Sepsis andintravascular thrombosis
نویسنده
چکیده
1 Gedde-Dahl TW, Bjark P, H0iby EA, H0st JH, Brunn JN. Severity of meningococcal disease: assessment by factors and scores and implications for patient management. Rev InfectDis 1990; 12:973-91. 2 Ferguson JH, Chapman OD. Fulminating meningococcic infections and the so-called Waterhouse-Friderichsen syndrome. Am J Pathol 1947; 24: 76395. 3 Margaretten W, McAdams AJ. An appraisal of fulminant meningococcemia with reference to the Shwartzmann phenomenon.AmJMed 1958; 25: 868-76. 4 Colman RW, Robboy SJ, Minna JD. Disseminated intravascular coagulation (DIC): an approach. AmJ Med 1972; 52: 679-89. 5 Evans RW, Glick B, Kimball F, Lobell M. Fatal intravascular consumption coagulopathy in meningococcal sepsis. AmJ Med 1%9; 46: 910-8. 6 McGehee WG, Rapaport SI, Hjort PF. Intravascular coagulation in filminant meningococcemia. Amn Intern Med 1%7; 67: 250-60. 7 Gimbrone MA. Vascular endothelium: nature's blood container. In: Gimbrone MA, ed. Endothelium in hemostasis and thrombosis. Edinburgh: Churchill Livingstone, 1986: 1-12. 8 Bone RC. Modulators of coagulation: a critical appraisal of their role in sepsis. Arch InternMed 1992; 152: 1381-9. 9 Renesto P, Kadiri C, Chignard M. Combined activation of platelets by cathepsin G and platelet activating factor, two neutrophil-derived agonists. BrJ Haematol 1992; 80: 205-13. 10 Brandtzaeg P, Jo0 G, Brusletto B, Kiemrf P. Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease. Thromb Res 1990; 57: 271-8. 11 Luacher EF. Activated leukocytes and the hemostatic system. Rev Infect Dis 1987; 9 (suppl 5): S546-52. 12 Fourrier F, Lestavel P, Chopin C, et al. Meningococcemia and purpura fulminans in adults: acute deficiencies ofproteins C and S and early treatment with antithrombin III concentrates. Intensive CareMedicine 1990; 16: 121-4. 13 Heyderman RS, Klein NJ, Shennan GI, Levin M. Deficiency of prostacyclin production in meningococcal shock. Arch Dis Child 1991; 66: 1296-9. 14 Heyderman RS, Klein NJ, Shennan GI, Levin M. Modulation of the anticoagulant properties ofglycosaminoglycans on the surface of the vascular endothelium by endotoxin and neutrophils: evaluation by an amidolytic assay. Thromb Res 1992; 67: 677-85. 15 van der Poll T, Buller HR, ten Cate H, et al. Activation of coagulation after administration of tumor necrosis factor to normal subjects. N Engi J Med 1990; 322: 1621-7. 16 Girardin E, Grau GE, Dayer J-M, et al. Tumour necrosis factor and interleukin-1 in the serum ofchildren with severe infectious purpura. N Engl J'Med 1988; 319: 397-400. 17 Wachtfogel YT, Abrams W, Kuccich U, Weinbaum G, Schapira M, Colman RW. Fibronectin degradation products contsining the cytoadhesive tetrapeptide stimulate human neutrophil degranulation. J Clin Invest 1988; 81: 1310-6. 18 Jafari HS, McCracken GH. Sepsis and septic shock: a review for clinicians. Pediatr Infect DisJ 1992; 11: 739-49. 19 Glynn MFX, Silver E, Redmond MD. A randomised trial of cryoprecipitate replacement offibronectin deficiencies in the critically ill. AmRev Respir Dis 1984; 129: A102. 20 Lundsgaard-Hansen P, Doran JE, Rubli E, et al. Purified fibronectin administration to patients with severe abdominal infections: a controlled trial. Ann Swrg 1985; 202: 745-9. 21 Braude Al, Douglas H, Davis CE. Treatment and prevention of intravascular coagulation with antiserum to endotoxin.JInfectDis 1973; 128: S15744. 22 Corrigan JJ, Ray WL, May N. Changes in the blood coagulation system associated with septicemia. NEnglJMed 1968; 279: 851-6. 23 Gerard P, Moriau M, Bachy A, Malvaux P, De Meyer R. Meningococcal purpura: report of 19 patients treated with heparin. J Pediair 1973; 82: 780-6. 24 Zhang CW, Xie WM, Li YF, He ML, Wang ND, Yue JS. Estimation of free heparin in blood and observation of the therapeutic effect of protamine in epidemic hemorrhagic fever. ChungHua NeiKo Tsa Chih 1981; 20: 711-5. 25 Klein N, Shennan G, Heyderman R, Levin M. Alteration in glycosaminoglycan metabolism and urface charge on human umbilical vein endothelial cells induced by cytokines, endotoxin and neutrophils. J Cell Sci 1992; 102: 821-32. 26 Ditter H, Matthias FR, Voss R, Lohmann E. Beneficial effects of prostacyclin in a rabbit endotoxin shock model. Thromb Res 1988; 51: 403-15. 27 Nava E, Palmer RMJ, Moncada S. Inhibition of nitric oxide synthesis in septic shock: how much is beneficial? Lancet 1991; 338: 1555-7. 28 Taylor FJ, Chang A, RufW, et al. Lethal E coli septic shock is prevented by blocking tissue factor with monoclonal antibody. Circ Shock 1991; 33: 12734. 29 Angelini GD, Cooper GJ, Lamarra M, Bryan AJ. Unorthodox use of aprotinin to control iife-threatening bleeding after cardiopulmonary bypass. Lancet 1990; 335:799-800.
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