REVIEWS
Published 2015-10-10
Keywords
- SEPSIS,
- POLYMORPHISM,
- GENETIC PREDISPOSITION,
- GENETIC VARIATION,
- GENE
How to Cite
Sergeev, S., Strunin, O., & Litasova, Y. (2015). Role of genetic polymorphism in the development of sepsis in infants. Patologiya Krovoobrashcheniya I Kardiokhirurgiya, 17(4), 59–62. https://doi.org/10.21688/1681-3472-2013-4-59-62
Copyright (c) 2013 Sergeev S.A., Strunin O.V., Litasova Ye.Ye.

This work is licensed under a Creative Commons Attribution 4.0 International License.
Abstract
Sepsis and its consequences continue to be a major cause of morbidity and mortality in the intensive care unit (ICU). The evidence that endogenous mediators actually mediate an individual response to the infection has led to the development of different approaches to assess the impact of each person on the course of the disease. The role of the genetic background and the susceptibility to human inflammatory response amplitude are determined by the variability of the genes encoding endogenous mediators which are produced during inflammation. Pro-and anti-inflammatory reactions influence the susceptibility and the outcomes in patients with sepsis and systemic inflammation. Thus, all genes encoding proteins involved in the transduction of inflammatory genes are candidates for detection of a human's genetic background responsible for the difference in interpersonal systemic inflammatory reaction.References
- Ziegeler S., Tsusaki B.E. et al. // Anest. 2003. V. 99. P. 212-219.
- Members of the American College of Chest Physicians // Crit. Care Med. 1992. V. 20. P. 864-874.
- Angus D.C., Linde-Zwirble W.T., Lidicker J. // Crit. Care Med. 2001. V. 29. P. 1303-1310.
- Martin G.S., Mannino D.M., Eaton S. et al. // N. Engl. J. Med. 2003. V. 348. P. 1546-1554.
- Ефремов А.В., Березикова Е.Н., Шилов С.Н. и др. // Патология кровообращения и кардиохирургия. 2011. Т. 3. С. 63-66.
- Cohen J. // Nature. 2002. V. 420. P. 885-891.
- Wong H.R., Shanley T.P. Genetic Basis of Acute Lung Injury. New York, 2007.
- Sorensen T.I., Nielsen G.G., Andersen P.K. et al. // N. Engl. J. Med. 1988. V. 318 (12). P. 727-732.
- Arbour N.C., Lorenz E., Schutte B.C. et al. // Nat. Genet. 2000. V. 25 (2). P. 187-191.
- Allen A., Obaro S., Bojang K. et al. // Pediatr. Infect. Dis. J. 2003. V. 22 (11). P. 1018-1019.
- Holmes C.L., Russell J.A., Walley K.R. // Chest. 2003. V. 124 (3). P. 1103-1115.
- Stuber F., Klaschik S., Lehmann L.E. et al. // Clin. Infect. Dis. 2005. V. 41 (Suppl. 7). P. 416-420.
- Van Deventer S.J. // Intensive Care Med. 2000. V. 26 (Suppl. 1). P. 98-102.
- Odwyer M. et al. // Crit. Care. 2007. V. 11 (Suppl. 2). P. 448.
- Michalek J., Svetlikova P., Fedora M. et al. // Intensive Care Med. 2007. V. 33 (12). P. 2158-2164.
- Knoell D.L., Julian M.W., Bao S. et al. // Crit. Care Med. 2009. V. 37 (4). P. 1380-1388.
- Прохорова Д.С., Нарциссова Г.П., Горбатых Ю.Н., Синельников Ю.С., Субботин Д.В. // Патология кровообращения и кардиохирургия. 2011. № 2. С. 17-20.