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)

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

The effects of E. coli lipopolysaccharide (LPS) on washed platelets of the healthy volunteers were studied by measuring ADP induced aggregation and intracellular ionized calcium concentration ([Ca2+]i) by fluorescent calcium indicator, quin 2. Addition of LPS in platelets suspension in saline, caused an increased platelet aggregation. Adding LPS, however, in platelet suspension in Na(+)-citrated platelet poor plasma inhibited ADP aggregation. These trends were not affected by cyclooxygenase inhibitor, but partially antagonized by dibutyryl cyclic AMP, and verapamil. The intracellular calcium ion concentration ([Ca2+]i) was significantly increased (334 +/- 141 nM to 150 +/- 45 nM in control) on addition of LPS in platelet suspension containing ionized calcium. On the other hand, there was no significant difference observed with those suspended in calcium free solution (50 +/- 16 to 45 +/- 15 in control). These results indicate that changes of platelet aggregation by LPS were mediated by cyclic AMP and Ca2+, but not by arachidate derivatives. The author concludes that LPS changed the mechanism of Ca2+ influx of platelet membrane and elevated [Ca2+]i of platelets. These findings, however, probably are not the cause of aggregation of platelets during DIC.
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PMID:[Effects of E. coli LPS on human platelet aggregation]. 818 78

The effects of E. coli endotoxin (ET) on human erythrocyte cytosolic free calcium concentration ([Ca2+]i) and membrane calcium pump (Ca(2+)-Mg(2+)-ATPase) activity were observed in vitro. The changes of erythrocyte [Ca2+]i, Ca(2+)-Mg(2+)-ATPase activity, calmodulin activity, the deformability of erythrocytes, membrane protein electrophoresis, and the fluidities of membrane lipids were investigated in the ET-induced disseminated intravascular coagulation (DIC) model to study the significance of erythrocyte factors in the occurrence of microangiopathic hemolytic anemia. The [Ca2+]i of human erythrocytes was 86 +/- 9.2 nmol/L in normal cells, and it was increased to 124 +/- 22 nmol/L, 174 +/- 41 nmol/L and 220 +/- 92.1 nmol/L, respectively, when the erythrocytes were incubated with 0.5 mg/ml, 1 mg/ml and 2 mg/ml ET, respectively. At the same time, the Ca(2+)-Mg(2+)-ATPase activities decreased from 1031 +/- 131 nmol/mg.h in normal to 870 +/- 182 nmol/mg.h, 684 +/- 124 nmol/mg.h and 718 +/- 144.4 nmol/mg.h in groups receiving 0.5 mg/ml, 1 mg/ml and 2 mg/ml ET, respectively (P < 0.01). The [Ca2+]i of rabbit erythrocytes was elevated from 76.6 +/- 14.9 nmol/L in normal to 224 +/- 74 nmol/L (P < 0.01), and the Ca(2+)-Mg(2+)-ATPase activity was inhibited from 220 +/- 26.8 nmol/mg.h in normal to 146.1 +/- 30.6 nmol/mg.h during ET-induced DIC in vivo. In addition, erythrocyte deformability decreased and the membrane protein electrophoresis showed changes in the 4.5 KD band area. However, there was no significant difference in the calmodulin activity and fluidities of membrane lipids of erythrocytes in DIC rabbits. These results suggest a possible alternative mechanism for the formation of microangiopathic hemolytic anemia in ET-induced DIC rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The changes in erythrocyte calcium is one of the mechanisms of anemia formation in rabbit endotoxin-induced DIC]. 824 17

