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)

DIC is a hemorrhagic syndrome frequently encountered as a complication in severe gram-negative bacterial sepsis. An animal model for sepsis-associated DIC was developed in order to permit study of the appearance and development of this syndrome in relation to the entire disease process. Rhesus monkeys (4 to 6 kg) were infected by intravenous injection of 10(9) Salmonella typhimurium organisms and studied for a period of 7 to 10 days following infection. Ten of 23 infected monkeys developed petechial rash characteristic of DIC, which appeared on days 1 to 2 infection and lasted 4 to 5 days. In the group of monkeys developing rash, activation of coagulation was suggested by an 80% decrease in platelet count and 20% to 30% increases in PT and APTT. Fibrinolytic system activation was indicated by the appearance of FDP. Kinin system activation was evidenced by decreases in both prekallikrein nad kininogen. Changes in laboratory tests suggestive of subclinical DIC were also noted in infected monkeys which did not develop a rash. Pathologic evidence of DIC was obtained through observation of numerous fibrin thrombi in the kidneys of the only monkey which died in the course of infection. Occurrence of DIC in association with this experimental infection in rhesus monkeys was established on the basis of clinical, laboratory, and pathologic criteria. Expression of the syndrome on days 1 to 2 following infection correlated with the period of increasing bacteremia.
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PMID:Model for disseminated intravascular coagulation: bacterial sepsis in rhesus monkeys. 9 3

We report a patient with urinary sepsis who, during intravenous urography with iodinated contrast (70 mg Na, Ca diatrizoate and meglumine) developed dyspnea, tachypnea, sinus tachycardia and moderate hypoxemia (pO2: 72 with FiO2 of 0.21). She subsequently developed adult respiratory distress syndrome (ARDS) with refractory hypoxemia (pO2: 40 mmHg with FiO2 of 0.5) and disseminated intravascular coagulation (DIC) (prothrombin index: 5%, platelets: 20,000/mm3, APTT: 102/37 min, FDP: 80 ng/ml, and fibrinogen: 120 mg %). The patient required mechanical ventilation and treatment with inotropic drugs, antibiotics, corticosteroids, plasma, platelets and erythrocytes. The outcome was favorable, and she could be discharged from the Reanimation Service 7 days after admission. In severe systemic reactions to iodinated contrasts (SRIC), ARDS and DIC are common. In our patient, the close temporal association between the administration of iodinated contrast and the development of the clinical picture made us suspect their possible causal relation. A higher predisposition to SRIC in patients with sepsis has been reported. We review the SRIC in which the anesthesiologist may play a role for reanimation.
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PMID:[Respiratory distress in adults and disseminated intravascular coagulation after administration of iodinated contrast]. 238 76

Plasma and serum from patients with liver disease and elevated fibrin(ogen) degradation product (FDP) levels as measured by latex agglutination were analyzed by immunoblotting to characterize the FDP in these patients. An antihuman fibrinogen antibody was used that recognizes fibrinogen, fibrin monomer, soluble high molecular weight fibrinogen and fibrin polymers, as well as high molecular weight cross-linked degradation fragments, and the smaller fragments X, Y, D-dimer, D, and E. The analytic procedures were validated with plasma and serum from patients known to have intravascular fibrinolysis associated either with disseminated intravascular coagulation (DIC) or with thrombolytic therapy. The samples demonstrated a spectrum of plasmin degradation fragments on the immunoblots. Twenty-eight of 35 patients with liver disease (80%) had no evidence of plasmin degradation fragments in their plasma or serum. The cause of the elevated FDP levels as measured by latex agglutination was thought to be fibrin monomer or unclottable fibrinogen that was retained in the sera of some of these patients. Seven patients (20%) were found to have circulating plasmin degradation fragments. In addition to liver disease, however, these patients all had an illness (sepsis, shock, and pancreatic carcinoma) independently associated with intravascular coagulation and fibrinolysis. Three patients who lacked plasmin fragments also had pancreatic carcinoma or sepsis. The two groups of liver disease patients could not be clearly differentiated on the basis of clinical or laboratory evidence, but the blotting procedure proved to be a useful discriminator.
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PMID:Analysis of elevated fibrin(ogen) degradation product levels in patients with liver disease. 293 48

To evaluate the availability of the fibrinolytic system in patients suffering from acute respiratory distress syndrome, ARDS, induced by septicemia or trauma, the following parameters were analysed: fibrinogen, FG, antithrombin III, AT III, plasma prekallikrein, PPK, plasminogen, PG, alpha 2-antiplasmin, alpha 2-AP, alpha 2-macroglobulin, alpha 2-MG, urokinase-inhibitor, UK-I, streptokinase-inhibitor, SK-I, C1-inhibitor, C1-I, alpha 1-antitrypsin, alpha 1-AT, and fibrinogen-fibrin degradation products, FDP. Survivors and non-survivors of septicemia induced ARDS showed a characteristic feature: marked increase of FG and pronounced decrease of AT III and PPK in the coagulation system; concerning the fibrinolytic system a decrease of PG, alpha 2-AP and alpha 2-MG as well as an increase of inhibitors of PG-activators (PG-antiactivators) UK-I, SK-I, C1-I and alpha 1-AT; the FDP-titer was elevated. This constellation of parameters is interpreted as indicative of a marked procoagulant stimulation rendering the organism a state of hypercoagulability coinciding with a diminished availability of the fibrinolytic system, due to exhaustion of the fibrinolytic potential and increase of PG-antiactivators. In the trauma group initially the rise of FG, SK-I, C1-I and alpha 1-AT is absent independent of the outcome, but develops with progression of the disease. As ARDS is more frequently associated with septicemia, diminished availability of the fibrinolytic system simultaneously with increased procoagulant stimulation may be a particular pathophysiologic mechanism in the pathogenesis of ARDS.
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PMID:Fibrinolysis inhibition in acute respiratory distress syndrome. 386 24

