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)

Renal function was monitored in 24 patients with systemic envenoming following proven Russell's viper bite. In all patients, blood clotted within 20 min on admission. In 15 cases severe defibrination (systemic envenoming) developed during the next 3-5 d. None of the patients received antivenom before admission but enzyme-refined monospecific antivenom was given to those who developed signs of systemic envenoming. Specific antigen was detected by enzyme immuno-assay in all 21 subjects tested. Nine patients whose renal function remained normal did not develop systemic envenoming, and recovered without any treatment even though venom antigen was detectable in their serum. Ten patients developed mild renal dysfunction and systemic envenoming, but recovered after treatment with antivenom alone. The remaining 5 patients, all of whom were oliguric from admission, developed acute renal failure despite treatment with antivenom, but some recovered after peritoneal dialysis. Serum venom antigen levels were high in the last 2 groups, but there was some overlap. Albuminuria, found only in patients who became systemically envenomed, was associated with high fractional sodium excretion in those who developed acute oliguric renal failure. Albuminuria may appear before a gross clotting defect is detectable. It is an indication for antivenom and spot measurements might prove a useful early predictor of outcome.
 ...
PMID:Development of renal function abnormalities following bites by Russell's vipers (Daboia russelii siamensis) in Myanmar. 183 90

A prostate biopsy was carried out in a 53-year-old male outpatient with disseminated prostatic carcinoma. Two days later, he was admitted with severe acute anaemia (haemoglobin: 48 g.l-1) and macroscopic haematuria. Biological investigations revealed a disseminated intravascular coagulation (DIC). Symptomatic treatment was undertaken (transfusion of packed red blood cells, platelets, fresh frozen plasma and fibrinogen). However, the patient's condition worsened, and he was admitted to the intensive care unit 48 h later. Despite appropriate symptomatic treatment, the patient's condition continued to worsen. The prostatic origin of this condition was therefore suspected, and anti-androgenic treatment was started on day 9 (1,200 mg.day-1 ketoconazole and 2,000 mg.day-1 sodium fosfestrol). Within 48 h, the patient had began to recover in quite a spectacular manner. Ketoconazole starts blocking steroid synthesis within 4 h of giving it. This treatment can be used until oestrogen therapy starts having an effect (about one week). The low levels of testosterone in this case, before starting treatment, suggest that ketoconazole acted on the DIC by a possible cytotoxic effect on the carcinomatous cells.
 ...
PMID:[Favorable outcome of neoplastic disseminated intravascular coagulation treated with ketoconazole and estrogen derivative]. 192 64

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.
 ...
PMID:Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation. 245 67

We described here a seventy-one year-old male, who had repeated disseminated intravascular coagulation related to atherosclerosis and aneurysm of the aorta, and was successfully treated with self-subcutaneous injection of heparin sodium. He developed gingival bleeding and purpura in 1977. He was first treated with prednisolone (30 mg/day) and ACTH-Z under the diagnosis of idiopathic thrombocytopenic purpura associated with chronic thyroiditis, since platelet count (0.2 x 10(4)/microliters) was markedly decreased and megakaryocytes in the bone marrow were increased. By the treatment, platelet count recovered to 16.7 x 10(4)/microliters, while fibrin-degradation product levels were increased and hypofibrinogenemia developed, suggesting disseminated intravascular coagulopathy. Additional treatment with heparin was effective, and the coagulation studies became normal. In 1980, he again developed the episode with thrombocytopenia. At this time, prednisolone did not improve the episode, but heparin was effective. Since 1983, an enlargement of abdominal aorta had been recognized and gradually progressed. In 1983, he developed lumbago and abdominal pain, and received an emergency operation using artificial Y-graft vessel under the diagnosis of rupture of the aneurysm. There was no evidence of consumption coagulopathy at that time. He had been well until 1987, when he developed the third episode of thrombocytopenia with gingival bleeding. Thrombocytopenia was controlled with the treatment of heparin, but needed a continuous treatment with heparin. Thereafter, he has been well managed with self-injection of the anticoagulant, heparin sodium.
 ...
PMID:[Disseminated intravascular coagulation related to atherosclerosis and aneurysm of aorta: successful management with subcutaneous self injection of heparin sodium]. 259 49

