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)

We investigated the imbalance between thrombin and plasmin activity in vivo with various grades of severity of disseminated intravascular coagulation (DIC) in relation to the underlying diseases. Plasma thrombin-antithrombin-III complex (TAT) and plasmin-alpha 2-antiplasmin complex (PAP) levels were measured in 133 blood samples obtained from patients with DIC. The TAT/PAP ratio was higher in patients with sepsis or solid cancer than in those with hematologic malignancies. In acute promyelocytic leukemia (APL), the TAT levels were the highest, but the PAP levels were even higher and the TAT/PAP ratio was the lowest. As for the severity of DIC, in mild DIC, both thrombin and plasmin activities were increased. In moderate DIC, the TAT/PAP ratio increased, and thrombin activity was much more predominant. However, in severe DIC, the ratio decreased, and plasmin activity became excessive. In 3 patients with acute myeloblastic leukemia, APL and pancreatic cancer, respectively, the PAP level remained high during heparin therapy although the TAT level was decreased. When tranexamic acid was given, the PAP level was selectively reduced, and the TAT/PAP ratio was markedly decreased along with clinical improvement. These results indicate that monitoring of the TAT/PAP ratio may contribute to decisions regarding the institution and performance of combination therapy for DIC using anticoagulants and antifibrinolytic agents.
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PMID:Imbalance between thrombin and plasmin activity in disseminated intravascular coagulation. Assessment by the thrombin-antithrombin-III complex/plasmin-alpha-2-antiplasmin complex ratio. 146 20

Both surgical trauma and infection can disturb the proteinase to proteinase inhibitor balance in the circulation. We sought to assess the effect of Candida albicans infection (INFX) on postoperative mortality, to correlate mortality with total serum proteolytic activity (PA), and to assess the impact of exogenous proteinase inhibitors (PI) on this mortality. Mice underwent midline laparotomy (LAP) and immediate postoperative intravenous C. albicans infection. LAP + INFX shortened mean survival compared to INFX or LAP alone. Quantitative renal cultures confirmed that death in the LAP + INFX and INFX groups was due to Candida sepsis. PA was measured using an 125I-labeled protein assay, yielding micrograms of acid-soluble peptides/100 microliters of serum. In control, sham-operated, and LAP groups, PA averaged less than 9.0, and mortality was 0. In INFX and LAP + INFX groups, PA averaged greater than 14.5 and mortality was high. To determine if high PA was related to high mortality, LAP + INFX mice were treated immediately preoperatively with a single dose of PI (1 mg alpha 1-proteinase inhibitor, 1 mg antithrombin, and 1000 KIU aprotinin). Mean survival increased with PI treatment. In conclusion, the addition of Candida infection to surgical trauma hastened mean time to death. More rapid death correlated with elevated PA and may reflect systemic imbalance in the proteinase to proteinase inhibitor ratio in the circulation. PI improved survival, suggesting that proteinase inhibition may prove useful in the future in the treatment of fungal sepsis in surgical patients.
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PMID:Surgical trauma, Candida infection, and serum proteolytic activity. 152 52

The effect of burn wound size on the activation of fibrinolysis, coagulation, and contact factors was analyzed in 60 thermal injury patients. Blood samples from 47 male patients and 13 female patients, (average age 37 years; range 1.5-70 years) were collected within the first 36 hours and at 5-7 days following injury. The patient population was categorized by percentage of burn (second degree and/or third degree): less than 20%, n = 22; 20%-40%, n = 18; greater than 40%, n = 20. The average percentage of burn was 32% (range, 4%-95%). The mechanism of injury was by flame (25), explosion and flame (19), scald (12), electric (3), or chemicals (1). An associated inhalation injury was present in 12 patients. The overall mortality rate was 13% (8). Sepsis or serious infection occurred in 23% (14) of the patients. On admission, 83% of the patients had normal prothrombin times (PT) and activated partial thromboplastin times (APTT). However, specific hemostatic variables showed marked changes. Admission hemostatic markers that correlated with the severity of injury were: tissue-plasminogen activator (tPA), plasminogen activator inhibitor (PAI), D-dimer (D-di), plasminogen (Plg), proteins C and S (PrC and PrS), antithrombin III (ATIII), thrombin-antithrombin complex (TAT), kallikrein (Kal:c), kinin (Kin), C1 esterase inhibitor (C1Inh), and factor VII clotting and antigen (FVII:c, FVII:ag). These data suggest that during the early course following burn injury, thrombogenicity is increased (TAT increases) because of a decrease in ATIII, PrC, and PrS; and fibrinolysis activation (D-di increases) occurs via an increase in tPA with a p value increase in PAI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of burn wound size on hemostasis: a correlation of the hemostatic changes to the clinical state. 163 6

