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)

A patient with typical varicella (chickenpox) developed several complications: nephrotic syndrome following glomerulonephritis, trombocytopenic purpura, gastrointestinal bleeding, disseminated intravascular coagulation, encephalitis and bronchopneumonia. The course was satisfactory having been given antibiotics, heparin and peritoneal dialysis. Recovery was 100%.
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PMID:[Complications of chickenpox]. 61 25

Human plasma prekallikrein (Fletcher factor) clotting activity and antigen levels have been examined in various clinical conditions. Prekallikrein antigen was measured by a newly developed, specific, and sensitive radioimmunoassay. The assay had no demonstrable cross-reactivity with human urinary kallikrein nor, in the species tested, animal plasma prekallikrein. This assay was able to measure plasma kallikrein after its biological functions had been inactivated by plasma inhibitors. Normal human pooled plasma contained approximately 50 microgram/ml prekallikrein. Quantitative measurement of plasma prekallikrein was possible for concentrations as low as 0.3% of that of normal pooled plasma. A good correlation (correlation coefficient = 0.71) existed between titers of plasma prekallikrein measured by Fletcher factor clotting assays and radioimmunoassays among 40 normal subjects. Both prekallikrein clotting activity and antigen were significantly reduced in plasmas of patients with advanced hepatic cirrhosis or DIC. Prekallikrein activity and antigen were mildly decreased in plasmas or serums of patients with chronic renal failure and nephrotic syndrome but were normal in those of patients under treatment with warfarin or suffering from SLE, rheumatoid arthritis, sarcoidosis, or HANE. Human cord serum contained a lower titer of prekallikrein antigen than adult serum. Strenuous physical exercise did not significantly change plasma prekallikrein levels.
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PMID:Human plasma prekallikrein (Fletcher factor) clotting activity and antigen in health and disease. 65 66

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

Acquired antithrombin III (AT III) deficiency is based on either decreased activity or synthesis, increased loss or increased consumption. The activity of AT III is decreased in metabolic acidosis, hyperlipoproteinemias and by lipid peroxides. Chronic liver diseases especially liver cirrhosis are associated with very low levels of AT III due to insufficient hepatic synthesis, reduced transcapillary flux ratios, diffuse intravascular coagulation and loss in the ascites. Gastrointestinal loss of AT III may occur in patients with active inflammatory bowel diseases. AT III deficiency is observed in nephrotic syndrome when urinary loss of protein exceeds 5 g/d. During hemodialysis we have not found low AT III levels. Disseminated intravascular coagulation is characterized by activation of the coagulation system and increased consumption of AT III. AT III complexes with activated coagulation factors are subsequently cleared by the reticuloendothelial system.
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PMID:[Acquired antithrombin III deficiency]. 158 93

Cases with a pathological diagnosis of renal venous thrombosis (RVT) associated with nephrotic syndrome (NS) were studied retrospectively for clinicopathological evaluation. The material consisted of 21 RVT cases which were diagnosed in 2000 consecutive pediatric necropsies, with an overall incidence of about one percent. Eight of the 21 RVT cases were associated with nephrotic syndrome (34%), and this group formed 0.4 percent of the total necropsies in our pediatric center. The glomerulopathies of these nephrotic patients consisted of three cases of Finnish-type congenital NS (FCNS), three cases of renal amyloidosis secondary to familial Mediterranean fever, and two cases of membranoproliferative glomerulonephritis (MPGN). The presence of sepsis associated with disseminated intravascular coagulation, and the morphological age of the thrombi suggested that the RVT was secondary to sepsis in the FCNS cases. In the MPGN and secondary renal amyloidosis cases, the long duration of both the nephrotic state and the administration of diuretics along with glucocorticoid treatment and also the newly formed thrombi without infarction are strong evidences, although not definite, that the RVT developed as a complication of the glomerulopathy. Even though there were no definite clinical criteria for the diagnosis of most of the RVT cases, we would like to emphasize the importance of flank pain, the rapid deterioration of renal functions in a stable nephrotic patient, as well as the hypercoagulable state in the consideration of the development of RVT which indicate the need for appropriate radiological studies for confirmation of this condition during life.
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PMID:The association of nephrotic syndrome and renal vein thrombosis: a clinicopathological analysis of eight pediatric patients. 260 31