In a controlled study of fibronectin supplementation in sepsis, 11 ICU patients in septic shock were scheduled to receive either cryoprecipitate from 20-40 donors (n = 6) or 250-300 ml of stored plasma (n = 5) (two infusions over 24 h). We wanted to: compare some "conventional" DIC variables in the ICU (platelet count, prothrombin complex = NT, FDP) to additional variables: Fibronectin (Fn), fibrinogen (Fg), F V, FVIII R:Ag, F VIII:C activity, F XII, plasminogen (Plg), antiplasmin (AP), antithrombin (AT), kallikrein inhibiting activity (KI) and spontaneous proteolytic activity (SPA): study the effects of cryoprecipitate or plasma infusion on three variables. Samples were taken before the first infusion, and 24 and 48 h after. At onset, high levels (p less than .001 when compared to blood donors) of Fg, VIIIR:Ag and VIII:C were seen. KI levels were within the normal range. F V was low (p less than .05). Fn, NT, XII, Plg, AP and AT were markedly low (p less than .001). SPA showed great variation. When compared to 28 patients with severe infections, but not in septic shock, the ICU group had higher VIIIR:Ag (p less than .05) and VIII:C (p less than .01), and lower XII, Plg, AP and AT (p less than .001). FDP was elevated in all ICU patients. Five patients were thrombocytopenic, and in these a pattern with low levels of Plg and AT was observed. Fn did not correlate well to the other variables measured. These results indicate a marked activation of coagulation and fibrinolysis in these severely ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibronectin and other DIC-related variables in septic ICU patients receiving cryoprecipitate. 393 20

The purpose of this study is to elucidate the pathophysiology of the acute pancreatitis and set up the criteria for assessing the severity of this disease. One hundred and fifty seven cases of acute pancreatitis were treated at the First Surgical Department of Tokyo University Hospital and its affiliated hospitals. They consisted of 24 severe cases, 76 moderate cases, and 57 mild cases according to our classification. In early stage ten parameters, namely, abnormalities of white cell count, platelet count, hematocrit, lactic acid dehydrogenase, blood urea nitrogen, serum calcium, base excess, PaCO2 and fasting blood glucose and age within 24 hours after admission and X-ray CT scan within 48 hours as early prognostic signs, enabled us to predict severe, moderate, or mild pancreatitis. More than 4 weeks later than the onset of acute pancreatitis, X-ray CT scan, white blood cell count, elevation of serum FDP level, endotoxemia and fall of plasma opsonic index served as good indicators to evaluate the severity of abdominal sepsis. In experimental pancreatitis, CH50 and opsonic index were remarkably decreased at 6 and 12 hours after induction of acute pancreatitis. As the above results, determination of early prognostic signs immediately after onset and late prognostic signs 3-4 weeks after onset is very important to evaluate and manage the acute pancreatitis patients.
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PMID:[Pathophysiology and prognosis of acute pancreatitis--early and late prognostic signs]. 408 48

Acute respiratory failure is a common complication in patients with disseminated intravascular coagulation associated with sepsis. To elucidate the role of coagulation abnormalities in acute lung injury in sepsis, we investigated the effect of anticoagulants on the pulmonary vascular injury in rat induced by lipopolysaccharide (LPS). When administered intravenously, LPS (5 mg/kg body weight) significantly increased the accumulation of 111indium-labeled neutrophils in lung 30 min after administration. Subsequently, the pulmonary vascular permeability and the serum level of fibrin and fibrinogen degradation products (E) [FDP (E)] increased and remained elevated for several hours. Neither heparin alone, heparin plus antithrombin III, or dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa, a selective inhibitor of thrombin generation, prevented LPS-induced vascular injury 6 hours after LPS administration, whereas these substances significantly inhibited the increase in serum FDP (E) at that time. LPS-induced pulmonary vascular injury was significantly attenuated in rats with methotrexate-induced leukocytopenia or treated with ONO-5046, a potent granulocyte elastase inhibitor, although ONO-5046 did not inhibit the LPS-induced increase in serum FDP (E). Thus, activated leukocytes play a more important role than coagulation abnormalities in the pathogenesis of LPS-induced pulmonary vascular injury in an experimental rat model of endotoxemia.
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PMID:Endotoxin-induced pulmonary vascular injury is mainly mediated by activated neutrophils in rats. 748 29