Sepsis is often associated with hemostatic dysfunction. This study aimed to relate changes in fibrinolysis and coagulation parameters to sepsis and sepsis outcome. Urokinase-type plasminogen activator (u-PA) antigen, tissue-type plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor (PAI) type 1 antigen, PAI activity, antithrombin (AT) III activity, and protein C activity were measured in 24 patients suffering from sepsis or septic shock and the results were compared with those observed in 30 non-sepsis patients with severe infectious disease. The u-PA level was markedly increased in plasma of sepsis patients as compared to non-sepsis patients (11.5 +/- 9.4 versus 1.6 +/- 1.5 ng/ml, p less than 0.0001). PAI-1 antigen and t-PA activity showed a significant increase in sepsis patients (320 +/- 390 ng/ml versus 120 +/- 200 ng/ml, and 3.0 +/- 3.6 IU/ml versus 1.0 +/- 0.7 IU/ml, respectively, p less than 0.01). AT III was decreased in sepsis patients (58 +/- 28% in sepsis versus 79 +/- 26% in severe infectious disease, p less than 0.01) as was protein C (30 +/- 18% versus 58 +/- 27%, p less than 0.001). No significant difference was found for t-PA antigen nor for PAI activity. Nonsurvivors of sepsis were distinguished mainly by a high u-PA antigen level and increased t-PA activity. It is concluded that plasma u-PA antigen showed the strongest significant difference, among the parameters evaluated, between sepsis and severe infection. u-PA antigen may be of prognostic value in patients admitted to the medical intensive care unit for severe infectious disease.
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PMID:Fibrinolysis and coagulation in patients with infectious disease and sepsis. 190 55

Optimal expectant management of preterm premature rupture of membranes (PROM) requires the early detection of chorioamnionitis. To date, however, no universally sensitive and specific marker for chorioamnionitis has been identified. Recently, the serial determination of plasma fibronectin, antithrombin, and prekallikrein has been reported to facilitate the early detection of sepsis in critically ill neonates and adult surgical patients. A cross-sectional study was undertaken to determine if plasma levels of these markers change significantly in patients with overt chorioamnionitis following expectant management of preterm PROM. Plasma levels of fibronectin and prekallikrein were not significantly different between the study (30 patients with overt chorioamnionitis following preterm PROM) and control (30 undelivered patients without antenatal complication matched for gestational age) groups. Antithrombin levels were significantly lower in the study group (p less than 0.05), but the magnitude of the difference (102% versus 94%) is not likely to be of clinical significance. We conclude that determination of plasma levels of fibronectin, prekallikrein, and antithrombin is not likely to aid in the early detection of chorioamnionitis in the setting of preterm (PROM).
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PMID:Evaluation of potential early markers of chorioamnionitis associated with preterm premature ruptured membranes. 229 8