A 12 month old boy weighing 6.4kg with esophageal varices caused by congenital biliary hypoplasia was scheduled for emergency sclerotherapy under general anesthesia. Anesthesia was induced with thiamylal sodium 3mg.kg-1 i.v. and then maintained with nitrous oxide, oxygen and a low concentration of enflurane, paralysed with pancuronium bromide. As soon as a small dose of sclerosant (5% ethanolamine oleate) was injected, transient moderate bradycardia and hypotension occurred. As his spontaneous breathing was very weak and the movements of extremities convulsive and his consciousness drowsy, prophylactic respiratory care was carried out. He had pneumonia and manifestation of DIC 4 days after sclerotherapy. He died of a massive tracheal hemorrhage. The cause of the patient's death seemed largely due to the several toxicities of sclerosant itself. We stress that although this therapy is effective for the child with portal hypertension, the incidence of complications might be high in patient with severely damaged liver function. Therefore, anesthetic and postoperative management in injection sclerotherapy should be performed very carefully.
 ...
PMID:[Death after delayed recovery and respiratory failure following injection sclerotherapy in a small infant under general anesthesia]. 261 9

Inhibition of Factor VIIa-tissue factor activity by a plasma component(s) that requires factor Xa has been described recently. In this communication, we have developed a specific radiometric assay (which utilizes 3H-Factor IX and is sensitive to less than 1% of plasma level) for this inhibitor and have measured its activity in various disease states. Strikingly, the levels of this inhibitor were found to be normal in patients with advanced chronic hepatocellular disease but low in patients with disseminated intravascular coagulation (DIC). When endotoxin was used to induce DIC in rabbits, the levels of this inhibitor fell by 25-90%. Human umbilical vein endothelial cells (HUVE), bovine pulmonary artery endothelial cells, and a human hepatoma cell line (HepG2) all synthesized and secreted this inhibitor, whereas a promyelocytic cell line (HL-60) did not and a monocytic cell line (U937) appears to synthesize only small amounts. When ammonium sulfate-fractionated human plasma and serum-free conditioned media from both HUVE and HepG2 cells were electrophoresed on sodium dodecyl sulfate acrylamide gels, two activity peaks corresponding to Mr approximately 45,000 and Mr approximately 33,000 were eluted in each case. These observations suggest that (a) the inhibitor is consumed in DIC and that (b) endothelial cells (or other cells) synthesize sufficient amounts of this inhibitor in vivo to compensate for any decreased production by liver cells.
 ...
PMID:Inhibitor of the factor VIIa-tissue factor complex is reduced in patients with disseminated intravascular coagulation but not in patients with severe hepatocellular disease. 303 84

Neutrophil-mediated oxidative stress on the rat mesenteric microcirculation was studied in the experimental model of endotoxin-induced disseminated intravascular coagulation (DIC) by using an intravital fluorescent technique and luminol-dependent chemiluminescence (ChL) analysis. Leukocytes sticking to the venules were visualized by the injection of acridine orange, a fluorochrome tracer which shows high affinity to white cells. Endotoxin (E coli, O-111B4, Difco, USA) was infused intravenously at a dose of 2 mg/kg/hr. After starting the infusion of endotoxin, the number of sticking cells were gradually increased on the venular endothelium followed by a transient neutropenia. In order to investigate the distribution of infused endotoxin in the microvasculature, FITC-labeled endotoxin (Sigma, USA) was used. After administration of FITC-endotoxin, multiple patches of fluorescence along the venular walls were observed, while no fluorescent conjugates were found at the sticking neutrophils and along the arteriolar walls. ChL activities of neutrophils were also dramatically elevated, which may reflect the enhanced ability to generate oxyradical species. To investigate the inhibitory effects of heparin sodium and gabexate mesilate which was a synthetic protease inhibitor on locomotive and metabolic changes of neutrophils induced by endotoxemia, both agents were administered prior to endotoxin infusion. Gabexate mesilate attenuated these changes, but heparin sodium did not show any improving effects. It was concluded that endotoxin primarily affects the venular endothelial cells, resulting in the activation of neutrophils. Gabexate mesilate was more likely to attenuate neutrophil-mediated oxidative stress on microvasculature in endotoxin-induced DIC than heparin sodium.
 ...
PMID:Microcirculatory disturbances in endotoxin-induced disseminated intravascular coagulation. The effects of heparin and gabexate mesilate on locomotive and metabolic changes of neutrophils. 314 69