Native hirudin is a heterogenous polypeptide obtained from the medicinal leech, Hirudo medicinalis. Recent advances in molecular biological techniques have led to the availability of large amounts of hirudin in the recombinant form. Recombinant hirudins (rH) are currently being investigated for potential use in the prophylaxis and treatment of deep venous thrombosis (DVT), in disseminated intravascular coagulation (DIC) and during cardiovascular bypass surgery. In this study, one specific variant of rH with a lysine residue in position 47 (rHV2-Lys 47) was administered in dogs in a multiple dose regimen of 2 mg/kg (i.v. bolus) for three weeks with a dosing interval of one week. After each dose, blood samples were collected at regular time intervals, plasma separated and stored at -4 degrees C. Concentrations of rHV2-Lys 47 in each sample were determined using an enzyme-linked immunosorbent assay (ELISA). Ex vivo antithrombin responses measured included activated partial thromboplastin time (APTT), calcium-thrombin time (Ca++TT-10 NIH units/ml) and a chromogenic anti-IIa assay. It was the purpose of this study to detect any sensitization or desensitization of antithrombin responses when rHV2-Lys 47 is used in a repeated fashion such as would be expected in the prophylaxis of DVT. The results indicated that there was no attenuation in the responses; however, there was a sensitization of response as measured by the Ca++TT (10 NIH units/ml). These findings could have major implications in the clinical use of rH where this drug is expected to be used in a multiple dose regimen.
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PMID:Alteration of pharmacokinetics and pharmacodynamics of recombinant hirudin (rHV2-Lys 47) after repeated intravenous administration in dogs. 846 75

Although the low molecular weight degradation products of fibrinogen (FgDP) and fibrin (FbDP) are known to inhibit lymphocyte blastogenesis, the effect of purified macro-molecular FgDP and FbDP (molecular weight, 90 to 200 Kd) is unclear. We have examined the effect of these latter FgDP and FbDP and find that products that contain the D domain inhibit lymphocyte proliferation in response to T-cell mitogens, allogeneic mononuclear leukocytes, and anti-CD3 in vitro. Plasmic digestion of D1 in the absence of calcium with removal of the C-terminal end of the gamma chain or disruption of the gamma-gamma C-terminal cross-link site of D-dimer (DD) by puffadder venom (PAV-D) abrogates their inhibitory potential. Prior incubation of monocytes with DD or D1 inhibits subsequent lymphocyte transformation. Binding studies with radiolabeled DD and PAV-D confirm that monocytes interact only with DD. This specific binding may be competitively inhibited by monoclonal antibodies to CD11b/CD18 or by peptide analogues of the C-terminal gamma chain of fibrinogen that mimic the adhesion recognition site of integrins. We postulate that DD and D1 bind to CD11b/CD18 on adherent monocytes and modulate lymphocyte activation. These products are typically present in the plasma of patients with disseminated intravascular coagulation with sepsis and could therefore influence inflammatory processes in vivo.
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PMID:Fibrin and fibrinogen degradation products with an intact D-domain C-terminal gamma chain inhibit an early step in accessory cell-dependent lymphocyte mitogenesis. 849 35

Fifty-two severely wounded patients, admitted directly from a battlefield or after surgical treatment in a war hospital, were treated in the Surgical Intensive Care Unit of the 'Sisters of Mercy' University Hospital in Zagreb during the 1991 war in Croatia. Considering the severity of the wounds, blood loss was not as severe as expected. This can be attributed to the nature of the injuries as most of the patients were wounded by fragments of explosive devices which cause less tissue destruction than military bullets. Low serum potassium levels, metabolic acidosis, low total protein levels and consequently low serum calcium levels correlated with wound severity. Low serum potassium levels were caused by its redistribution. Reperfusion liver injury was also present. Consumption coagulopathy was one of the characteristic disturbances in this type of injury. There was a relatively big difference between fluid input and output caused by fluid loss through drain sites and large open wound surfaces. The low mortality of the severely wounded was due to their young age and the well-organized military medical service which was developed from the civilian medical service in a short time.
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PMID:Clinical course in 52 severely wounded patients treated in the intensive care unit during the war in Croatia. 855 Jan 36

