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Query: UMLS:C0243026 (sepsis)
52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental gram-negative sepsis was induced in the rat by Klebsiella pneumoniae. Although bacteria are susceptible to the treatment with the antibiotic Tobramycin, DIC could not be prevented. DIC was manifested by a leuko- and thrombocytopenia, decreases in fibrinogen and AT III and an increase of the aPTT. In this model the therapeutic treatment with human AT III was evaluated. To determine the optimal concentration of AT III a prestudy in a LPS induced DIC in the rat was performed. It was shown that a bolus i.v. injection of 500 U/kg improved survival and DIC, and was thus chosen for the Klebsiella sepsis model. The infectious load was adjusted to yield a mortality rate of 90-100% in the untreated Klebsiella group and a reduction to about 40-50% of the mortality rate by Tobramycin. It was found that AT III reduced mortality in the Klebsiella induced sepsis not only when given prophylactically but was effective even when administrated in a late stage of the DIC, i.e. 3 or 5 h post infection.
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PMID:Reduction of mortality with antithrombin III in septicemic rats: a study of Klebsiella pneumoniae induced sepsis. 845 37

This review presents the rationale for and main results of coagulation inhibitor substitution during experimental and human sepsis. Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficiency of biologically active C1-Inh. Substitution with concentrations of C1-Inh has been safely performed and preliminary results are consistent with a possible beneficial effect on hypotension and vasopressor requirement in septic shock. The extrinsic pathway is the main initial coagulation process involved in sepsis-induced DIC. Endothelial and monocyte generation of tissue factor (TF) is activated by bacterial products and endotoxin. Activation of TF is counteracted by a specific tissue factor pathway inhibitor (TFPI). The potential for TFPI substitution to inhibit the activation of the coagulation cascade in sepsis requires further study. Thrombin generation is inhibited by antithrombin III (AT III) and the protein C-protein S system. During sepsis, AT III is consumed and degraded by elastase. Animal studies have shown that DIC and death were prevented by high doses of AT III concentrates. Although a significant reduction in the duration of biological symptoms of DIC has been reported in most human studies, the usefulness of AT III substitution in human sepsis is still debated. None of the studies was able to document a statistically significant reduction in mortality. Protein C is activated by thrombomodulin and, with its cofactor protein S, inhibits factors Va and VIIIa. The free level of protein S depends on the level of the C4b binding protein (C4bBP), an acute-phase complement regulatory protein. During sepsis, protein C activity is significantly reduced, either by acute consumption or by thrombomodulin down-regulation, and increased levels of plasma C4bBP inhibit protein S. Infusion of activated protein C and protein S substitution both protect animals from the lethal effects of bacteria. Combining these different coagulation inhibitors should be carefully studied before its use in septic patients is recommended.
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PMID:Coagulation inhibitor substitution during sepsis. 863 34

We report two cases of sepsis and meningoencephalitis with listeriosis. They died in despite of administering sensitive antibiotics. A 2 day old girl was admitted to our hospital because of fever and cyanosis. Listeria monocytogenes type 4b was cultured from blood, CSF, throat, urine, ear. She was treated with twice exchange transfusion and sensitive antibiotics (ABPC, TOB), but died from DIC. A 48 year old man suddenly experienced an unconscious condition. A CSF culture grew L. monocytogenes type 1/2a. He was treated with sensitive antibiotics (ABPC, CEZ etc), but went bad conditions. Listeria infection of this cases developed as unfortunate infection.
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PMID:[Two cases of Listeria monocytogenes infection in Osaka Municipal Hospital]. 874 12

Prediction of outcome of acute renal failure (ARF), particularly in patients with multisystem organ failure (MSOF), is a very important issue and a very difficult task. In patients with ARF as a consequence of severe polytrauma, frequent complications (e.g., sepsis, respiratory insufficiency, DIC, hepatic insufficiency, etc.) contribute to a hyperbolic state, and in the case of synergistic action, they start the mechanism of MSOF. In 33 patients (1 female, 32 male, 38.61 +/- 8.79 years) with severe polytrauma acquired in war combat, ARF developed requiring hemodialysis (HD) treatment. Seventeen out of 33 (51.4%) recovered renal function. In 12 out of 33 patients, MSOF occurred with less successful recovery results. The analysis of pathophysiologic mechanisms of MSOF appearance and ARF outcome has shown the importance of blast injuries, bowel injury, respiratory insufficiency requiring assisted ventilation, and sepsis. Although severe hemorrhage and shock are the common mechanism of ARF appearance in these patients, it seems that wounds by themselves can be of great importance, as abdominal wounds are more frequently associated with ARF and MSOF than in other types.
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PMID:Acute renal failure in polytraumatized patients: prediction of outcome. 887 86

