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Sepsis ve İnflamasyon Mediatörleri

Sepsis and inflammatory mediators

Journal Name:

  • İnönü Üniversitesi Tıp Fakültesi Dergisi

Publication Year:

  • 1996

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
Septicemia and septic shock are dramatic clinical syndromes which result from acute invasion of the bloodstream by certain microorganisms or their toxic products. The clinical manifestations of septicemia and septic shock are the result of an interplay between microbial products and host mediator systems. Sepsis provokes a neuroendocrine and inflammatory response to promote survival. A variety of host mediators have been implicated in the pathogenesis of septic shock including active metabolites of the complement, kinin, and coagulation systems as well as factors released from stimulated cells, particularly, the cytokines. From the standpoint of vascular perfusion and organ function a vicious circle is established that results in altered blood flow in the microcirculation and progressive injury to the capillary endothelium and tissue. Now, all of the cytokines are not identified thus far, TNFcc appears to be the most potent mediator the pathophsiology of the sepsis syndrome. In addition, other many inflammatory mediators have been identified as inflammatoy factors in sepsis. It is also likely that in the near future we will be able to take advantage of the recent developments in molecular biology and a better understanding of the pathogenesis of the septic process. [Journal of Turgut Özal Medical Center 1996;3(4):374-381]
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Abstract (Original Language): 
Sepsis ve septik şok; bazı mikroorganizmaların veya bu organizmaların toksik ürünlerinin akut olarak kan dolaşımı ile yay ılımı sonucunda gelişen dramatik bir klinik tablodur. Bu tablonun klinik bulguları mikroorganizma ve ürünleri ile konakçının medyatör sistemleri arasındaki mücadelenin bir sonucudur. Sepsis konakçının nöroendokrin, immün ve inflamatuar sistemlerini uyarır ve bu cevabın şiddeti de klinik seyri belirler. Septik şokun patogenezini; konakçı mediatörlerinin bir bölümü; kompleman, kinin, koagülasyon sistemlerinin aktif metabolitleri ve özellikle sitokinler oluşturur. Kapiller endoteldeki ve dokudaki sürekli zedelenme, mikrosirkülasyondaki kan akımı değişikliği, vasküler perfüzyonun durumu ve organ fonksiyonlarındaki kısır döngüyü belirler. Günümüzde sitokinlerin tamamı ayrıştır ilam am ıştır, ancak TNF anın sepsis sendromu patofizyoloj"isinde en potent mediator olduğu açıktır. Ayrıca diğer pekçok inflamatuar mediatörün de sepsiste rol aldığı tespit edilmiştir. Muhtemelen yakın bir gelecekte mole kül er biyolojideki yeni gelişmeler sonucunda septik sürecin patogenezini daha iyi anlayabileceğiz. Bu da yeni tedavi yaklaşımları oluşturmamızı sağlayacaktır. [Turgut Özal Tıp Merkezi Dergisi 1996;3(4):374-381]
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  • 4
374-381
  • Turkish

REFERENCES

References: 

1. American Collage of Chest Physicions/Society of Critical Care Medicine Consensus Conference Committee Deffinitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20: 864-74
2. Bone RC. The pathogenesis of sepsis. Ann Intern Med 1991; 115: 457-69.
3. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis: Chest 1992; 110: 1644-55.
4. Banerjee SN, Emori TG, Culver DH, et al. Secular trends in nasocomial primary bloodstream infections in the United States, 1980-1989. Am J Med 1991; 91(Suppl 3B): 86-9.
5. Wolff SM, Bennett JV. Gram negative rod bacteremia (editorial). N Engl J Med 1974; 291: 733.
6. Centers for Disease Control and Prevention. Increase in National hospital discharge survey rates for septicemia-United States, 1979-1987. MMWR 1990; 39:31-4.
7. Istorico-Sanders LJ, Cobbs CG. Gram-negative bacteremia and the sepsis syndrome. In: Stein JH (ed), Internal
Medicine, 4. Edition. Mosby-Year Book Inc, 1994; 1941¬52.
8. McCabe WR and Jackson GG. Gram-negative bacteremia,
Arch Intern Med 1962; 110:83.
9. Balk RA, Parrillo JE. Septic shock: clinical syndrome, management, outcome, and sequelae. In:.Fishman AP (ed),
McGrave-Hill Inc. 1992;185-97.
10. Krager BE, Groven DE, McCabe WR. Gram-negative bacteremia. 4. reevalution of clinical features and
thereatment in 612 Patients. Am J Med 1980; 68:344.
11. Harris RL, Musher DM, Bloom K. Manifestations of sepsis.
Arch Intern Med 1987; 147: 185-96.
12. Young LS, Proctor Ra, Beutler B, et al. University of California/Davis inter-departmental conference on Gram-negative septicemia. Rev Infect Dis 1991; 13: 666-87.
13. Young LS. Sepsis syndrome. In: Mandell GL, Bennett JE, Dolin R, Ed(s). Infectious Diseases; 4th ed. Churchill
Livingstone 1995; 690-704.
14. Michie HR, Manogue KR, Spriggs DR, et al. Detection of
circulation tumor necrosis factor after endotoxin
administration. N Engl J Med 1988; 318:1481-6.
15. Blick M, Sherwin SA, Rosenblum M, et al. Phase I study of recombinant TNF in cancer patients. Cancer Res 1987;
47:2986-9.
16. Tracey KJ, Frong Y, Hesse DG, et al. Anti-cahectin/TNF monoklonal antibodies prevent septic shock during lethal
bacteremia. Nature 1987; 330; 662-4.
17. Aderka D, Le J, Vilcek J. IL6 inhibits lipopolysaccharide-induced TNF production in cultured human monocytes,
U937 cells and in mice. J Immunol 1989; 143:3517-23.
18. Cannon JG. Cytokines and shock. In: Kimball ES, Ed. Cytokines and Inflammation. Boca Raton: CRC Press:
1991; 307-29.
19. De Waal MR, Abrams J, Bennet B, et al. Interleukin 10
inhibits cytokine syntesia by human monocytes: an autoregulatory role of IL-10 produced by monocytes. J Exp
Med 1991; 174:1209-20.
20. Jaffe HS, Sherwin SA. Immunomodulators. In: Stites DP, Terr AI, (Ed)s. Basic and Clinical Immunolgy 7th edition.
Lange Medical Book 1992; 780-5.
21. Pepke-Zeba J, Higenbottom TW, Dinh-Xuan AT, et al.
Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmanary hypertention. Lancet 1991; 338:
11733-4.
22. Moncada S, Higgs A. The L-arginine-nitric oxide pathway.
N Engl J Med. 1993; 329:2002-12.
23. Hack CE, Ogilvie AC, Eisele B. Initial studies on the administration of C1-esterase inhibitor to patients with septic shock or with a vascular leak syndrome induced by
interleukin-2 therapy. Prog Clin Biol Res 1994; 388: 335¬57.

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