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

A radioimmunoassay for fibrinopeptide A (FPA) has been developed. This assay uses rabbit antibodies induced by injection of native FPA-human serum albumin conjugates and 125I introduced into tyrosine-FPA synthesized in out laboratory. Plasma FPA is separated from fibrinogen by TCA extraction. The assay is capable of detecting as little as 50 pg/ml of FPA. In 20 normal donors this assay revealed a mean concentration of 0.9 ng/ml (0.3 SD). In five patients with disseminated intravascular coagulation, FPA concentrations ranged from 13.0 to 346 ng/ml. Two groups of patients with systemic lupus erythematosus (SLE) whose disease had achieved complete remission were studied; one consisted of four patients with no history of lupus nephritis and another with a history of nephritis. Mean FPA concentrations of 1.5 ng/ml (range, 0.7-1.8 ng/ml) and 2.7 ng/ml (range, 1.1-5.6 ng/ml) were found in these two groups, respectively. Another group of nine patients with active SLE, but without evidence of lupus nephritis, had a mean FPA concentration of 4.5 ng/ml (range, 2.4-7.8 ng/ml). Finally, a group of seven patients with active SLE, including active nephritis, had a mean FPA concentration of 10.2 ng/ml (range, 5.3-17.0 ng/ml). A positive correlation was found between the concentration of plasma FPA and serum DNA-binding activity and an inverse correlation was found between plasma FPA and the concentration of serum C3. No correlation existed between plasma FPA and concentration of serum creatinine. Several possibilities for the origin of plasma FPA in patients with SLE were considered; at present it seems most likely that FPA arises through the action of thrombin on fibrinogen.
 ...
PMID:Fibrinopeptide A in plasma of normal subjects and patients with disseminated intravascular coagulation and systemic lupus erythematosus. 93 2

To estimate the degree of coagulopathy in abdominal sepsis, we measured the plasma levels of prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PIC) by the enzyme-linked immunosorbent assay in 38 patients with disseminated intravascular coagulation (DIC). In 20 patients with DIC due to abdominal sepsis, plasma levels of F1 + 2, TAT and PIC were 2.6 nmol/l, 27.9 micrograms/l and 1.5 micrograms/ml, respectively, with a mean antithrombin III (AT III) activity of 41.7%. F1 + 2, TAT, PIC and AT III levels were 4.7 nmol/l, 75.8 micrograms/l, 8.8 micrograms/ml and 70.9% in 18 patients with DIC as the result of malignancy. Though AT III levels in DIC due to sepsis were lower than those in DIC due to malignancy, the levels of F1 + 2, TAT and PIC in the former were not significantly more increased than those in the latter. The plasma levels of F1 + 2 were positively correlated with TAT and PIC in DIC patients with malignancy; however, there was no correlation between F1 + 2 and TAT or PIC in DIC patients with sepsis. In addition, the levels of serum albumin in the two groups were similar. These results suggest that activation of coagulation and fibrinolytic systems may not be so prominent in cases of DIC due to abdominal sepsis, compared to related events in DIC due to malignancy. It is also suggested that the depletion of AT III in cases of sepsis is not only caused by a consumption related to intravascular coagulation or to an alternate distribution of protein.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Coagulopathy in disseminated intravascular coagulation due to abdominal sepsis: determination of prothrombin fragment 1 + 2 and other markers. 138 63

The pathogenesis of disseminated intravascular coagulation (DIC) in the early stage after burn injury remains still unclear. We investigated 12 burn injured patients by serial determination of anti-thrombin III (AT-III) activities and thrombin-antithrombin III complex (TAT) levels. Of these patients 4 developed DIC (DIC group) and the others had no hematological complications (non-DIC group). The mean levels of TAT increased markedly and peaked at 6 hr; the increment being more pronounced in DIC group (p less than 0.001). A significant correlation was recognized between TAT and Burn Index (r = 0.871, p less than 0.001). We also observed low AT-III activities those inversely related to Burn Index (r = 0.875, p less than 0.001), whereas closely correlated with serum albumin levels (r = 0.864, p less than 0.001), suggesting that this depression might be caused by both massive infusion and shifts of plasma into the extravascular space rather than consumption. These findings suggest that massive thrombin generation and decrease of anticoagulant activity, correlated to the severity of burns, might concurrently develop. Non-DIC group may remain to latent activation of coagulation cascade where anticoagulants could inactivate thrombin generated. This compensatory mechanism may fail in severe burn patients who have Burn Index of more than 90, developing DIC with high levels of TAT (316.3 +/- 104.5 ng/ml) and low AT-III activities (19.5 +/- 8.7%).
 ...
PMID:[Disseminated intravascular coagulation in the early stage after severe burn: the role of excessive thrombin generation]. 194 44