Greenfield filters for prevention of pulmonary emboli may be placed in the inferior vena cava by surgical cutdown or by percutaneous insertion through the femoral or jugular veins. We evaluated the use of the percutaneous techniques 52 times in 50 patients. The right femoral vein was used in 37 of the procedures, the right internal jugular vein in 12, and the left femoral vein in three. Twenty-two patients had altered coagulation factors: 11 were receiving heparin, four were receiving warfarin sodium, six had hepatic cirrhosis, and one had disseminated intravascular coagulation and had been receiving warfarin sodium. Filter placement was successful in 51 of 52 procedures. In the unsuccessful case, placement was attempted via the left femoral vein; the carrier could not be advanced from the common iliac vein to the inferior vena cava. This patient required surgical occlusion of the cava. There was one major complication, a hematoma in the right side of the groin that required transfusion. This occurred in the patient with disseminated intravascular coagulation who had extensive scarring from multiple previous vascular surgical procedures. Two patients required second filters because of severe angulation of the filter found 1 and 4 days after implantation. Clinical thrombosis of the femoral vein after femoral vein access occurred in two (5%) of 40 patients and was proved by venogram in one. Our experience shows that the percutaneous method is highly successful and suggests that this technique should be the primary method for filter placement in the inferior vena cava.
 ...
PMID:Greenfield filter: percutaneous placement in 50 patients. 325 35

Protamine-agarose chromatography is introduced as a rapid and efficient method for the isolation of fibrinogen/fibrin degradation products from biological fluids such as human plasma. All fibrinogen/fibrin fragments above a MW of 35000, including fragments D and E are quantitatively adsorbed to insolubilized protamine and can be eluted with a buffer containing 0.2 M sodium citrate/citric acid pH 5.3, following previous elution of non-fibrinogen proteins with a buffer containing 0.8 M NaCl at neutral pH. Fragments D and E are separated by stepwise elution. The efficiency of the method is - evaluated by applying it to plasma samples obtained from healthy donors and from patients with clinical and laboratory evidence of disseminated intravascular coagulation.
 ...
PMID:Isolation and purification of fibrinogen/fibrin degradation products by chromatography on protamine-agarose. 342 89

Recently, monoclonal antibody (DD-3B6) to fibrin D-dimer was prepared and coupled to latex beads to provide a specific test (Dimertest) for fibrinolysis. The purpose of this study was to evaluate the Dimertest assay as a clinical laboratory test for the measurement of plasma fibrin D-dimer derivatives. The Dimer-test assay specifically detected 2 micrograms/mL of purified fibrin D-dimer or fibrin D-dimer/fragment E complex added to afibrinogenemic plasma but did not detect 500 micrograms/mL of either fibrinogen fragments X, D, E, or 160 micrograms/mL cross-linked fibrinogen. The fibrin(ogen) degradation product (FDP) assays of American Dade or Wellcome Diagnostics detected 5.0 micrograms/mL of fibrin D-dimer and from 1 to 10 micrograms/mL of the other FDPs. Twenty-eight percent of 150 random plasma samples assayed from hospitalized patients were positive for fibrin D-dimer derivatives. Plasma samples from 152 patients suspected of having disseminated intravascular coagulation (DIC) were assayed for serum FDP (Wellcome Diagnostics) and plasma fibrin D-dimer derivatives. Samples from 69% of patients with serum FDP levels less than 10 micrograms/mL, and more than 90% of those with serum FDP levels greater than 10 micrograms/mL, were positive for fibrin D-dimer derivatives. Dimertest results were not modified by heparin, streptokinase, freeze-thawing, or clotting plasma. Serum fibrinogen-related antigens were immunoadsorbed from Dimer-test positive sera by anti-fibrinogen antibody and formalin-fixed Cowan I strain Staphylococcus aureus. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and protein blotting with the use of monoclonal antibody DD-3B6 demonstrated a protein band with similar mobility to purified D-dimer. The measurement of plasma fibrin D-dimer derivatives by the Dimertest assay is a rapid, sensitive, and specific laboratory test for fibrinolysis. The Dimertest assay has proven to be a useful addition to the clinical laboratory and should be helpful in the diagnosis and management of patients with diseases associated with fibrinolysis.
 ...
PMID:Measurement of plasma fibrin D-dimer levels with the use of a monoclonal antibody coupled to latex beads. 354 76


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>