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)

Reported are 2 cases of an advanced gastric cancer with a "diffuse carcinomatosis of the bone marrow" (DCMB) showing a widespread osteoplastic bone metastasis. In a DCBM, a widespread invasion of cancer cells to the bone marrow occurs, causing leukoerythroblastosis, anemia, and disseminated intravascular coagulation. The local reaction in the bone, namely being osteoplastic or osteolytic, has not been discussed in previous papers. Our cases were characterized by an extremely high serum alkaline phosphatase, a "superscan" view of the bone scintigram, and a diffuse osteoplastic bone metastasis with an osteoid increase. Thus we think there are DCBM subtypes with a diffuse osteoplastic bone metastasis.
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PMID:[Two cases of advanced gastric cancer with diffuse carcinomatosis of the bone marrow showing a widespread osteoplastic bone metastasis]. 215 82

A veterinarian dealing with critical and trauma patients must be proficient with techniques for tracheostomy, thoracostomy tube placement for chest drainage, diagnostic peritoneal lavage, and autotransfusion. The utilization of these techniques may be life-saving in the critical patient. A tracheostomy is indicated in any patient with upper airway obstruction that cannot be managed with supplemental oxygen and/or orotracheal intubation. A tracheostomy tube with an inner cannula is preferred. Tracheostomy tubes should be cleaned at 3- to 4-h intervals, and methods should be employed to decrease thick tracheal secretions and to remove them from the trachea. A patient with a tracheostomy tube should be monitored continuously. A thoracostomy tube is indicated in any patient with large and/or continuous accumulation of air, blood, fluid, or chyle in the pleural space. The thoracostomy tube should be at least the same size as the patient's main stem bronchus. The thoracostomy tube is placed aseptically at the seventh intercostal space at the junction of the upper one third and lower two thirds of the lateral chest wall. Fluid or air may be removed from the chest intermittently with a three-way stopcock attached to the thoracostomy tube and a 60-ml syringe. If continuous drainage is needed, a continuous underwater seal and suction system should be used. Diagnostic abdominal paracentesis and peritoneal lavage are useful techniques in the determination of abdominal trauma, hollow viscus rupture, peritonitis, hepatic trauma, and urinary system trauma. When a multiholed catheter and lavage are used, the accuracy of detecting abdominal trauma is 95 per cent. When only needle paracentesis is used, the accuracy drops to 47 per cent. Abdominal lavage fluid can be analyzed for bacteria, whole blood, white blood cells, free bilirubin, creatinine, blood urea nitrogen, amylase, alkaline phosphatase, and alanine aminotransferase. Large volumes of whole blood recovered from abdominal or thoracic paracentesis can be reinfused into the patient if needed, providing it is not contaminated or markedly hemolyzed. The blood should be collected aseptically into blood bottles or bags. If the bleeding is ongoing or the blood only a few hours old, anticoagulants should be used. If the hemorrhage is several hours old, then clotting and defibrination has already occurred and the blood can be collected into "dry" bags or bottles. Before use, abdominal blood should be analyzed for urine, bile or fecal contamination. Blood collected from the thoracic cavity is much less likely to be contaminated. Autotransfused blood is administered through a standard blood administration set.
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PMID:Critical care surgical techniques. 268 82

Gram-negative septicemia/endotoxemia remains a serious clinical disorder that is often complicated by disseminated intravascular coagulation (DIC). Plasma antithrombin-III (AT-III) levels usually decrease during gram-negative septicemia/endotoxemia, and even moderate decreases in this major inhibitor of the coagulation system are associated with serious DIC. We demonstrated in an earlier study that prophylactic treatment of rats with 250 U/kg of AT-III followed by endotoxin challenge markedly attenuates DIC, indices of organ damage, and metabolic dysfunction. The present study was to determine whether treatment with 250 U/kg AT-III 1 hr after endotoxin challenge would be similarly efficacious. Rats treated with 250 U/kg of AT-III inactivated by human sputum elastase (ATX) served as protein controls. Blood samples for analysis were obtained 4 hr after AT-III or ATX treatment (5 hr after endotoxin challenge). Rats in the ATX treatment group exhibited abnormalities characteristic of endotoxemia, i.e., decreased fibrinogen levels and platelet counts, increases in prothrombin time and activated partial thromboplastin time, elevated serum glutamic oxaloacetic transaminase (SGOT) and alkaline phosphatase (AKP), and hypoglycemia. Treatment with AT-III markedly and significantly (P less than .05) attenuated all of these abnormalities, although survival was not increased. This study strongly suggests that supplementation of plasma AT-III is efficacious after the development of sepsis, although not as efficacious as prophylactic treatment.
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PMID:Antithrombin-III treatment limits disseminated intravascular coagulation in endotoxemia. 273 21

