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 apoprotein (AP) of tissue factor (TF) has been purified 72,000-fold to homogeneity from human placenta using acetone delipidation, sodium deoxycholate (DOC) extraction, Sephacryl S-300 column chromatography, preparative polyacrylamide-gel electrophoresis (PAGE) in DOC and tryptic digestion. The purified AP had an apparent molecular weight of 54,000 by sodium dodecyl sulfate/PAGE. A radioimmunoassay (RIA) for quantitation of the TF-AP using an antibody against this purified AP of TF was devised which was sensitive enough to measure as small a quantity as 100 pg/ml of TF-AP accurately with high reproducibility. In addition to TF clotting activity (TFA), the immunoreactive TF-AP (IR-TFR) in the homogenates of leukemic leukocytes from patients with acute non-lymphoid leukemia (ANLL) was determined using this RIA. In 30 patients with ANLL, the mean IR-TFR with standard deviation (SD) of 21 cases with DIC was 157.9 +/- 188.1 ng/10(8) cells, which was significantly higher than that (37.1 +/- 29.9 ng/10(8) cells) of 9 cases with no DIC during remission induction chemotherapy (p less than 0.01).
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PMID:Radioimmunoassay of human tissue factor. 373 65

Heparin-induced thrombocytopenia with thromboembolism calls for an immediate substitution of the heparin with other potent anticoagulants, such as coumarin derivatives. The occurrence of this adverse effect in pregnancy poses an additional dilemma because the use of coumarin derivatives is not acceptable during pregnancy, while other medications may not be as effective. In a pregnant patient treated with mucous sodium heparin for deep vein thrombosis, recurrent heparin-induced thrombosis and disseminated intravascular coagulation (DIC) occurred. Replacing the heparin with a different brand of the same drug resulted in reversal of the DIC and in clinical improvement. If severe heparin-induced thrombosis occurs in a patient in whom anticoagulation with other drugs is contraindicated, substituting one brand of heparin for another could be of value.
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PMID:Heparin-induced thrombocytopenia and recurrent thrombosis in pregnancy. A case report. 378 42

Severe homozygous protein C deficiency is a rare but serious problem in the newborn, with a clinical presentation of purpura fulminans. We have presented such a case in an 1,870 gm female neonate. Salient clinical findings in this case include DIC associated with extensive ecchymosis and subsequent gangrene of the skin, thrombotic complications that began on the third day of life. There was no precipitating infection. The progressive gangrenous necrosis of heel and toes was refractory to heparin therapy, but there was clinical improvement after treatment with fresh frozen plasma. Our patient's level of protein C antigen was less than 3% (normal 70% to 130%). Levels of other vitamin-K-dependent factors, as well as factor V, factor VIIIC, and antithrombin III were normal. A heterozygous protein C deficiency was documented in the mother and father. Presently the child is receiving warfarin sodium (Coumadin) therapy and is clinically stable.
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PMID:Protein C deficiency. 381 Feb 23

Following the administration of fluphenthixol (a depot phenothiazine) for a psychotic illness, a 44-year-old woman developed weakness, rhabdomyolysis and renal failure, together with hyperthermia (42 degrees C) and signs of both autonomic and central nervous system dysfunction. She died following massive intestinal haemorrhage, intra-abdominal sepsis and probable disseminated intravascular coagulation. A diagnosis of neuroleptic malignant syndrome had been made, but treatment with dantrolene sodium was probably instituted too late to prevent the progress of the complications she had developed. This syndrome, which follows the use of phenothiazines or butyrophenones, is rare, potentially fatal and probably underdiagnosed. It has been likened to malignant hyperthermia, but a review of the literature points to many differences. Both dantrolene sodium and dopaminergic drugs (bromocriptine, amantidine and L-dopa) have been shown to be efficacious and their continued use, despite a failure in this case, is advocated until more is known about this syndrome.
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PMID:The neuroleptic malignant syndrome. Case report with a review of the literature. 382 73