Mesenteric venous thrombosis is a clinical entity, which is rarely recognized on admission. The patients are admitted with vague abdominal complaints and, eventually, abdominal sepsis might occur requiring laparotomy. Nowadays, underlying hypercoagulable states such as antithrombin-III, protein-C and protein-S deficiencies are recognized more frequently as a distinct cause of mesenteric venous thrombosis. In this paper, a case of mesenteric venous thrombosis due to protein-C deficiency is presented. The patients generally have a history of thromboembolism of the deep veins of the legs at young age. The combination of vague abdominal complaints and a history of thrombosis of the deep veins of the legs should arouse the suspicion of mesenteric venous thrombosis. In these cases, contrast-enhanced computerized tomography is a non-invasive diagnostic means which may provide the diagnosis. If infarction of the gut is present, resection is mandatory and a second-look operation should be performed. After surgery, heparinization is essential. This must be followed by administration of oral anticoagulants for an indefinite period in case of an underlying antithrombin III, protein-C or protein-S deficiency.
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PMID:Mesenteric venous thrombosis caused by deficiency of physiologic anti-coagulants: report of a case. 232 Feb 74

Fatal multiple organ failure after severe infection may be related to an early activation of protease cascade systems. This study aimed to relate changes in coagulation, fibrinolysis, and kallikrein to shock and outcome. Of 53 patients with severe infection, 30 did not develop shock, 12 survived septic shock, and 11 died from organ failure after septic shock. No patient had overt disseminated intravascular coagulation. We measured 17 components of the coagulation/fibrinolysis/kallikrein pathways on admission and on the next 2 days. High values for fibrinogen, factor VIII:C, von Willebrand factor antigen, and D-dimer were seen in all patients; factor XII, prekallikrein, factor VII, antithrombin, protein C, and fibronectin were low. The patients thus appeared to be hypercoagulable. These disturbances were more pronounced in septic shock survivors, who also had low plasminogen and antiplasmin, indicating ongoing fibrinolysis. Nonsurvivors of sepsis were distinguished mainly by high plasminogen activator inhibitor values; this suggests an impaired functional fibrinolysis in fatal sepsis, with possible therapeutic implications. Cryoprecipitate infusion increased the fibronectin concentration, but did not influence the other factors studied.
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PMID:Coagulation, fibrinolysis, and kallikrein systems in sepsis: relation to outcome. 250 62

We have evaluated the quantitative relationship between lipopolysaccharide (LPS, endotoxin), fibrinopeptide A (FPA), antithrombin (AT), protein C (PC) and extrinsic pathway inhibitor (EPI) in plasma from 39 consecutively admitted patients with systemic meningococcal disease (SMD). The most severely ill patients with fulminant meningococcal septicemia (n = 13, 6 dead) had significantly (p less than 0.01) higher plasma levels of LPS and FPA and lower levels of PC and AT on admission as compared with the less severe clinical presentations (n = 26, 1 dead). The levels of EPI on admission were significantly (p less than 0.05) higher in nonsurvivors vs survivors with fulminant septicemia. As the disease progressed, the levels of LPS, FPA, AT and PC declined, while the levels of EPI increased. Three of six nonsurviving septicemic patients had levels of EPI greater than 200% within 16 hours of admission vs two of 30 survivors (p = 0.02). The results suggest that increasing levels of LPS in SMD elicit increasing consumption coagulopathy, contributing to the organ pathophysiology. The kinetics of EPI, inhibiting the thromboplastin-FVIIa-FXa complex, differs markedly from the kinetics of AT and PC i.e. increases as opposed to decreases.
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PMID:The quantitative association of plasma endotoxin, antithrombin, protein C, extrinsic pathway inhibitor and fibrinopeptide A in systemic meningococcal disease. 251 Mar 54

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

The treatment of disseminated intravascular coagulation (DIC) in infants with sepsis should be instituted after multimodality therapy of pyo-inflammatory diseases taking into account the degree of hemostatic disorders. In stage I DIC (hypercoagulation one), it is necessary to reach an adequate level of the inhibitors of the thrombin and plasmin systems. In this case it is quite sufficient to use donor's cryoplasma without heparin administration. In stage II DIC (transitory one) and stage III (hypocoagulation one), it is required that the drugs possessing antithrombin and antiplasmin activity, substitution therapy with blood preparations and components as well as measures to control hemorrhagic diathesis may be used.
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PMID:[Disseminated intravascular coagulation in newborn infants with infection]. 276 53


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