Five patients who developed acute renal failure due to acute tubular necrosis following multiple hornet (Vespa orientalis) stings are described. All of them had intravascular hemolysis. Evidence for rhabdomyolysis was present in 2 patients. Two patients had elevated transaminase and alkaline phosphatase levels and in 1 of these, liver biopsy showed centrilobular necrosis. Two patients had thrombocytopenia in the absence of disseminated intravascular coagulation. Two patients died of infections while the remaining 3 recovered completely. Acute renal failure following multiple hornet stings appears to result mainly from intravascular hemolysis or rhabdomyolysis although a direct nephrotoxic effect of venom cannot be excluded.
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PMID:Acute renal failure following multiple hornet stings. 341 46

Concentrations of plasma fibrinopeptide A (FPA) were measured by radioimmunoassay in 50 patients with venous thromboembolism or disseminated intravascular coagulation or both. A consistent discrepancy was observed in values obtained with two anti-FPA antisera. Analysis of extracts from plasma of these patients by high-performance liquid chromatography (HPLC) revealed the presence of a phosphorylated and an unphosphorylated form of the A peptide. Differences in concentrations of FPA measured with the two antisera could be accounted for by their different reactivity with phosphorylated FPA (FPA-P). The differences were abolished by treatment with alkaline phosphatase. A good correlation was observed between the FPA-P content of free A-peptide material and of fibrinogen in plasma as determined by HPLC (r = .88, P less than .001, n = 11). In patients with elevated FPA levels, the mean FPA-P content of fibrinogen was significantly higher (P less than .002, n = 13) than in patients with normal FPA levels (n = 8) and in healthy controls (n = 14). Phosphorus in fibrinogen did not correlate with fibrinogen degradation products or fibrinogen levels and became normal on adequate anticoagulation. Therefore, blood-clotting activation may lead to a high phosphate content of fibrinogen and of free FPA in plasma.
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PMID:Fibrinopeptide A and the phosphate content of fibrinogen in venous thromboembolism and disseminated intravascular coagulation. 369 10

A 35-year-old woman tuffering from gastric cancer associated with disseminated carcinomatosis of the bone marrow is reported. Total gastrectomy combined with splenectomy and distal pancreatectomy was performed. The patient was treated with mitomycin C, FT-207, OK-432, and PSK. But serum ALP (alkaline phosphatase) and CEA (carcinoembryonic antigen) values showed gradual elevations followed by deterioration of the patient's general condition. Consequently, chemotherapy program consisting of 5-fluorouracil, Adriamycin (intra-arterially), and cisplatin (intravenously) was initiated. Serum CEA and ALP values were considerably improved, and patient was restored to a better condition. She survived 17 months and died of disseminated intravascular coagulation.
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PMID:[Effective postoperative chemotherapy of gastric cancer associated with disseminated carcinomatosis of the bone marrow]. 393 24