A novel platelet-agglutinating protein (PAP) was purified approximately 2,000-fold from the plasma of a patient with thrombotic thrombocytopenic purpura (TTP) by ammonium sulfate fractionation, DEAE-Sephacel and concanavalin A-Sepharose chromatographies. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, with and without reduction, this preparation revealed a major protein band with a molecular weight of 37,000, and a minor band with a molecular weight of 32,000-34,000. After elution from the gel, only the 37,000-mol wt protein corresponding to the major band induced the platelet agglutination. When four normal plasmas and the recovery plasma from the same TTP patient were subjected to the similar purification steps, the 37,000-mol wt major band was absent. The 125I-PAP bound to the platelets in a concentration-dependent manner. The platelet agglutination induced by PAP was not inhibited by hirudin, heparin in the presence of antithrombin III, phenylmethylsulfonyl fluoride, apyrase, aspirin, or prostaglandin I2. However, it was inhibited by IgG from normal adults and from the same TTP patient after recovery. The anti-37,000-mol wt PAP antiserum prepared in the rabbit formed a single precipitin line against the highly purified PAP. Using this antiserum in the Western immunoblotting, the 37,000-mol wt protein band was found in the three TTP plasmas, of which the platelet-agglutinating activity was inhibited by the anti-37,000-mol wt PAP IgG. The 37,000-mol wt immunoprecipitin band was absent in the plasmas obtained from another two TTP patients, two normal subjects, two patients with idiopathic thrombocytopenic purpura, and two patients with disseminated intravascular coagulation. These results suggest that the 37,000-mol wt PAP is present only in certain cases of TTP, and is likely to be responsible for the formation of platelet thrombi in the microcirculation.
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PMID:Novel platelet-agglutinating protein from a thrombotic thrombocytopenic purpura plasma. 393 64

Factor VIII antigen (VIII:CAg) exhibits molecular weight heterogeneity in normal plasma. We have compared the relative quantities of VIII:CAg forms present in normal individuals (n = 22) with VIII:CAg forms in renal dysfunction patients (n = 19) and in patients with disseminated intravascular coagulation (DIC; n = 7). In normal plasma, the predominant VIII: CAg form, detectable by sodium dodecyl sulfate polyacrylamide gel electrophoresis, was of molecular weight 2.4 X 10(5), with minor forms ranging from 8 X 10(4) to 2.6 X 10(5) D. A high proportion of VIII:CAg in renal dysfunction patients, in contrast, was of 1 X 10(5) mol wt. The patients' high 1 X 10(5) mol wt VIII: CAg level correlated with increased concentrations of serum creatinine, F1+2 (a polypeptide released upon prothrombin activation), and with von Willebrand factor. Despite the high proportion of the 1 X 10(5) mol wt VIII:CAg form, which suggests VIII:CAg proteolysis, the ratio of Factor VIII coagulant activity to total VIII:CAg concentration was normal in renal dysfunction patients. These results could be simulated in vitro by thrombin treatment of normal plasma, which yielded similar VIII:CAg gel patterns and Factor VIII coagulant activity to antigen ratios. DIC patients with high F1+2 levels but no evidence of renal dysfunction had an VIII:CAg gel pattern distinct from renal dysfunction patients. DIC patients had elevated concentrations of both the 1 X 10(5) and 8 X 10(4) mol wt VIII:CAg forms. We conclude that an increase in a particular VIII:CAg form correlates with the severity of renal dysfunction. The antigen abnormality may be the result of VIII:CAg proteolysis by a thrombinlike enzyme and/or prolonged retention of proteolyzed VIII:CAg fragments.
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PMID:Abnormal factor VIII coagulant antigen in patients with renal dysfunction and in those with disseminated intravascular coagulation. 393 66