Disseminated intravascular coagulation (DIC) is characterized by extreme activation of intravascular coagulation, and clinical manifestations such as bleeding and/or multiple organ failure is sometimes observed in advanced cases of DIC. The balance of coagulation and fibrinolysis activation varies according to the underlying diseases of DIC. DIC cases are classified as the type with predominant coagulation activation and the type with predominant fibrinolysis activation in former type plasma levels of thrombin-antithrombin III complex (TAT) are greatly increased, and those of plasmin-alpha 2 plasmin inhibitor complex (PIC) are slightly increased. In addition plasma levels of plasminogen activator inhibitor 1 (PA1) are greatly increased, multiple organ failure is a major clinical manifestation in advanced cases and sepsis is a representative underlying disease. In the second type both plasma levels of TAT and PIC are greatly increased, plasma levels of PA1 are almost within normal limits. Bleeding is a major clinical manifestation in advanced cases and acute promyelocytic leukemia (APL) is a representative underlying disease. The classification of DIC should be considered when choosing treatment with DIC. Diagnosis of pre-DIC status is based on gradually decreasing platelets counts in sepsis and on mild elevation of FDP and D dimer in APL, leukemia and cancer.
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PMID:[Classification and treatment of DIC]. 778 36

A 26-year-old male who had been diagnosed as pulmonary tuberculosis three years ago with an antituberculous chemotherapy of only two months, complained of tiredness, exertional dyspnea and fever since a month ago. Bloody sputum, bloody stool and hematuria have developed three days before admission. Petechiae over the body trunk and lower extremities were observed on admission. Peripheral blood examination revealed lymphocytopenia (672/microliters), low hemoglobin content (6.2 g/dl), thrombocytopenia (3,000/microliters), elevated FDP (36.2 micrograms/ml) and D-dimer (25.0 micrograms/ml) values. Chest radiograph showed a massive pleural effusion in the right hemithorax, bilateral pulmonary infiltrates and a cavity on CT scan. Together with positive acid-fast bacilli in sputum, diagnoses of relapsed pulmonary tuberculosis, tuberculous pleurisy associated with DIC (disseminated intravascular coagulation) were made. Left hydronephrosis which was presumed to be a consequence of infundibulum stenosis due to renal tuberculosis, was detected by abdominal ultrasonography. Treatment with antituberculous drugs and protease inhibitors were started with thoracic tube drainage. DIC condition was improved by the 20th hospital day and sputum culture turned to be negative after the 4th week, however, fever up to 38 degrees C continued until the end of the 7th week and a D-dimer which is a representative marker for secondary fibrinolysis, continuously showed a high level up to the 10th week of hospitalization. The patient was uneventful during the three months follow up period after discharge. DIC is a well known complication of sepsis including miliary tuberculosis, whereas it is rarely associated with cavitary tuberculosis and no case of prolonged elevation of D-dimer have been reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of pulmonary, pleural, and renal tuberculosis associated with DIC and a prolonged increase in D-dimer]. 804 Oct 60

We measured various coagulable factors and molecular markers in plasma and serum in the disease group including DIC, DIC suspect, thrombosis, acute myocardial infarction, angina pectoris, sepsis, malignant tumor and type II diabetes and the healthy subject group, and surmised the intravascular coagulative-fibrinolytic activity in each disease group compared with the healthy group. Additionally we selected parameters useful for early detection of the pre-thrombotic state and hypercoagulable state. As a result, of the parameters for the coagulative system, those considered useful were the assay of soluble fibrin monomer complexes using the synthetic substrate (FM.Oita), assay of soluble fibrin monomer complexes using HPLC(SFMC.Oita) and thrombin-anti-thrombin III complex (TAT) in this order. Of the parameters for the fibrinolytic system, those considered useful were FDP assay using ELISA (FDP.Oita) and plasmin-alpha 2 plasmin inhibitor complex (PIC). This FDP.Oita had a considerably high detection sensitivity compared with the FDP assay (Diayatron Co.) using the latex photometric immunoassay which has been commercially available. When measurement was made with plasma and serum in the subject disease group as the sample by the high sensitivity assays mentioned above, it was made clear that both the coagulative activity and fibrinolytic activity are increased, albeit with some differences in intensity, in all the disease groups compared with the healthy group. In order for the hypercoagulable state and pre-thrombotic state to be detected, it is important to know the balance between the coagulative activity and fibrinolytic activity. According to the results of the present experiment, a significant directly proportional correlation was recognized between FM.Oita and FDP.Oita and between TAT and FDP.Oita. Therefore, examination of these ratios will be a more detailed indicator of coagulative-fibrinolytic activity than the TAT/PIC ratio, PAI-1/TPA ratio and ATIII/alpha 2 PI ratio hitherto in use. If useful molecular markers such as FM.Oita are measured over time in various cases and these data are compiled and analyzed statistically, it will not be long before the criteria for the hypercoagulable state and pre-thrombotic state are established.
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PMID:[Molecular marker for detecting hypercoagulable state]. 810 79


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