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)

Systemic inflammatory response syndrome (SIRS) is characterized by body temperature abnormalities, tachypnea or hyperventilation, tachycardia, and leukocytosis or leukopenia. Although it is typically associated with a serious infection and referred to as sepsis, SIRS can stem from noninfectious causes, as well. We report the cases of four patients with toxic serum levels of salicylate (33.5 to 67.6 mg/dL) and SIRS, and we discuss mechanisms responsible for SIRS. Our patients showed temperature disturbances (35.5 degrees C to 39.8 degrees C), noncardiogenic pulmonary edema, and mixed acid base disturbances. Other abnormalities included coagulopathy (disseminated intravascular coagulation), encephalopathy, and hypotension. All four patients recovered from SIRS, probably due to early recognition and treatment; only one patient did not survive the hospitalization. Chronic salicylate toxicity should be considered as a cause of SIRS in the absence of a source of infection, since survival appears to be dependent on prompt diagnosis and management.
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PMID:Systemic inflammatory response syndrome caused by chronic salicylate intoxication. 863 72

Pathophysiologic concept of SIRS has been proposed for the better management of postoperative severe infection and septic MOF, and the concept has been found to be very useful. It is very important to identify the high risk SIRS patients of the development of septic MOF and to treat those patients aggressively to prevent the development of septic MOF. In the prevention and treatment of septic MOF, the blood purification has been found to be very effective. Among the blood purifications, continuous blood purification, such as continuous hemodiafiltration (CHDF) should be chosen for this purpose. CHDF has been claimed to be very effective to removal of causative humoral mediators from the blood stream. The concept of DIC has been changed recently and the concept of DII (disseminated intravascular inflammation) should be applied instead of DIC, since the main feature of this pathologic condition is the damage of endothelial cells due to extensive systemic inflammation.
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PMID:[Prevention and treatment of postoperative septic MOF and DIC and efficacy of blood purification]. 903 85

Antithrombin (AT) is a single-chain glycoprotein in plasma and belongs to the family of the serpins. It is synthesized in liver parenchymal cells, and its plasma concentration is between 112-140 mg/L. AT is a unique inhibitor of the clotting system and neutralizes most of the enzymes generated during activation of the clotting cascade, especially thrombin, factors Xa and IXa. Equimolar, irreversible complexes are formed between AT and the enzymes. The interaction between AT and the activated clotting factors is at least 1,000-fold increased in the presence of heparins. Heparins bind to multiple sites of the AT molecule resulting in a steric reconfiguration. Heparins contain a specific pentasaccharide unit which is the minimum requirement for AT binding. The glycosaminoglycan (GAG) heparan sulfate found on endothelial cell surfaces also contains this pentasaccharide and can thus "activate" AT. It is believed that much of the physiological inactivation of enzymes by AT occurs on the endothelium, mediated by heparan sulfate. The binding of AT to the GAGs also releases prostacyclin which possesses strong antiinflammatory properties. Deficiencies of AT are inherited or acquired. Only acquired defects due to increased consumption are discussed, most notably AT in DIC, especially DIC in sepsis. During acute DIC, clotting factors and inhibitors are consumed faster than they can be reproduced. This consumption of AT is of great significance in DIC and sepsis, and plasma AT levels predict outcome. AT levels drop early in sepsis and laboratory signs of DIC can already be found in patients with SIRS and early sepsis. The important role of AT in DIC and sepsis is the basis for considering antithrombin concentrates as an additional therapeutic modality.
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PMID:Antithrombin: its physiological importance and role in DIC. 951 76

The prognosis of extensively burned patients is dependent upon the presence of sepsis. The more extensive the burns, the more likely patients are to become septic. Although recently the frequency of burn wound sepsis has been decreased due to the early excision of necrotic tissue, that of sepsis resulting from respiratory tract infection has increased. Staphylococcus aureus (methicillin-resistant S. aureus) and Pseudomonas aeruginosav are the agents most likely to cause infections. Sepsis syndrome also results from bacterial translocation (BT), in which gut bacteria and/or endotoxins are thought to enter the portal bloodstream and/or lymphosystem. The pathophysiological mechanism of sepsis is the increased release of inflammatory mediators and resulting imbalances between these substances and their antagonists. In cases of severe sepsis, the sequelae of the imbalance between inflammatory mediators and their antagonists can lead to endothelial injury, DIC, and finally MODS. Strategies against the occurrence of sepsis include hospital-wide infection control measures, blockage of infection routes, and administration of antibiotics. The early initiation of nutritional management, preferably by the enteral route, to enhance immune system function and minimize the occurrence of BT is recommended. Several drugs to control inflammatory mediator release are currently under development and are expected to be used clinically in future.
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PMID:[Sepsis in extensive burned patients]. 954 45