Proteins C and S are two vitamin K-dependent plasma proteins that work in concert as a natural anticoagulant system. Activated protein C is the proteolytic component of the complex and protein S serves as an activated protein C binding protein that is essential for assembly of the anticoagulant complex on cell surfaces. The anticoagulant activity is expressed through the selective inactivation of Factors Va and VIIIa. Many patients deficient in proteins C and S have been described and have an associated thrombotic tendency, but not all heterozygous protein C and S deficient individuals experience thrombotic complications. Multiple mechanisms and/or drugs can lead to acquired deficiencies of these proteins: oral anticoagulation, liver disease, DIC and in the case of protein S, lupus erythematosus, nephrotic syndrome, pregnancy and certain hormones. The anticoagulant activity of protein C decreases rapidly after administration of warfarin (i.e., with a time course similar to Factor VII). This rapid decrease may lead to a transient imbalance and contribute to coumarin induced skin necrosis. Protein S antigen levels do not decrease as rapidly, but protein S functional levels are often low in patients with an acute thrombus. The discrepancy between antigen and function results from elevations in C4b-binding protein, which complexes reversibly with protein S. Unlike free protein S, the complex does not function in the anticoagulant pathway. The available information all suggest that deficiency of protein C and protein S should be considered a risk factor contributing to recurrent thrombotic disease and that the function of these proteins is altered by many common clinical conditions which have associated an increased risk of thrombosis.
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PMID:Anticoagulation proteins C and S. 295 34

This article focuses on the pathophysiology of thrombosis in patients with acquired antithrombin III deficiency. Antithrombin III is an important natural inhibitor of the hemostatic mechanism, and a hypercoagulable state is often induced in diseases causing antithrombin III deficiency. Laboratory determination of antithrombin III activity is particularly useful in the clinical evaluation and therapeutic management of patients with disseminated intravascular coagulation, nephrotic syndrome, and severe hepatopathy.
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PMID:Pathophysiology of antithrombin III deficiency. 328 88

A 71-year-old male with disseminated intravascular coagulation (DIC) caused by abdominal aortic aneurysm was successfully treated surgically. He had aortic regurgitation, an old myocardial infarction, and nephrotic syndrome. The infrarenal part of the inferior vena cava, which was on the left side of the aneurysm, was temporarily transected during the surgical procedure. Preoperative heparin therapy was insufficient, but infusion of blood components during the operation and minimal dissection of the aneurysm were effective in controlling intraoperative hemorrhage. Hypofibrinogenemia and thrombocytopenia were normalized immediately after operation, and hemorrhagic diathesis was completely cured. In this case, the definitive treatment of DIC caused by an abdominal aortic aneurysm war removal of the lesion and the infusion of coagulation factors during the operation was effective in minimizing blood loss.
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PMID:Disseminated intravascular coagulation caused by abdominal aortic aneurysm. 341 54

Eleven of 204 children with nephrotic syndrome had thrombotic complications: arterial thrombosis in five, venous thrombosis in four, and pulmonary embolism in two. Fifty-one episodes of thromboembolism were recognized in 116 adult patients with nephrotic syndrome. Despite the lower incidence, thromboembolic complications tended to be more severe in children. In vitro indices of hemostasis and clinical evidence of thromboembolic complications were compared in children and adults. Antithrombin III concentrations and activities were abnormal in seven of 10 children, but in only two of 32 adults. In both groups, alpha 2-macroglobulin was elevated, but more markedly so in children. No evidence for circulating granulocyte-derived proteases (elastase/antielastase complexes) was noted in either group. Protein C was significantly elevated in children with nephrotic syndrome, but was normal in adults. Children also differed from adults with nephrotic syndrome in laboratory evidence of subthreshold disseminated intravascular coagulation (i.e., elevated soluble fibrinogen monomeric complexes and fibrin degradation products) and indicators of in vivo platelet activation (elevated beta-thromboglobulin). The more severe coagulation abnormalities in children may be linked to the more pronounced hypoalbuminemia.
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PMID:Hemostasis and thromboembolism in children with nephrotic syndrome: differences from adults. 358 1

The significance of acquired antithrombin III (AT III) deficiency must be interpreted in close relation to the underlying disease process. In patients with acute or chronic liver impairment, the AT III activity is related to a decrease of procoagulatory factors, whereas, in protein loss syndromes such as nephrotic syndrome, the AT III indicates an increased risk of thromboembolic events. The effect of oral contraceptives (OC) on AT III levels in young healthy females (n = 30) was determined prospectively. AT III decreases during OC usage could not be related to the estrogen content of the examined oral contraceptives, and there was no parallel decrease of AT III activity and concentration in each type of OC. In a prospective study, the extent of AT III decrease was determined in patients undergoing cardiopulmonary bypass operations (CPB) receiving different anticoagulant schedules during extracorporeal circulation (n = 49). There was no significant influence on the effectiveness of anticoagulation by the observed AT III decreases. AT III deficiency during CPB was primarily the result of hemodilution. However, the AT III kinetics were significantly influenced by the different protamin dosages and were not affected by the different heparin dosages. Correction of diminished AT III levels by substitution of AT III concentrates is beneficial in cases, in which an interruption of an enhanced coagulatory process such as disseminated intravascular coagulation is necessary or in patients requiring high dosage heparinization as in deep vein thrombosis. In those cases the quality of AT III correction correlates to the course of the disease. However, the potency of concentrates as well as the individual AT III recovery and half-life must be considered for an appropriate treatment with AT III substitution.
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PMID:[Clinical aspects of acquired antithrombin III deficiency]. 371 7


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