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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A brief explanation of the molecular markers of coagulation, fibrinolysis and endothelial cell activation was done. The clinical significance of markers, such as, soluble fibrin monomer complex, FDP D-dimer, prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasmin-alpha 2 plasmin inhibitor complex and plasma thrombomodulin in our patients with disseminated intravascular coagulation (DIC) due to abdominal sepsis and malignancy is discussed. The coagulopathy in the DIC patients due to abdominal sepsis had a different aspect from that in the DIC patients due to malignancy. Activation of the coagulation and fibrinolytic systems in sepsis was milder than that in malignancy, despite the decrease of antithrombin III activity in the patients with sepsis. In the patients with sepsis, granulocyte elastase was increased. It was proposed that the coagulopathy was caused not only thrombin formation but also by granulocyte proteinase. It could be expected that the pathophysiology of disseminated intravascular coagulation should be clarified, because of the high sensitivity.
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PMID:[Advancement in the diagnosis of disseminated intravascular coagulation for the surgeon]. 838 85

In the present study soluble fibrin complexes and fibrin(ogen) degradation products are determined in patients with sepsis and liver-cirrhotic simultaneously by means of FM-Test, FDP-Kit and SCT in order to detect the different and early phases of disseminated intravascular coagulation. According to the possible configuration of test results 43 patients (sepsis n = 23, liver cirrhotic n = 20) could be grouped in 4 phases. The FDP-concentrations and the FM-Test-result appear to be independent from one another. A positive FM-Test was found at least once in 35% of patients with liver-cirrhotic and 26% of patients with sepsis. The correlation coefficient for the two FDP-Tests (FDP-Kit and SCT) was r = 0.97 (p < 0.001) for liver-cirrhotic and r = 0.98 (p < 0.001) for sepsis.
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PMID:[Differential determination of fibrinogen degradation products in assessment of the stages of plasma consumption in patients with infection and liver cirrhosis]. 844 74

We studied the influence of age on mortality and severity of clotting abnormalities in 79 children (median age: 3.1 years) with meningococcal sepsis. Parameters of coagulation and fibrinolysis and plasma levels of cytokines were prospectively measured on admission. The mortality rate was 27%. The age of survivors was significantly different from that of non-survivors (p = 0.013). With the exception of FVII, vWF and t-PA, parameters of coagulation and fibrinolysis, as well as plasma cytokine levels were related to outcome. Patients were divided in two groups: younger and older than median age. The mortality in children < or = 3.1 years was 40% versus 13% in children > 3.1 years (p = 0.006). In contrast to cytokine levels, which were not different between the two age groups, fibrinogen, prothrombin, factors V, VII, VIII, vWF, protein C, antithrombin, FDP, and the ratio PA1-1/t-PA were related to age, indicating a more severe coagulopathy in children < or = 3.1 years despite a similar degree of inflammatory response. A relative deficiency of coagulation factors due to an immature state of the clotting system, as well as an inadequate fibrinolytic response, both related to age may have caused this more severe coagulative response in younger children, and may have contributed to the higher mortality rate.
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PMID:Age-related differences in outcome and severity of DIC in children with septic shock and purpura. 897 13

Upon stimulation, polymorphonuclear leucocytes (PMNs) release potent serine proteases, i.e. elastase, cathepsin G and proteinase 3, which contribute to the degradation of tissue and plasma components. Here, we describe the development of a plasma test to assess PMN-mediated fibrinogenolysis as a biochemical marker for actual PMN-derived proteolysis in vivo, useful for monitoring therapeutic efficacy, i.e. of elastase inhibitors. We generated a monoclonal antibody (MAb), designated 1-1/B3, with a high affinity for elastase-degraded fibrinogen (EDF). The epitope for 1-1/B3 becomes exposed in a time-dependent manner during digestion of fibrinogen with purified PMN-derived serine proteases and with isolated PMNs in vitro. However, 1-1/B3 does not react with plasma fibrinogen or with fibrin(ogen) degradation products generated by plasmin or by other active proteases that may occur locally, i.e. metalloproteases and lysosomal cathepsins. On the basis of MAb 1-1/B3, we developed a plasma test for the assessment of PMN-mediated fibrin(ogen) degradation products (PMN-FDP). In a panel of control plasmas, we observed concentrations of PMN-FDP of 8.2 +/- 0.9 ng mL-1 (n = 18). These values were increased twofold in patients with alpha 1-proteinase inhibitor deficiency (18.6 +/- 3.3 ng mL-1; n = 12; P < 0.0001) and even more in patients with sepsis (365.7 +/- 97.7 ng mL-1; n = 16; P < 0.0001). Furthermore, synovial tissue extracts from patients with rheumatoid arthritis contained increased levels of PMN-FDP, compared with synovial tissue extracts (P < 0.005) from patients with osteoarthritis.
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PMID:An enzyme immunoassay for polymorphonuclear leucocyte-mediated fibrinogenolysis. 906 9

