Genetic Polymorphism and the Rate of Development of Complications in Pneumonia of Varying Genesis

Objective: to study the genetic polymorphism of the genes of phase I and II xenobiotic detoxification (GSTM1, GSTP1, GSTT1, CYP1A1), as well as ACE, CCR5, MTHFR, and those of the cytokines IL-6 and TNF-a to reveal hereditary predisposition to pneumonia of varying genesis and its complications. Mater...

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Published inObshchai͡a︡ reanimatologii͡a Vol. 7; no. 2; p. 10
Main Authors Smelaya, T. V., Salnikova, L. Ye, Moroz, V. V., Golubev, A. M., Zarzhetsky, Yu. V., Rubanovich, A. V.
Format Journal Article
LanguageEnglish
Published Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russia 20.04.2011
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Summary:Objective: to study the genetic polymorphism of the genes of phase I and II xenobiotic detoxification (GSTM1, GSTP1, GSTT1, CYP1A1), as well as ACE, CCR5, MTHFR, and those of the cytokines IL-6 and TNF-a to reveal hereditary predisposition to pneumonia of varying genesis and its complications. Materials and methods. The frequency of the allele variants of 7 genes was studied in the groups of patients with pneumonia (n=524) and healthy donors (a control group (n=178). Results. There were are genotypes associated with predisposition to community-acquired and nosocomial pneumonia (CAP and NP): GSTM I*, CYP1A1 606T/T, ACE D/D and those associated with a higher risk for complicated CAP. There were effects of the allelic variants of the ACE gene in developing complications, such as acute respiratory distress syndrome, multiple organ dysfunction, and sepsis: ACEI/I insertion homozygotes linked to survival and the alternative ACE D/D genotype to mortality. Conclusion: The study revealed an association of detoxification gene polymorphism with predisposition to CAP and NP and with the development of complications in CAP. Key words: xenobiotic detoxification genes, key ACE renin-angiotensin system gene, chemokine receptor 5 (CCR5) gene, pneumonia, acute respiratory distress syndrome, sepsis, multiple organ dysfunction.
ISSN:1813-9779
2411-7110
DOI:10.15360/1813-9779-2011-2-10