Systematic clotting studies were performed in 157 patients with de novo acute nonlymphoblastic leukemia (ANLL) prior to treatment. Sixteen patients had disseminated intravascular coagulation (DIC). Three of the patients with DIC (two with M3, one with M5 leukemia) had a marked isolated factor-X deficiency (factor X:C 21%, 33%, and 41%, respectively). Another four patients had a mild isolated factor-X deficiency (factor X:C 55%-68%). In these seven patients the remaining liver-synthesized clotting factors (factors II, VII, IX, V) as well as serum albumin and cholinesterase were within the normal range. Liver disease or vitamin-K deficiency could therefore be excluded. In none of the 141 patients without DIC was a marked isolated factor X deficiency observed; two patients had moderately reduced factor X:C levels but normal liver-synthesized proteins. Induction treatment led to the control of DIC with an almost parallel increase of fibrinogen and factor X up to normal in all patients with factor-X deficiency who achieved complete remission. In one patient, recurrence of leukemia was associated with reoccurrence of DIC and marked factor-X deficiency. We conclude that there is a coincidence of isolated factor-X deficiency and DIC in some patients with ANLL. In some patients, this factor-X deficiency may be severe enough to contribute to the bleeding tendency.
 ...
PMID:Coincidence of acquired factor-X deficiency and disseminated intravascular coagulation in patients with acute nonlymphoblastic leukemia. 204 64

Measurements of the principal protease inhibitors were carried out in patients with two types of chronic liver disease: alcoholic cirrhosis and primary biliary cirrhosis. Measurement of the two major protease inhibitors operative in the haemostatic mechanism--that is, antithrombin III and alpha 2-antiplasmin--showed significantly reduced levels in the alcoholic cirrhosis group, who satisfied clinical and biochemical criteria of impaired hepatocellular function, but not in the primary biliary cirrhosis group, who had relatively good preservation of hepatocellular function. Significant correlation of levels of both these major protease inhibitors with the serum albumin concentration was also found. No evidence of disseminated intravascular coagulation was detected, and therefore failure of synthesis by the liver is the likely explanation of the low levels noted.
 ...
PMID:Protease inhibitors in liver disease. 245 4

Changes of high molecular weight kininogen (HMW-K) clotting activity, antigen and cleavage in the plasma in the health and various diseases were studied. In 20 healthy individuals clotting activity of HMW-K, as measured by APTT one stage method, was 99 +/- 12% (male) and 84 +/- 15% (female). Antigen as measured by Laurell method were 106 +/- 24% (male) and 91 +/- 21% (female). In 35 patients with disseminated intravascular coagulation (DIC), both activity (78 +/- 33%) and antigen (69 +/- 31%) were statistically lower than those in normal individuals (p less than 0.01). In DIC both activity and antigen of HMW-K was correlated with serum albumin level. These results suggest that the cause of the lower level of HMW-K in DIC especially with septicemia is the result of lower production rather than consumption. In vivo cleavage of HMW-K was detected in plasma of a patient with septicemia and DIC by immunoblotting. The change of HMW-K was also assessed in other pathological states including liver cirrhosis, collagen disease, cardiopulmonary bypass and pregnant women.
 ...
PMID:[Changes of high molecular weight kininogen in various states]. 259 37

To examine the pathogenesis of thrombocytopenia associated with liver cirrhosis, the platelet count, spleen size and serum cholinesterase levels were measured together with plasma concentration of beta-thromboglobulin, fibrinopeptide A and serum albumin in 38 patients with histologically proven, severe but stable liver cirrhosis. The spleen size contributed most significantly to thrombocytopenia in this disorder and the serum cholinesterase level also correlated with the platelet count, both in decompensated and compensated liver cirrhosis. Plasma beta-thromboglobulin, serum fibrinopeptide A levels and serum albumin did not correlate with the platelet count. These findings indicate that disseminated intravascular coagulation is not likely to be the cause of thrombocytopenia in liver cirrhosis. Splenomegaly as well as the diminished protein synthetic activity of the liver participates in the pathogenesis of the thrombocytopenia in this disease.
 ...
PMID:Thrombocytopenia in liver cirrhosis. 261 53

