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)

In newborn infants, the influence of gestational age (GA), postnatal age (PA), and health status on the plasma protease inhibitors alpha 2-macroglobulin (alpha 2-M), alpha 1-antitrypsin (alpha 1-AT), C1 esterase inhibitor (C1E-INH), alpha 2-antiplasmin (alpha 2-AP), and antithrombin III (AT-III) was investigated. Inhibitor levels were measured by radial-immunodiffusion and expressed as a percentage of pooled plasma from adults (mean +/- SEM). In total, 54 premature infants (28-36 weeks gestation) were classified at birth as healthy (N = 22) (IV fluids, antibiotics only) or sick (N = 32) (all other support, but excluding infants with disseminated intravascular coagulation (DIC] and studied on Days 1 and/or 7 of life. Healthy term infants (N = 18) and infants with DIC (N = 10) were studied on Day 1 only. All inhibitors except C1E-INH increased with increasing gestational age (P less than 0.01). In healthy premature infants all inhibitor levels reached the normal adult range by 1 week of age. In contrast, at 1 week of age, sick infants had lower levels of alpha 2-M and alpha 2-AP, and higher levels of alpha 1-AT compared to healthy infants (P less than 0.01). The presence of DIC depressed all of the inhibitors on Day 1 except alpha 1-AT when compared to healthy controls (P less than 0.01). Thus, gestational age, postnatal age, and health status all significantly influenced the levels of these plasma protease inhibitors.
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PMID:Plasma protease inhibitors in premature infants: influence of gestational age, postnatal age, and health status. 619 32

An enzyme-linked immunosorbent assay (ELISA) has been developed for the quantification of alpha 1-antitrypsin-human leukocyte elastase (alpha 1AT-E) complexes. In the ELISA, the alpha 1AT-E complex is bound to a surface by rabbit antileukocyte elastase antibody, and the inhibitor-proteinase complex is quantified by a second antibody, rabbit anti-alpha 1-antitrypsin F(ab')2, labeled with alkaline phosphatase. alpha 1AT-E complexes were detected when a final concentration of 2.2 nmol/liter of leukocyte elastase was added to plasma. The concentration of these complexes increased with additional elastase. In clotting blood, alpha 1AT-E complexes were generated in parallel with the conversion of 125I-fibrinogen to fibrin, whereas alpha 2-plasmin inhibitor-plasmin (alpha 2PI-P) complexes were not formed. The concentration of alpha 1AT-E complexes in 19 of 21 controls was less than 2.2 nmol/liter. Patients with laboratory evidence for disseminated intravascular coagulation (DIC) demonstrated elevated alpha 2PI-P complexes with either increased or normal concentrations of alpha 1AT-E complexes. Patients without evidence for DIC, but who demonstrated prolonged reptilase clotting times, were studied. This group had increased alpha 1AT-E but normal alpha 2PI-P complex levels, raising the possibility that elastase release in vivo may be accompanied by limited degradation of fibrinogen. These assays thus serve as useful probes for the study of leukocyte activation and of the interactions between cellular and plasma proteolytic enzyme systems.
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PMID:Alpha-1-antitrypsin-human leukocyte elastase complexes in blood: quantification by an enzyme-linked differential antibody immunosorbent assay and comparison with alpha-2-plasmin inhibitor-plasmin complexes. 621 25