An enzyme-linked differential antibody immunosorbent assay has been developed for the quantification of alpha2-plasmin inhibitor-plasmin and alpha2-macroglobulin-plasmin complexes. In this method the inhibitor-plasmin complex is bound to a surface by an inhibitor-specific antibody, and the plasmin bound to the inhibitor is quantified by a second antibody, rabbit antiplasminogen F(ab')2, labeled with alkaline phosphatase. The hydrolysis of p-nitrophenyl phosphate by the alkaline phosphatase is expressed in femtomoles of plasminogen per milliliter, by reference to a standard plasminogen curve. Inhibitor-enzyme complexes were generated in plasma by the addition of plasmin or of urokinase. The concentration of plasmin added was well below the plasma concentration of alpha2-plasmin inhibitor (1 microM) or of alpha2-macroglobulin (3.5 microM), so that neither inhibitor would be fully saturated with enzyme. Under these conditions increasing amounts of plasmin generated an increase in both alpha2-plasmin inhibitor-plasmin and alpha2-macroglobulin-plasmin complexes. Varying amounts of plasmin were incubated with each of the purified inhibitors in the concentration found in plasma, and the complexes. Varying amounts of plasmin were incubated with each of the purified inhibitors in the concentration found in plasma, and the complexes that formed were quantified by immunoassay. These studies made it possible to quantify the distribution of plasmin between the two inhibitors in plasmin or urokinase-treated plasma. In plasmin-treated plasma, 10% or less of the plasmin bound to both inhibitors was in complex with alpha2-macroglobulin. In contrast, between 19 and 51% of the plasmin generated in urokinase-activated plasma was bound to alpha2-macroglobulin. Thus, major changes in the distribution of plasma were observed, according to whether plasmin was added to plasma or whether plasminogen was activated endogenously. The pattern of inhibitor plasmin complexes generated in vivo by the therapeutic infusion of urokinase was similar to that found for urokinase-activated plasma. 23 normal individuals had low levels of alpha2-plasmin inhibitor-plasmin complexes, whereas six patients with laboratory evidence for disseminated intravascular coagulation demonstrated a 16- to 35-fold increase in he concentration of these complexes. These data indicated that a useful new probe for the study of the fibrinolytic enzyme system had been developed.
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PMID:Alpha2-plasmin inhibitor and alpha2-macroglobulin-plasmin complexes in plasma. Quantitation by an enzyme-linked differential antibody immunosorbent assay. 616 34

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

Sixty-seven cases of eclampsia were managed between August 1977 and July 1980. Routinely acquired laboratory tests of these cases have been analyzed. In addition, the group of patients with eclampsia was compared with a group of 24 healthy pregnant women. There was no significant difference in platelet count, serum fibrinogen, and bilirubin values. The activated partial thromboplastin time was abnormal in 42% of patients with eclampsia. There was no clinical evidence of disseminated intravascular coagulation in any patient. Patients with eclampsia had abnormalities of lactic dehydrogenase, alkaline phosphatase, SGOT, uric acid, BUN, and creatinine. However, in any individual patients there was no single test of great clinical usefulness and no test predictive of maternal or fetal outcome. At present the authors recommend complete blood count (including blood smear and platelet count), clot observation, and serum creatinine tests. Liver function tests are reserved for the patient with upper abdominal pain. Additional tests are recommended if the diagnosis of eclampsia is questionable or if an additional disease process is suspected.
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PMID:Eclampsia II. Clinical significance of laboratory findings. 707 59

Erythema multiforme major and disseminated intravascular coagulation developed in a dog 24 hours after exposure to a d-limonene-based insecticidal dip. Clinical signs included severe lethargy and weakness, ulceration of the oral mucosa, and erythematous serpiginous, annular, and arciform lesions on the head, trunk, and limbs. Clinicopathologic abnormalities included leukocytosis with neutrophilia, normocytic normochromic anemia, thrombocytopenia, prolongation of prothrombin and partial thromboplastin times, increased fibrin degradation products, hypoproteinemia, hyponatremia, hypochloremia, azotemia, high serum alanine aminotransferase and alkaline phosphatase activities, and high serum bilirubin concentration. Despite intensive supportive care, the dog developed severe intrathoracic and abdominal hemorrhage and died. Necropsy revealed severe diffuse epidermal necrosis and widespread hemorrhage within organs. Insecticidal dips containing d-limonene have the potential to induce various toxic effects, including, possibly, erythema multiforme major, and should be used cautiously.
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PMID:Erythema multiforme major and disseminated intravascular coagulation in a dog following application of a d-limonene-based insecticidal dip. 759 26


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