Infrared differential interference contrast (IR DIC) videomicroscopy was used to measure and characterize cell swelling induced by activation of glutamate receptors (GluR) in a neostriatal brain slice preparation. This swelling is, in many cases, a prelude to necrotic cell death. Activation of N-methyl-D-aspartate (NMDA) and non-NMDA ionotropic GluRs caused cell swelling. The concentration-response relationships and the time courses of the onset of agonist-induced swelling were very similar for NMDA and kainate (KA). However, cells were able to recover from KA but not NMDA-induced swelling. Results from ion substitution experiments suggest that sodium, chloride and to a lesser extent calcium ions play critical roles in this swelling. Heterogeneity in the response to NMDA occurred within cells of the neostriatum. Approximately 15% of the cells did not swell when exposed to NMDA. The magnitude of the NMDA-induced swelling also varied depending on the region of the nervous system. Swelling was greater in the neostriatum and neocortex than in the hippocampus and it did not occur in the suprachiasmatic nucleus. In conclusion, IR DIC videomicroscopy can be used to follow quantitatively the dynamics of GluR-evoked responses in single cells and should be instrumental in determining the factors capable of modifying excitotoxicity.
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PMID:Glutamate receptor-induced toxicity in neostriatal cells. 882 70

A pregnant woman with severe preeclampsia developed HELLP syndrome and acute pancreatitis. She underwent an emergency caesarean section. In this patient, attention had to be paid to complicating cranial hemorrhage, rupture of liver subcapsular hematoma, acute renal failure, DIC, hypovolemic shock and sepsis. Therefore, we used a calcium blocker, diuretics and a protease inhibitor and examined the liver and pancreas by abdominal X ray-CT.
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PMID:[HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome and acute pancreatitis complicated with severe preeclampsia]. 909 10

The effects of Bitis gabonica venom have been studied in several animal species, including the monkey, dog, rabbit, rat and guinea pig. Further information has been provided by observations on the effects of snake bite in man. Bitis gabonica venom exerts a number of cytotoxic and cardiovascular effects: cytotoxic effects include widespread hemorrhage, caused by the presence of two hemorrhagic proteins. These hemorrhagins bring about separation of vascular endothelial cells and extravasation of blood into the tissue spaces. Metabolic alterations include decreased oxygen utilization by tissues and increased plasma glucose and lactate concentrations. Metabolic non-compensated acidosis has also been seen in the rat as a consequence of the cytotoxicity of the venom. Cardiovascular effects include disturbances in atrio-ventricular conduction and reduction in amplitude and duration of the action potential brought about by a decreased calcium membrane conductance. A progressive decrease in myocardial contractility can also be attributed to the decreased calcium conductance, which together with the severe acidosis may cause death in experimental animals. A severe, though reversible, vasodilatation was observed after envenomation due to unidentified compounds in the venom. In man, envenomation causes a variable clinical picture depending on the time course and severity of envenomation. Frequently seen effects include hypotension, hemorrhage at the site of the bite and elsewhere and disseminated intravascular coagulation. Envenomation can be satisfactorily treated with antivenom.
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PMID:The Gaboon viper, Bitis gabonica: hemorrhagic, metabolic, cardiovascular and clinical effects of the venom. 927 5

The clinical characteristics of and outcome for 75 children with meningococcal septic shock were studied. In addition, a new prognostic scoring system was developed. The median age of the patients was 3.2 years (range, 3 weeks to 17.9 years). The most common phenotype of Neisseria meningitidis was B:4:P1.4 (27%). A mortality rate of 21% was observed. Ten (17%) of the 59 survivors had serious sequelae. Calcium levels were significantly lower in patients with seizures. Disseminated intravascular coagulation occurred in 58% of the patients who were tested. Logistic regression analysis identified four laboratory features independently associated with mortality: serum C-reactive protein level, base excess, serum potassium level, and platelet count. These features were used to develop a novel scoring system with a predictive value for death and survival of 71% and 90%, respectively. The outcome was predicted correctly for 86% of the patients, which is higher than rates previously reported for scoring systems.
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PMID:Meningococcal septic shock in children: clinical and laboratory features, outcome, and development of a prognostic score. 931 53


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