A new method is described for identifying low concentrations of circulating derivatives of fibrinogen and fibrin, even when present in heterogeneous mixtures. This technique is applicable to plasma and serum and uses electrophoresis in 2% agarose in the presence of sodium dodecyl sulfate (SDS) followed by immunological identification of separated derivatives, using radiolabeled antifibrinogen antiserum and autoradiography. Unique electrophoretic patterns distinguish plasmic derivatives of crosslinked fibrin from those of fibrinogen and also identify crosslinked fibrin polymers produced by the combined action of thrombin and factor XIII on fibrinogen. The assay is sensitive to a concentration of 0.1 micrograms/mL of fibrinogen in serum or plasma. Fibrin polymers, plasmic degradation products of fibrinogen, and plasmic degradation products of crosslinked fibrin were detected in the plasma or serum of a patient with disseminated intravascular coagulation. Plasmic derivatives of both fibrinogen and crosslinked fibrin appeared in serum in the course of fibrinolytic therapy for pulmonary embolism, whereas during acute myocardial infarction a marked increase in the proportion of fibrin polymers in plasma was found in comparison with normal controls. Thus, the procedure can distinguish between the simultaneous processes of fibrin polymer formation, fibrinogenolysis, and fibrinolysis, and is sufficiently sensitive to detect relevant quantities of derivatives in pathologic conditions.
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PMID:Specific identification of fibrin polymers, fibrinogen degradation products, and crosslinked fibrin degradation products in plasma and serum with a new sensitive technique. 397 Oct 42

We present the case of a 35-year-old man who developed symptoms of the neuroleptic malignant syndrome (NMS) after taking prescribed, moderately high, therapeutic doses of haloperidol. When brought to the emergency department, he was comatose, hypotensive, and had rigid muscle tone and a core body temperature of 42.2 C. Although initial treatment was supportive, intubation, ventilator support, and further care in the intensive care unit were necessary. Ensuing disseminated intravascular coagulation was treated successfully and the patient was weaned from the ventilator on the third day after admission. He was discharged from the hospital 11 days after admission. Recently recognized drug therapy for NMS, such as bromocriptine mesylate and dantrolene sodium, was not used in this case.
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PMID:Neuroleptic malignant syndrome. 398 49

Heparin cofactor II (HCII) is a glycoprotein in human plasma which inactivates thrombin rapidly in the presence of heparin or dermatan sulfate. We have developed a functional assay for HCII in which inhibition of thrombin by plasma is determined in the presence of dermatan sulfate. The assay is specific for HCII by the following criteria: (a) under the conditions of the assay, 125I-thrombin forms complexes in plasma which comigrate with the thrombin-HCII complex during sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE); (b) activity detected by the assay is decreased in plasma absorbed with monospecific antibodies against HCII; and (c) purified antithrombin III (ATIII) is unreactive in the assay system. Addition of Polybrene to the assay permits determination of HCII activity in samples containing less than or equal to 12 U/mL of heparin. The range of HCII concentrations in normal individuals is 1.2 +/- 0.4 mumol/L (mean +/- 2 SD, n = 34). HCII activity was determined in 54 consecutive patients undergoing evaluation for the possibility of disseminated intravascular coagulation (DIC). Ten of the 11 patients with documented DIC had decreased HCII activity as compared with only 7 of the 43 patients without DIC (chi 2 = 19.3, P less than .0001). The concentrations of HCII and ATIII varied in parallel in most of the patients tested. A significant correlation between decreased HCII activity and decreased serum albumin concentration was also observed in these patients and in eight additional patients with hepatic failure in the absence of DIC. We conclude that HCII activity is decreased in many patients with DIC and hepatic failure.
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PMID:Heparin cofactor II activity in patients with disseminated intravascular coagulation and hepatic failure. 404 18

Three antimicrobial agents were evaluated as to their ability to neutralize the toxic effects of endotoxin in rabbits. These consisted of two cyclic polypeptides, polymyxin B sulfate and colymycin M (sodium colistimethate), and an aminoglycoside, gentamicin sulfate. Polymyxin B regularly prevented endotoxin-induced leukopenia, thrombocytopenia, and disseminated intravascular coagulation. Colymycin M had similar activity but was not as effective as polymyxin B. Gentamicin demonstrated no neutralizing ability in this study.
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PMID:Comparison between the polymyxins and gentamicin in preventing endotoxin-induced intravascular coagulation and leukopenia. 434 9


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