A sensitive radioimmunoassay (RIA) for the fragment that is liberated from factor X when this zymogen is activated by factor VII/VIIa-tissue factor or factor IXa was developed. Antisera were raised in rabbits to a synthetic 15 amino acid peptide containing the COOH-terminal sequence of the activation fragment coupled to bovine serum albumin with glutaraldehyde. The reactivity of the antibody population obtained toward the factor X zymogen was negligible (less than 1/36,000 that of the activation peptide on a molar basis). However, because other plasma constituents contributed to a nonspecific basal signal in the RIA, a procedure by which the peptide could be reproducibly extracted from plasma was developed. The mean level of this species in normal individuals younger than the age of 40 was 66.4 pmol/L, and elevations up to 550 pmol/L were observed in patients with evidence of disseminated intravascular coagulation. The validity of these measurements of factor X activation is supported by the fact that the RIA signal migrates on reverse-phase high pressure liquid chromatography in a manner identical to that of the native peptide and can be quantitatively recovered. The mean concentration of the activation fragment was markedly decreased to 25.7 pmol/L in patients with hereditary factor VII deficiency (P = .0001 v normal controls), whereas the mean level in subjects with factor VIII deficiency was 61.1 pmol/L (P greater than .1 v normal controls). These data indicate that the basal (ie, in the absence of thrombosis or provocative stimuli) levels of FXP under in vivo conditions result mainly from the activity of the extrinsic pathway.
 ...
PMID:Detection of factor X activation in humans. 280 45

Twelve New Zealand white rabbits were intoxicated with aflatoxin B1. Most rabbits developed a coagulation defect near the time of death. Immediately prior to death there were significant decreases in factors V, VII, and VIII coagulant activities and fibrinogen concentration without a change in plasma fibrin(ogen) degradation product concentration, platelet number, and detectable plasma fibrin monomers. Microscopic evidence of disseminated intravascular coagulation was present in one rabbit with marked, diffuse hepatic necrosis. Terminal serum albumin concentration was significantly correlated to plasma factors V and VII activities and fibrinogen concentration. The coagulation defect of aflatoxicosis is primarily due to diminished hepatic synthesis of coagulation factors except when hepatic necrosis is severe enough to initiate intravascular coagulation and consumption of coagulation factors.
 ...
PMID:Coagulation defects of aflatoxin intoxicated rabbits. 310 13

Coumarins inhibit metastasis in a number of animal models, but the mechanism of this effect remains unclear. We have investigated the relationship between the coagulation system and metastasis using a new model system, involving i.v. injection of Mtln3 rat mammary carcinoma cells into Fischer 344 rats, and subsequent estimation of pulmonary seeding. Injection of factors II, VII, IX and X elevated the median number of surface pulmonary seedlings per animal to 182, and injection of factors II, IX and X to 181, compared with a median for control animals of 12 (P less than 0.001). Injection of factor VII alone, or of bovine serum albumin did not significantly affect pulmonary seeding. In a second experiment, arvin defibrination reduced the mean plasma fibrinogen concentration to 76.8 mg dl-1 from a control value of 228 mg dl-1. This degree of defibrination had no significant effects on pulmonary seeding, nor on the enhancing effects of factor complex injection (median numbers of seedlings per animal; control 15, arvin 21, arvin plus factors II, VII, IX and X 170, factors II, VII, IX and X only, 157). Factor complex injections did not detectably shorten thrombotest clotting times. In vitro testing suggested that Mtln3 cells contain little or no conventional factor X activating cancer procoagulant. The complex of coagulation factors II, IX and X appears to contain a component which greatly enhances metastasis in this model. This may explain the previously reported antimetastatic effect of coumarin anticoagulants, which suppress factors II, VII, IX and X. The enhancing effect of the factor complex does not appear to be altered by significant reductions in fibrin forming capacity, and defibrination itself has no effect on metastasis. These findings suggest the possibility that the effect of this factor complex on metastasis may be mediated via mechanisms other than the formation of a fibrin clot.
 ...
PMID:Promotion of metastasis by a specific complex of coagulation factors may be independent of fibrin formation. 316 6


1 2 3 4 Next >>