Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma fibronectin was assayed in 179 hospitalized patients referred for workup of possible acquired coagulopathy. Based on laboratory results and chart review, these patients were classified as having no coagulopathy (N = 36), defibrination syndrome (N = 31), compensated defibrination syndrome (N = 100), microangiopathic thrombocytopenia (N = 7), and primary fibrinolysis (N = 5). Compared to patients with no coagulopathy, fibronectin concentration was reduced in patients with defibrination syndrome (p less than 0.005) and compensated defibrination syndrome (p less than 0.10). Fibronectin concentration was not reduced in patients with microangiopathic thrombocytopenia and primary fibrinolysis. In patients with defibrination syndrome, the reduction of fibronectin was correlated to the degree of liver impairment. This finding is consistent with the liver being the primary site of synthesis of plasma fibronectin. Fibronectin was significantly correlated to plasminogen and antithrombin III. The sensitivity of fibronectin for the diagnosis of coagulopathy is low except for patients with defibrination syndrome.
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PMID:Plasma fibronectin concentration in patients with acquired consumptive coagulopathies. 652 49

Plasma fibronectin levels in 66 medical ICU (MICU) patients were measured daily. Mean values of initial levels were significantly higher in survivors (266 +/- 14 mg/L) than nonsurvivors (179 +/- 13 mg/L; p less than .0003). There was extensive overlap between survivors and nonsurvivors. The clinical categories of sepsis, disseminated intravascular coagulation (DIC), adult respiratory distress syndrome (ARDS), and hepatic failure with GI bleeding were associated with low fibronectin levels. Within all diagnostic categories the mean initial fibronectin level of the survivors was higher than that of nonsurvivors. This difference was significant only in the septic group (p less than .02). Patients with minimum fibronectin levels less than 195 mg/L had a 65% mortality rate; patients with minimum levels greater than or equal to 195 mg/L had a 17% mortality rate. Fibronectin, via its role in reticuloendothelial system (RES) function, may have a pathophysiologic role in a variety of medical illnesses.
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PMID:Plasma fibronectin in medical ICU patients. 672 31

The plasma fibronectin level was determined by immunoelectrophoresis in patients under intensive care. The decrease in plasma fibronectin concentration was most pronounced in patients with sepsis and DIC. Survival of these patients was related to the extent of decrease of the plasma fibronectin concentration. Burn injury and the associated surgical treatment were followed by a decrease in fibronectin concentration which then normalized in 24-48 h after the burn injury. It is concluded that serial determinations of plasma fibronectin are essential for studying the relation of a low plasma fibronectin with the clinical condition.
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PMID:Plasma fibronectin concentration in patients admitted to intensive care unit. 672 57

Plasma fibronectin is a nonspecific opsonin which mediates phagocytosis of particulate matter by macrophages. Fibronectin depletion results in depression of reticuloendothelial system phagocytic function. This may potentiate microvascular embolization and sludging in critical illness. It has been hypothesized that sepsis is a major cause of fibronectin depletion. To explore this hypothesis, plasma fibronectin concentrations were measured in rats with intraabdominal abscesses and in rabbits subjected to the generalized Shwartzman reaction (spaced doses of endotoxin). In both groups of animals there was a significant increase (P less than 0.05) rather than decrease in fibronectin concentrations at times when sepsis and disseminated intravascular coagulation were manifest. This study does not support the hypothesized relationship between sepsis and fibronectin depletion. Until the kinetics of fibronectin production and utilization are further delineated, caution must be exercised in the interpretation of immunoreactive plasma fibronectin levels.
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PMID:Plasma fibronectin concentration in animal models of sepsis and endotoxemia. 682 8

Plasma fibronectin (FN) binds fibrin in vitro by both noncovalent and covalent bonds and is decreased in DIC. In rabbits, conventionally purified 125I-FN had a complex blood clearance with a late t1/2 of 71 hr. A large portion was apparently altered, as evinced by rapid clearance and an intravascular/total body ratio (C1) of 0.28-0.51. 3H-labeled FN, made in vivo by injection of 3H amino acids, had a t1/2 of 73 hr. Crosstransfusion of 131I-FN and 3H-FN into a second set of animals gave similar t1/2s and C1s of 0.74-0.82, indicating the altered 125I-FN was biologically screened in the first animals. Other animals were given 125I-fibrinogen and "screened" 131I-FN. Intravenous thrombin (50-60 U/kg/1 hr) caused a 25%-50% decrease in both 125I-fibrinogen and 131I-FN. Ancrod injection reduced fibrinogen by greater than 90% but had no effect on 131I-FN. 131I-FN levels did not change when thrombin was given after ancrod. No cross-linked FN-fibrinogen alpha-chain was found in the plasma, nor was the thrombin-induced fall in FN affected by spermidine blockade. These experiments demonstrate that FN and fibrin bind in vivo during defibrination and are rapidly cleared from the blood. The abnormal fibrin resulting from ancrod either does not bind FN in vivo or does so reversibly.
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PMID:Fibronectin: blood turnover in normal animals and during intravascular coagulation. 710 86