The plasma level of soluble E-selectin (sE) reflects the activation of endothelial cells induced by cytokines such as tumor necrosis factor-alpha and interleukin-1 in vitro. These cytokines are important in the development of coagulation abnormalities in patients with sepsis. We compared the plasma levels of sE in patients with infections suspected of having disseminated intravascular coagulation (DIC) (n = 33) and in patients with underlying disorders other than infections, including solid tumors (n = 28), obstetric disorders (n = 13), hematologic malignancies (n = 13), and liver disease (n = 9), to clarify the involvement of cytokines in the development of coagulation abnormalities in patients with sepsis. Plasma levels of sE in patients with infection were significantly higher than in patients with the other underlying disorders. The plasma level of sE was also significantly higher in patients with infection with DIC (114.6 +/- 77.9 ng/ml, n = 21) than in patients with infection without DIC (54.5 +/- 53.1 ng/ml, n = 12, P < 0.02). There was no significant difference in sE level between patients with the other underlying disorders with and without DIC. The plasma level of sE was significantly correlated with the serum level of FDP(E) in patients with infection. The plasma level of sE was significantly higher in patients with infection with organ failure compared to patients without organ failure. There was no significant difference between patients with the other underlying disorders with and without organ failure. Plasma levels of tumor necrosis factor-alpha and interleukin-6 were detected in only 12.1% and 20.0% of patients with infections, respectively. These observations strongly suggest that plasma levels of sE reflect the activation of endothelial cells induced by cytokines, which may lead to DIC and organ failure in the presence of sepsis. Furthermore, determination of plasma level of sE may be useful for detecting the endothelial activation induced by cytokines in the pathologic conditions of sepsis, even when plasma levels of cytokines cannot be detected.
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PMID:Plasma levels of soluble E-selectin in patients with disseminated intravascular coagulation. 906 1

1.286 patients were diagnosed as DIC, among 123.231 patients who were admitted in the 285 departments of the university hospitals in Japan, in 1992. The incidence of DIC was high in acute promyelocytic leukemia, fulminant hepatitis, abruptio placentae, acute respiratory distress syndrome, and sepsis. In cases of DIC, bleeding tendency due to consumption coagulopathy is most important, but organ dysfunction due to circulatory disturbances by development of multiple thrombi is also noteworthy. As a whole, DIC may be divided in two types. The first type is cases of DIC with severe bleeding symptoms. However, except cerebral hemorrhage, organ dysfunction is rare in these cases. These cases may be called as "fibrinolysis-dominant DIC", because hemostatic thrombi as well as thrombi which cause organ dysfunction by circulatory disturbances are rapidly removed by abnormally enhanced fibrinolysis. The second type involves cases of DIC with severe organ dysfunction. Bleeding symptoms in these cases are usually not severe. These cases may be called as "coagulation-dominant DIC". The most typical causative disease of the fibrinolysis-dominant DIC is acute promyelocytic leukemia. The most typical causative disease of the coagulation-dominant DIC is sepsis. The presence of causative disease of DIC, elevation of FDP, and depletion of platelet count are most important to diagnose DIC. In the treatment of DIC, removal of cause of DIC, administration of heparin to protect further development of multiple thrombi, and replacement of platelets in cases of acute leukemia are most important.
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PMID:Clinical aspects of DIC--disseminated intravascular coagulation. 911 31

We describe a rapid and sensitive method for detection and quantification of D-dimer and other crosslinked fibrin degradation products (XL-FDPs), which are present in elevated concentrations in patients with sepsis and thrombotic disorders. The method utilizes a sandwich fluoroimmunoassay immobilized in the sensing region of an evanescent wave biosensor. Physiological concentrations of D-dimer and high molecular weight XL-FDP could be determined in buffer and plasma samples on calibrated fibers in 11 min. Samples from septic patients were assayed using ELISA and the fiber optic method; concentrations determined by fiber optic assay were strongly correlated with those determined by ELISA (r = 0.918); intra- and inter-assay errors were comparable to those from ELISAs. Given its accuracy and rapid response time, this fiber optic biosensor shows great potential for development as a diagnostic tool.
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PMID:Rapid detection of D-dimer using a fiber optic biosensor. 945 31