Systemic inflammatory response syndrome(SIRS) is a pathologic condition associated with infection and tissue injury and it frequently leads to multiple organ dysfunction syndrome and disseminated intravascular coagulation(DIC). Pathologic events observed in SIRS can be attributable to the actions of cytokines such as tumor necrosis factor-alpha(TNF-alpha) and interleukin-1 beta. These cytokines activate monocytes and endothelial cells to induce the expression of tissue factor on their cell surfaces. Tissue factor then activates the extrinsic pathway of the coagulation system to induce microthrombus formation. These cytokines also contribute to microthrombus formation by decreasing the endothelial expression of thrombomodulin and glycosaminoglycans that regulate the coagulation system. Consequently, these cytokines induce DIC. These cytokines can activate neutrophils to release various inflammatory mediators which are capable of damaging the endothelial cell. The resultant endothelial cell injury, together with the microthrombus formation, may lead to microcirculatory disturbance which plays a role in ischemic organ dysfunction. Although physiological anticoagulants such as antithrombin and activated protein C can prevent endothelial cell injury by inhibiting leukocyte activation, heparin does not. Thus, these anticoagulants except for heparin may be effective in treating DIC associated with SIRS.
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PMID:[SIRS and the coagulation of normality]. 1089 68

The serine-protease-inhibitor antithrombin III (AT III) has often been recommended for the therapy of septic patients as it provides anticoagulant and antiinflammatory actions. In animal studies the prophylactic treatment with AT III in a dose > 250 U/kg prevented the development of disseminated intravascular coagulopathy and vital organ dysfunction during sepsis and lowered the mortality rate. In clinical studies with septic patients therapy usually was started several hours after the start of the disease in dosages much lower than those used in animal studies. In these patients AT III-therapy improved laboratory changes of disseminated intravascular coagulopathy but was unable to lower the mortality rate. Hereditary AT III deficiency, lack of heparin effect due to low AT III levels, disseminated intravascular coagulation disorders are indications for the use of AT III while beneficial effects of AT III in patients suffering from SIRS, sepsis or septic shock have not yet been demonstrated.
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PMID:[Are there certified indications for the use of antithrombin III in intensive care]. 1132 45

Sepsis or its synonymously termed "SIRS (systemic inflammatory response syndrome)" is a common cause of individual morbidity and mortality in various clinical situations. In such conditions, high mobility group box-1 DNA binding protein (HMGB1), widely known as a nuclear structural protein, has been identified to act as a late mediator of delayed endotoxin lethality. Once released from necrotic damaged cells or secreted by activated monocytes/macrophage, it participates in the development of lethality and it activates downstream cytokine release. In this review, we describe herein the general features of sepsis focusing on the role of HMGB1 in the mechanism of development of systemic inflammation, and also introduce newly established therapeutic concept "Functional HMGB1 inhibition with thrombomodulin" against sepsis/SIRS/DIC.
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PMID:[Inflammation and its regulatory system]. 1559 89

Clinical observations of Babesia canis infection in 63 dogs during a 1-year period are summarised, demonstrating the pathogenicity of the Babesia strain endemic in Hungary. Most patients had babesiosis in the spring and autumn, correlating with the seasonal activity of ticks. Male animals appeared in higher numbers, probably due to an overrepresentation of outdoor dogs. Uncomplicated babesiosis was diagnosed in 32 cases. The disease affected dogs of any age in this study. Symptoms were similar to those published from other parts of the world: lethargy, fever, splenomegaly, pallor, icterus, haemoglobinuria and presence of ticks were the most common observations. Thrombocytopenia, lymphopenia and neutropenia were frequent haemogram changes. Imidocarb appeared to be highly effective in eliminating the Babesia infection. Thirty-one animals demonstrated babesiosis with complications. Most Rottweilers (7/9) developed complicated disease. Old age was a risk factor for multiple complications. Multiple organ manifestations had poor prognosis. Hepatopathy (44%), pancreatitis (33%), acute renal failure (ARF; 31%) and disseminated intravascular coagulation (DIC; 24%) were frequent complications, while immune-mediated haemolytic anaemia (IMHA; 10%), acute respiratory distress syndrome (ARDS; 6%) and cerebral babesiosis (3%) were rarely observed. There was a significant difference between the mean age of dogs having uncomplicated disease, babesiosis with a single complication and babesiosis with multiple complications (3.4, 4.8 and 8.6 years, respectively, p < 0.001). The recovery rate (78, 68 and 25%, respectively, p = 0.005) and mortality rate (3, 21 and 67%, respectively, p < 0.001) also tended to differ significantly in these groups. Systemic inflammatory response syndrome (SIRS) and DIC are two possible pathways leading to multiple organ dysfunction syndrome (MODS) in babesiosis. DIC was found to predict MODS more sensitively in this study than SIRS: there were 6 animals developing MODS out of 11 identified with DIC, while only 5 dogs developed MODS out of 22 having SIRS.
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PMID:Clinical manifestations of canine babesiosis in Hungary (63 cases). 1702 Jan 40