Plasma fibronectin was determined in 121 normal adults and in 149 patients. Fibronectin levels in normals were strongly influenced by sex and age. The mean value of the protein in cancer patients did not differ from that in normal controls; however, patients with cryofibrinogenaemia or extensive liver metastases had lower values whereas those with obstructive jaundice due to pancreatic carcinoma had higher values than normal controls. Fibronectin levels were greatly increased in patients with primary biliary cirrhosis and moderately elevated in nephrotic syndrome. In patients with severe infection or sepsis, plasma fibronectin did not show a consistent pattern. Patients with overt disseminated intravascular coagulation, irrespective of its cause, had the lowest plasma fibronectin concentrations.
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PMID:Plasma fibronectin in normal subjects and in various disease states. 725 92

Previous research has shown that disseminated intravascular coagulation causes a depression in RE function. Fibronectin, a high-molecular-weight surface-binding glycoprotein, is known to modulate RE function by facilitating opsonic activity and is sensitive to proteolytic cleavage by plasmin, yielding FNDP. The present investigation suggests that isolated FNDP, generated in vitro by incubation with plasmin, can depress phagocytosis in vivo as well as in vitro. Phagocytosis in rats was determined by a clearance technique employing CR51-RBCs and in vitro by employing a monolayer of peritoneal exudate macrophages. The in vivo studies demonstrated significantly reduced hepatic phagocytosis after the injection of FNDP an delayed clearance of injected test particles. Macrophage uptake in vitro, supported by either normal rat serum or purified fibronectin, was significantly reduced when incubated with FNDP. These results suggest that depression of the RE system and phagocytosis during intravascular coagulation may be mediated in part by the formation of plasmin degradation products of plasma fibronectin.
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PMID:Depression of phagocytosis by plasmin degradation products of plasma fibronectin. 725 34

The concentration of blood fibronectin and the state of the phagocytic function in the liver was studied in 19 patients with an emergency pathology of the abdominal cavity complicated by the infective-toxin shock and polyorganic insufficiency. Patients with severe abdominal pathology had a considerably decreased level of circulating fibronectin, disturbed phagocytic function of the liver and development of the hypercatabolic state. Hypofibronectinemia was accompanied by polyorganic disorders, systemic bacteriotoxemia and disseminated intravascular coagulation. Causes of hypofibronectinemia and its role in pathogenesis of systemic complications in patients with emergency abdominal pathology are discussed.
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PMID:[Blood fibronectin and liver phagocytic function in peritonitis patients]. 779 81

Postmyocardial infarction patients on hospital rehabilitation in case of no complications were examined for time course changes in the levels of fibrinogen degradation products (FDP), free hemoglobin (fHg) and fibronectin (Fn) using enzyme immunoassay. As shown by FDP and fHg values, the patients had DIC syndrome with its maximum on observation days 6-12 and 22-24. Fn fall occurred on the disease day 2-4 preceding maximum hemostasis activation up to 6-12th day. Less marked Fn reduction on the disease day 15-17 predicted a rise in hemocoagulation on day 22-24. It is recommended to determine FDP, fHg and Fn levels in blood of postmyocardial infarction patients to detect DIC syndrome and prevent hemostasis activation.
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PMID:[The detection of preventive hypofibronectinemia in diagnosing the development of disseminated intravascular coagulation in patients with myocardial infarction at the hospital rehabilitation stage]. 830 87

Some platelet alpha-granule contents were assessed in parallel with other markers of hemostatic imbalance in 50 patients with hepatosplenic schistosomiasis (15 patients with compensated hepatosplenomegaly, 15 patients with advanced hepatic fibrosis and ascites and 20 patients during an acute attack of hematemesis from ruptured esophageal varices). Platelet factor 4 (PF4), beta-thromboglobulin (beta-TG), fibronectin (FN), prothrombin fragment 1 + 2, thrombin-antithrombin (TAT) complexes, fibrin degradation products (FbDP) and D-dimer were assessed in schistosomal patients compared to controls (15 healthy subjects). A significant increase in both thrombin (high TAT and prothrombin fragment 1 + 2 levels) and plasmin (high FbDP and D-dimer levels) generation was detected in decompensated patients establishing the presence of a steady state of low-grade disseminated intravascular coagulation, with and without overt bleeding, in these patients. A decrease in plasma FN concentration was found in diseased groups compared to controls. The reduction in plasma levels of FN paralleled the defective liver function and matched the relative decrease in tissue FN in liver specimens of decompensated patients suggesting that FN levels can be used to evaluate the pathological staging of the disease. A significant increase in beta-TG and PF4 levels was noted in decompensated patients with ascites and/or acute hematemesis compared both to controls and compensated patients reflecting platelet alpha-granule release and consequently increased in vivo platelet activation which may initiate and/or perpetuate the pathophysiological mechanisms of the hemostatic imbalance underlying the hemorrhagic diathesis in hepatosplenic schistosomiasis.
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PMID:Fibronectin, platelet factor 4 and beta-thromboglobulin in endemic hepatosplenic schistosomiasis: relation to acute hematemesis. 909 85


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