Melanoma is rare in Singapore with an age-standardised rate (ASR) of 0.4-0.8 per 100,000 per year. Thirteen patients with metastatic or locally advanced melanoma were referred to the Department of Medical Oncology, Singapore General Hospital between Feb 1991 and Nov 1993. Ten patients were given combination chemotherapy comprising carmustine (BCNU), cisplatin, dacarbazine (DTIC) and tamoxifen. The remaining 3 patients either rejected chemotherapy or were too ill to receive chemotherapy. Patient characteristics were as follows: there were 6 males and 4 females; age range 29-75 years; all were Chinese; sites of primary disease: extremities 8, retroorbital 1, vagina 1; sites of metastases: lymph nodes 6, skin 2, pulmonary 3, liver 1. All received the same combination chemotherapy comprising iv BCNU 150 mg/m2 q8wk, iv DTIC 220 mg/m2 x 3 days q4 wk, iv cisplatin 25 mg/m2 x 3 days q4 wk and tab tamoxifen 40 mg daily. There were 6 partial responses and no complete responses, giving a response rate of 60% with a median survival of 11.5 months. Three patients with sites of disease in the vagina, retroorbital region and metastatic liver disease had progressive disease despite chemotherapy and one died of treatment related sepsis. The 6 responders include those with metastases to the skin, nodes and/or lung. Treatment was generally tolerable. Two patients experienced delays of their subsequent cycles of treatment by 1-2 weeks due either to neutropenia and/or thrombocytopenia. This regimen is a fairly active combination against metastatic melanoma, particularly those with metastases to the nodes, skin and the lung. Those with involvement of other sites tend to respond poorly.
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PMID:Combination chemotherapy (dacarbazine, carmustine, cisplastin, and tamoxifen) in advanced melanoma. 894 55

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

1.286 patients were diagnosed as DIC, among 123.231 patients who were admitted in the 285 departments of the university hospitals in Japan, in 1992. The incidence of DIC was high in acute promyelocytic leukemia, fulminant hepatitis, abruptio placentae, acute respiratory distress syndrome, and sepsis. In cases of DIC, bleeding tendency due to consumption coagulopathy is most important, but organ dysfunction due to circulatory disturbances by development of multiple thrombi is also noteworthy. As a whole, DIC may be divided in two types. The first type is cases of DIC with severe bleeding symptoms. However, except cerebral hemorrhage, organ dysfunction is rare in these cases. These cases may be called as "fibrinolysis-dominant DIC", because hemostatic thrombi as well as thrombi which cause organ dysfunction by circulatory disturbances are rapidly removed by abnormally enhanced fibrinolysis. The second type involves cases of DIC with severe organ dysfunction. Bleeding symptoms in these cases are usually not severe. These cases may be called as "coagulation-dominant DIC". The most typical causative disease of the fibrinolysis-dominant DIC is acute promyelocytic leukemia. The most typical causative disease of the coagulation-dominant DIC is sepsis. The presence of causative disease of DIC, elevation of FDP, and depletion of platelet count are most important to diagnose DIC. In the treatment of DIC, removal of cause of DIC, administration of heparin to protect further development of multiple thrombi, and replacement of platelets in cases of acute leukemia are most important.
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PMID:Clinical aspects of DIC--disseminated intravascular coagulation. 911 31

The etiology of acute pancreatitis is based on several causes, among which idiopathic nature (< 30%) is second to biliary stone disease (60-70%). It is still under debate whether alcohol as the main cause of chronic pancreatitic disease can cause acute pancreatitis. Based on Opie's "obstruction theory" of 1901 and experimental data, it is now widely accepted that the gallstone passage into or through the terminal biliopancreatic ductal system triggers acute (necrotizing) pancreatitis by causing pancreatic ductal obstruction. However, the sequential intracellular mechanisms in the pathogenesis of acute pancreatitis remain unclear. A co-localization hypothesis has been proposed to explain the premature intracellular activation of trypsinogen to trypsin: due to a yet unknown defect in the intracellular protein transport and sorting system within the acinar cell, lysosomal hydrolases (i.e. cathepsin B) and secretory proteins (i.e. trypsinogen) co-localize in a fragile postgolgi vacuole where activation can occur. In addition, alterations of exo- and endocytosis at the apical pole exist (i.e. secretion block). The pathophysiological events are characterized by local and systemic hypovolemia and (micro)circulatory failure aggravating necrosis, followed by ARDS, renal failure and several other severe complications (i.e. sepsis and DIC). The systemic overflow of proteolytic enzymes (i.e. PLA-2) and kinins plays a major role as mediating factor in severe cases, resulting in multiorgan failure.
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PMID:[Etiology, pathogenesis and pathophysiology of acute pancreatitis]. 928 10

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


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