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)

The therapeutic effect of highly purified protein C (PC) or activated protein C (APC) on three patients with disseminated intravascular coagulation (DIC) was tested. In two out of three cases, although therapeutic dose of heparin was not effective, PC or APC administration significantly improved the hypercoagulable state. In one case with acute leukemia who developed DIC with the severe gastrointestinal bleeding, APC corrected the hypercoagulable state without aggravating bleeding. These findings suggested that PC and/or APC might be effective in correcting hypercoagulable state without any adverse effect.
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PMID:Treatment of patients with disseminated intravascular coagulation by protein C. 231 13

The coagulation inhibitors are important components of control mechanisms which ensure the haemocoagulation equilibrium. One of them is protein C, whose level was followed in patients with DIC. and IM. In DIC. cases a significant decrease was noted with regard to the MI groups and healthy donors. EID and ELISA methods were used for testing. The patients exhibiting the protein C defect require a corresponding treatment which should suppress the thromboembolic complications.
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PMID:Clinical significance of protein C. 246 13

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

Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI-1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.
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PMID:Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation. 252

Heparin cofactor II (HC II) was measured by a chromogenic activity assay in normal preterm infants (gestational age, 28-36 weeks; n = 17; 29% +/- 11.5 [mean +/- 1 SD], range 11-51), normal full-term infants (n = 18; 49% +/- 6.6 [mean +/- 1 SD], range 36-58), and normal adults (n = 38; 101% +/- 14 [mean +/- 1 SD], range 73-130). Normal children attained adult levels at approximately 5 to 7 months of age. The lower values in preterm and term infants most likely reflect immature liver function. Neither adults and children with a history of thrombosis with prior negative evaluation (n = 74), patients with documented protein C and protein S deficiency (n = 4), nor sick infants without evidence of consumptive coagulopathy (n = 15) had significantly lower levels of HC II activity. Infants with disseminated intravascular coagulation (n = 2) had strikingly lower levels of HC II activity.
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PMID:Heparin cofactor II in adults and infants with thrombosis and DIC. 252 33

Plasma levels of protein S (PS) antigen, both total and free fractions, were measured together with C4b-binding protein (C4bp) and protein C (PC) antigen in 39 patients with disseminated intravascular coagulation (DIC), 34 with liver disease, 17 with collagen disease, 17 with diabetes mellitus, and 51 under stabilized warfarin treatment. In patients with DIC, mean concentrations of total PS and free PS were normal, while PC was reduced and C4bp were elevated. Total PS, free PS, C4bp and PC were all decreased in liver disease, elevated in diabetes mellitus, and normal in collagen disease. In warfarin-treated patients, total PS, free PS and PC were moderately decreased, but the decrease in C4bp was minimal. The concentration of PS correlated positively with PC in liver disease, diabetes mellitus, and during oral anticoagulation, but did not in DIC. These results indicate that PS and PC behave similarly when liver synthetic function is principally affected, but in contrast to PC, PS is hardly consumed during intravascular coagulation.
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PMID:Plasma protein S in disseminated intravascular coagulation, liver disease, collagen disease, diabetes mellitus, and under oral anticoagulant therapy. 252 31

Two unrelated families are described, of which four adult members were found to be suffering from severe protein C deficiency (less than or equal to 5% of normal plasma level). Newborn deaths were reported in the first family but the second family had no history of neonatal purpura fulminans and infant death. Thrombotic symptoms developed mainly in their early twenties, consisting chiefly of recurrent superficial and deep iliofemoral vein thromboses and pulmonary emboli. Other clinical features included generalized peritonitis due to massive mesenteric vein thrombosis, thrombosis of the cavernus sinus, renal vein thrombosis and priapism. In the second family, five members (all aged approximately 40 years) died of intravascular abdominal thrombosis. Massive thromboembolic episodes were associated with a compensated disseminated intravascular coagulation syndrome as evidenced by high concentrations of D-dimer (mean levels 5000 ng/ml plasma) and by a moderate reduction in platelet count and fibrinogen concentrations. D-dimer levels in noncrisis periods were also raised above normal (mean levels 400 ng/ml). The thrombotic problems of these patients were controlled satisfactorily by long-term administration of low molecular weight heparin alone or in combination with low dose warfarin.
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PMID:Congenital severe protein C deficiency in adults. 254 23

Enzyme-linked immunosorbent assays (ELISA's) were developed for the measurement of protein C inhibitor (PCI) antigen and activity and for its complexes with activated protein C (APC) in plasma. For PCI activity and antigen, APC or anti-PCI, respectively, was immobilized to microtiter plates and PCI bound was detected with labelled anti-PCI antibodies. For APC:PCI complexes, two different antibodies directed against protein C and PCI were used. The assays for PCI were calibrated with pooled normal human plasma (NHP) and with purified PCI, and for APC:PCI complexes with known concentrations of purified pre-formed complexes added to buffer or to plasma. The lower limit of sensitivity of the PCI activity and antigen assays was 10 ng/ml and 0.5 ng/ml, respectively and for plasma APC:PCI complexes 12 ng/ml. Mean coefficients of variation of 1.5% to 5.8% (intra-assay) and 2.1% to 9.8% (inter-assay) were found for the assays. For PCI antigen, a range of 56% to 162% of the NHP value was obtained in samples from 70 healthy donors (mean +/- SD = 98.6% +/- 23.1%). For PCI activity, the range was 59% to 148% (94.3% +/- 20.2). A good correlation (0.92) was obtained when both assays were compared. Plasma levels of APC:PCI complexes in 30 normals were under the detection limit (less than 12 ng/ml). In plasma samples from 10 patients with disseminated intravascular coagulation (DIC) PCI antigen concentrations were decreased (55.6% +/- 20%) and 8 of the patients had APC-PCI complex levels between 32 and 240 ng/ml (median, 35 ng/ml). After addition of 20 micrograms/ml APC to NHP or to protein C depleted plasma, 6.1 micrograms/ml complexes were recovered after 90 min incubation. Incubation of 10 micrograms/ml APC with NHP in the presence of 10 U/ml heparin yielded 11 micrograms/ml complexes after 90 min, which represent more than 90% of the maximum possible value. Thus, the method should be adequate to study complexes of APC in vivo in clinical conditions in which activation of protein C pathway may occur.
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PMID:Determination of functional and antigenic protein C inhibitor and its complexes with activated protein C in plasma by ELISA's. 255 Oct 66

We performed a blood coagulation study during the course of disseminated intravascular coagulation (DIC) in 34 patients with hematological malignancies. Risk factors of DIC such as increasing tumor mass, anti-tumor therapy and severe infections were frequently observed at onset of DIC, and influenced the prognosis of DIC. Before the onset of DIC, the DIC score and FDP value were slightly elevated, and they were significantly increased after the onset of DIC. Before the onset of DIC, the level of fibrinogen was significantly increased but it was decreased after the onset of DIC. These hemostatic abnormalities continued for about 2 weeks. Patients with DIC showing prolonged APTT and PT had a poor prognosis. The abnormalities of PT, FDP, fibrinogen, DIC score, FDP-D-dimer and fibrinopeptide A were significantly greater in DIC than in Pre-DIC defined as the period one week before the onset of DIC. FDP-D-dimer was also higher in Pre-DIC patients than in those without DIC. Although protein S and C 4 b binding protein were not decreased in DIC or Pre-DIC, Protein C activity decreased during the course of DIC, suggesting that FDP-D-dimer and Protein C activity were useful for diagnosis of Pre-DIC and DIC.
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PMID:[Hemostatic changes before and after the onset of disseminated intravascular coagulation]. 259 41


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