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 measured with Laurell's immunoelectroassay in 44 patients with meningococcal sepsis. The average value (15.0 +/- 7.9 mg/dl) was lower than that in normal children (27.4 +/- 8.7 mg/dl) (p less than 0.001). Fibronectin in patients correlated positively with antithrombin III (AT-III) values (p less than 0.02), but not with protein C (0.05 less than p less than 0.1). The decrease of fibronectin had no prognostic value. The fibronectin levels were lower in patients with disseminated intravascular coagulation (DIC+), than in those without DIC (DIC-) (p less than 0.02), but were lower in both groups than in a normal control group. A negative correlation between fibronectin and protein C was only present in DIC- patients (r: -0.773 = p less than 0.01). Fibronectin varied independent of AT-III and protein C in DIC+ patients. The study was repeated in 11 patients 24 hours after admission when fibronectin had decreased in 7/11 cases (mean decrease: -2.7 +/- 8.7 mg/dl). This variation correlated in a negative way with AT-III (r: -0.659 = p less than 0.05). In meningococcal sepsis fibronectin decreases very early, even in DIC- patients and its relationship to AT-III and protein C is different, depending on the presence of DIC and on the stage of evolution of the disease.
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PMID:Fibronectin in meningococcal sepsis. Correlation with antithrombin III and protein C. 231 65

A case is reported of a 60 year-old patient with chronic disseminated intravascular coagulation (DIC) which was increased by the therapeutic embolization of a renal tumour. The patient had 2 primary carcinomas (renal and prostatic) with vertebral metastases, severe chronic anaemia (due to haematuria), and chronic DIC, with thrombocytopaenia, soluble complexes, and fibrinogen and fibrin degradation products. Therapeutic embolization of the renal artery was carried out with fragments of dura mater. Although the result was anatomically very satisfactory, the patient's condition worsened, with continuing haematuria, and development of an haematoma in the lumbar fossa. Coagulation factors and antithrombin III (AT III) concentrations decreased, whereas the activated partial thromboplastin, thrombin and reptilase times increased. The patient also suffered from acute renal failure (creatinine: 690 mumol.l-1). Treatment consisted in fluid replacement, red blood cell and platelet transfusions, 150 IU.kg-1.d-1 heparin and 20 IU.kg-1.d-1 AT III. Haematological tests returned to pre-embolization values on the ninth day. The sudden worsening in the patient's condition was probably due to the sudden massive release of tissue thromboplastins related to the renal necrosis induced by the therapeutic embolization. The use of heparin AT III in the management of this patient is discussed.
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PMID:[Worsening of chronic disseminated intravascular coagulation after embolization of the renal artery]. 233 Oct 88

A syndrome in monozygotic twins that consists of a macerated twin fetus (fetus papyraceous) and a live-born twin with various anatomical defects has been described. The etiology is thought to be placental transfer of emboli or thromboplastic material through vascular shunts. Thromboplastic material precipitates disseminated intravascular coagulation (DIC) in the fetus, with a resultant hypercoagulable state due to relative fetal antithrombin III deficiency. Two cases of this syndrome will be discussed. The case of a live-born twin with intestinal atresia, who developed in utero with a fetus papyraceous, is reported. Emboli were demonstrated in vascular shunts of the diamniotic-monochorionic placenta. The hypothesis of intestinal atresia as a result of a vascular accident is reviewed. Another case involving a live-born twin with congenital skin defects, who developed in utero with a fetus papyraceous, is also reported. The skin defects were a congenital disruption from fetal DIC with resultant hypercoagulable state. Several other manifestations of the placental emboli syndrome will be discussed and the vascular etiology of the disruptions explained.
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PMID:Placental emboli from a fetus papyraceous. 235 89

During pregnancy an increase of antithrombin III can be observed. In hypertensive pregnant women this increase may be smaller. This fact may be a sign of hypertension induced disseminated intravascular coagulation and important for prognosis and therapy of pregnancy-induced hypertension. We carried out estimations of antithrombin III by double determinations using radial immundiffusion. Antithrombin III levels were lower in patient with pregnancy-induced hypertension.
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PMID:[Antithrombin III level in normal pregnancy and patients with pregnancy-induced hypertension]. 237 98

In order to assess precisely the fibrinolytic state in disseminated intravascular coagulation (DIC), plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP) and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 72 patients with DIC at presentation. Not only FbDP and TDP but also FgDP were markedly elevated in patients with DIC. When analyzed according to the underlying disease categories, the relative proportion of FgDP to TDP was high in patients with acute promyelocytic leukemia and vascular diseases, and it was the lowest in patients with sepsis. Correlation analysis revealed that plasma levels of FgDP correlated negatively with alpha 2-antiplasmin and positively with plasmin-alpha 2-antiplasmin complex (PAP) and a ratio of PAP to thrombin-antithrombin III complex (TAT). These findings indicate that besides fibrinolysis, fibrinogenolysis is markedly accelerated in the majority of the patients with DIC.
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PMID:Fibrinolysis and fibrinogenolysis in disseminated intravascular coagulation. 240 38

The changes in the level of glycated proteins and some factors of coagulation were studied in 30 patients with diabetes mellitus--15 with and 15 without diabetic retinopathy. The mean level of glycoalbumin was elevated (2.9 +/- 0.8 mg) HMF (mg protein) without an authentic difference in the two subgroups. Glycohemoglobin was also increased (means--13.6 +/- 1%) in all studied subjects The activity of antithrombin III was high (means--222 +/- 53%) and the concentration--reduced--means--22.1 +/- 2.2 mg%, without authentic difference in the two subgroups. The concentration of alpha-2-macroglobulin, as well as its activity showed no significant deviations. Factor VIII (von Willebrand) was within reference limits (means--97.04 +/- 15.06%) with a tendency to lower values in the group without diabetic retinopathy. Fibrinogen level (means--4.3 +/- 1.2 g) was within the reference range, and FDP--increased in the majority of the examined. A syndrome of intensified latent coagulability, equivalent to chronic decompensated DIC, determined by the basic dismetabolism and non-enzymatic glycating of proteins has been outlined. The changes are more marked in the cases with diabetic retinopathy.
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PMID:[Glycosylated proteins and various hemostatic indices in diabetic retinopathy]. 244 29

To determine the effects of preeclampsia and delivery, the hemostatic system was evaluated before and 24 to 48 hours after delivery in 59 nulliparous patients without clinical signs of disseminated intravascular coagulation. Fifteen patients with mild preeclampsia and 18 with severe preeclampsia were compared with 26 pregnant control patients. Preeclampsia was associated with high fibronectin (p less than 0.001), low antithrombin III (p less than 0.001), and low alpha 2-antiplasmin (p less than 0.005), suggesting endothelial injury, clotting, and fibrinolysis, respectively. After delivery, fibronectin decreased only in preeclamptic patients (p less than 0.005); alpha 2-antiplasmin increased in all groups (p less than 0.001). Endothelial injury in preeclampsia appeared to resolve soon after delivery, which could contribute to the rapid clinical improvement noted in the early puerperium.
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PMID:Preeclampsia, delivery, and the hemostatic system. 244 2

Decreases in platelet count, fibrinogen concentration, factor VIII, antithrombin III and alpha 2-antiplasmin activities, increase in FDP-D fraction, and pleural effusion were observed transiently at early fever stage of DHF at grade II, indicating DHF patients had manifestations of the acute type of DIC with increased permeability of vascular wall.
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PMID:DHF characterized by acute type DIC with increased vascular permeability. 244 85

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.
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PMID:Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation. 245 67

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.
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PMID:Protease inhibitors in liver disease. 245 4


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