fractions). It is yet necessary to confirm therapeutic role of FN.
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PMID:[Plasma fibronectin]. 641

The clinical scenario of multiple organ failure (MOF) is reviewed and its frequent correlation with sepsis emphasized. It is hypothesized that MOF is produced by the formation of immune complexes (IC) in response to infection with deposition on organs such as the liver, lung, and kidney. Such immune complexes trap macrophages which can directly damage endothelium. Such a pathologic picture is in keeping with that of MOF. Granular deposits of IgG, IgM, C3, C5, and fibrinogen have been identified in the organs of four patients dying of MOF and sepsis. Similar deposits have been identified using fluorescent antibody stains in the organs of rabbits following cecal perforation. It is hypothesized that sepsis may produce organ failure at a distance from the site of infection via deposits of immune complexes.
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PMID:Multiple organ failure: clinical and experimental. 644 89

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


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