Activation and inactivation of protein C during the clinical course of disseminated intravascular coagulation (DIC) was studied in three patients by qualitative (Western blotting) and quantitative (ELISA) analysis and the intensity of procoagulant activity monitored by the measurement of thrombin and factor Xa antithrombin III complexes. In one patient, inhibitor complexes of APC with protein C inhibitor (PCI) and alpha 1-antitrypsin (alpha 1-AT) were observed and the latter predominated at presentation. Both disappeared during the development of remission but the loss of alpha 1-AT complexes preceded PCI complexes which on Western blotting appeared to increase in intensity prior to disappearance. The two other patients bled to death from uncontrollable haemorrhage. In both cases, APC/inhibitor complexes with alpha 2-macroglobulin (alpha 2-M) in addition to PCI and alpha 1-AT were detected and persisted until death. Although PCI appeared to be the primary inhibitor in all three cases, alpha 1-antitrypsin and particularly alpha 2-macroglobulin appeared to assume greater roles in the two fatal cases. These data are similar to previous findings in an experimental animal model of DIC that suggested that alpha 2-macroglobulin and alpha 1-antitrypsin become more important inhibitors of APC as the primary inhibitor PCI is consumed in the face of a sustained procoagulant challenge.
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PMID:Activation of protein C and its distribution between its inhibitors, protein C inhibitor, alpha 1-antitrypsin and alpha 2-macroglobulin, in patients with disseminated intravascular coagulation. 768 92

C1-inhibitor (C1Inh), antithrombin III (ATIII), alpha 1-antitrypsin (a1AT), and alpha 2-antiplasmin (a2AP) are known inhibitors of factor XIa (FXIa). However, their precise contribution to FXIa inactivation in vivo is not known. We investigated FXIa inactivation in chimpanzees and assessed the contribution of these inhibitors to FXIa inactivation in patients with presumed FXI activation. Chimpanzees were infused with FXIa and the various FXIa-FXIa inhibitor complexes formed were measured. Most of FXIa was complexed to C1Inh (68%), followed by a2AP (13%), a1AT (10%), and ATIII (9%). Analysis of the plasma elimination kinetics revealed a half-life time of clearance (t1/2) for the FXIa-FXIa inhibitor complexes of 95 to 104 min, except for FXIa-a1AT, which had a t1/2 of 349 min. Due to this long t1/2, FXIa-a1AT complexes were predicted to show the highest levels in plasma samples from patients with activation of FXI. This was indeed shown in patients with disseminated intravascular coagulation, recent myocardial infarction or unstable angina pectoris. We conclude from this study that in vivo C1Inh is the predominant inhibitor of FXIa, but that FXIa-a1AT complexes due to their relatively long t 1/2 may be the best parameter to assess FXI activation in clinical samples.
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PMID:Inactivation of factor Xia in vivo: studies in chimpanzees and in humans. 890 95

The effects of experimental infection of calves with Sarcocystis cruzi on the blood coagulation cascade were investigated. Calves were inoculated orally with 1 x 10(5) sporocysts (group S1, n = 6) or with 5 x 10(5) sporocysts of S. cruzi (group S2, n = 3). A group of eight calves served as non-infected controls (group C). The animals were bled once during the first 4 weeks of infection and twice a week thereafter until day 40 p.i. The following parameters were measured: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time, thrombin coagulase time, factors XII, XI, X, IX, VIII:C, VII, V, prekallikrein, fibrinogen, alpha 2-antiplasmin, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin, haematocrit, haemoglobin, numbers of erythrocytes and thrombocytes. The infected calves developed acute sarcocystiosis from 25 (S1) or 29 (S2) days p.i. onwards. During the acute disease, antiproteases tended to elevated values and thrombocyte counts were generally reduced. In group S1 prolonged prothrombin time and reduced activities of factors VII or V were found. In group S2 accelerated prothrombin time and activated partial thromboplastin time, as well as elevated factor X activities, were recorded even before the onset of clinical disease at 19 days p.i. While prothrombin time returned to normal levels thereafter, activated partial thromboplastin time remained short. Activities of factor V, factor VII and factor X were significantly reduced in group S2 at the onset of acute sarcocystiosis, and one of the three calves died at 29 days p.i. The other parameters were not significantly affected by either dose of infection. No evidence for a classical disseminated intravascular coagulation syndrome could be found; however, it was demonstrated that S. cruzi alters plasma coagulation in a dose-dependent way.
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PMID:Blood clotting disorders during experimental sarcocystiosis in calves. 976 63


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