DIC is a thrombohemorrhagic syndrome which occurs in association with well-defined clinical disorders such as septicemia, acute leukemia, snake envenomation, hypoxic states, etc. These disease conditions trigger the coagulation cascade in vivo resulting in formation of microthrombi, activation of fibrinolysis and a bleeding tendency. The important and most frequently observed laboratory abberrations include reduced platelet counts, low levels of fibrinogen, factors V and XIII with increased FDP's. Therapy primarily consists of recognizing the cause of DIC, removing the triggering process and administering anticoagulant therapy in specific situations. Component replacement is required if patients continue to bleed inspite of instituting the above mentioned measures. Rarely, drugs which inhibit fibrinolysis may be indicated. Early recognition and prompt institution of appropriate remedial measures coupled with adequate laboratory monitoring help in reducing morbidity and mortality due to DIC.
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PMID:Disseminated intravascular coagulation: pathophysiology and principles of management. 970 78

The impact of clot stability affecting the vasculopathy and tissue necrosis in Shwartzman reaction was investigated using plasma Factor XIII A2-depleted rabbit (FXIII-DR). Plasma Factor XIIIA2 (FXIIIA2) was depleted by infusion of the mono-specific goat anti-rabbit FXIIIA2 IgG. Generalized Shwartzman reaction (GSR) was induced by priming and challenged by i.v. injection of LPS and local Shwartzman reaction (LSR) was primed by intradermal injection of LPS and challenged by i.v. injection of LPS. Histological examination of the GSR animals showed, extensive thrombi accumulation in renal tubules and bilateral cortical necrosis of kidney in 8 out of 10 rabbits but none in the FXIII-DR. Fibrinogen levels were elevated to 3 approximately 4 fold at 24 h and lowered at 48 h whereas a steady rise was seen in the FXIII-DR. FDP levels in GSR animals were significantly elevated at 24 h and further increased at 48 h but only slightly elevated in the FXIII-DR. Examination of the LSR tissues after 48 h showed an acute onset of progressive cutaneous vascular thrombosis, purpura, and secondary hemorrhagic necrosis whereas neither fibrin deposit nor necrosis of tissue were detected in FXIII-DR despite of an early edema formation. Fibrinogen levels were also increased two fold at 24 h but returned to basal levels at 48 h in control LSR animals but not affected at all in FXIII-DR. These results suggest that during the severe inflammatory conditions such as sepsis, the fibrinolytic system is functionally sufficient to dissipate the pathogenic accumulation of disseminated intravascular clots and exudated fibrin clots if those clots were prevented from getting crosslinked in plasma.
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PMID:Depletion of plasma factor XIII prevents disseminated intravascular coagulation-induced organ damage. 1130 16

An increased concentration of fibrin(ogen) degradation products (FDPs) commonly is used in conjunction with other hemostatic test abnormalities to identify patients with disseminated intravascular coagulation (DIC). Positive FDP results, however, have been observed in dogs without clinical evidence of DIC. The purpose of this study was to evaluate FDP concentrations in a group of clinically ill dogs with a variety of disorders. Dogs included in the study had the following hemostatic parameters evaluated: prothrombin time, activated partial thromboplastin time, fibrinogen concentration, platelet count, and FDP concentration. Two rapid latex agglutination methods were compared for detecting FDP in serum samples (Thrombo-Wellcotest, International Murex Technologies Corp) and plasma samples (FDP Plasma, American Bioproducts Inc). Results of the serum FDP method were positive in 8% (4/50) of the dogs tested: 3 with DIC and 1 with immune-mediated hemolytic anemia and liver disease. Results of the plasma FDP test were positive in 60% (30/50) of the animals tested: 6 with DIC, 3 with confirmed thrombosis, and 21 with a variety of conditions, including neoplasia, immune-mediated hemolytic anemia, pancreatitis, gastric dilatation-volvulus, heat stroke, severe trauma, sepsis, protein-losing nephropathy, liver disease, hyperadrenocorticism, and chronic heart failure. Because the plasma FDP test was positive more frequently than the serum FDP test in ill dogs, it may be more sensitive for the detection of canine FDP.
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PMID:Serum and plasma latex agglutination tests for detection of fibrin(ogen) degradation products in clinically ill dogs. 1202 12


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