Role of angiotensin-converting enzyme gene polymorphisms in children with sepsis and septic shock

Background: Sepsis is characterized by a systemic inflammatory response. Its development and outcome are associated with host defense, pathogenicity of the microorganism and genetic polymorphisms. Genetic polymorphisms of the immune system genes have been shown to have a close relationship with the...

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Bibliographic Details
Published in:Pediatrics international 2008-08, Vol.50 (4), p.477-480
Main Authors: Cogulu, Ozgur, Onay, Huseyin, Uzunkaya, Demet, Gunduz, Cumhur, Pehlivan, Sacide, Vardar, Fadil, Atlihan, Fusun, Ozkinay, Cihangir, Ozkinay, Ferda
Format: Article
Language:English
Subjects:
angiotensin-converting enzyme
Blood diseases
Child
Child, Preschool
children
Female
gene expression
Genetics
Genotype & phenotype
Humans
Infant
Infant, Newborn
Inflammatory diseases
Male
Pediatrics
Peptidyl-Dipeptidase A - genetics
Polymorphism, Genetic
Risk factors
sepsis
Sepsis - genetics
Shock, Septic - genetics
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Summary:Background: Sepsis is characterized by a systemic inflammatory response. Its development and outcome are associated with host defense, pathogenicity of the microorganism and genetic polymorphisms. Genetic polymorphisms of the immune system genes have been shown to have a close relationship with the clinical outcomes of sepsis. Angiotensin‐converting enzyme (ACE) plays a major role in the host defense against invading pathogens. It is therefore likely that polymorphisms in the ACE gene may have an important effect on determining the development and the outcome of sepsis. Methods: Ninety‐eight children diagnosed as having sepsis and 287 healthy children were included in the study. Insertion/deletion polymorphisms were analyzed using reverse‐hybridization assay. Results: The carriers of I allele (D/I genotype and I/I genotype) were found to have an increased risk of developing sepsis compared to the controls. Conclusion: DD genotype may play a positive role against the development of sepsis in healthy children.
ISSN:1328-8067
1442-200X
DOI:10.1111/j.1442-200X.2008.02583.x