Journal
JOURNAL OF PEDIATRICS
Volume 158, Issue 5, Pages 745-751Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jpeds.2010.10.043
Keywords
-
Categories
Funding
- National Institute of Child Health and Human Development [P01 HD 13021, R01 HD 059140, U10 HD 027853]
- National Institute of Diabetes and Digestive and Kidney Diseases [R03 DK61596, P30 DK078392]
- Translational Research Initiative of Cincinnati Children's Research Foundation
Ask authors/readers for more resources
Objective To investigate secretor gene fucosyltransferase 2 (FUT2) polymorphism and secretor phenotype in relation to outcomes of prematurity. Study design Study infants were <= 32 weeks gestational age. Secretor genotype was determined from salivary DNA. Secretor phenotype was measured with H antigen, the carbohydrate produced by secretor gene enzymes, in saliva samples collected on day 9 +/- 5. The optimal predictive cutoff point in salivary H values was identified with Classification and Regression Tree analysis. Study outcomes were death, necrotizing enterocolitis (NEC, Bell's stage II/III), and confirmed sepsis. Results There were 410 study infants, 26 deaths, 30 cases of NEC, and 96 cases of sepsis. Analyzed by genotype, 13% of 95 infants who were non-secretors, 5% of 203 infants who were heterozygotes, and 2% of 96 infants who were secretor dominant died (P = .01). Analyzed by phenotype, 15% of 135 infants with low secretor phenotype died, compared with 2% of 248 infants with high secretor phenotype (predictive value = 76%, P < .001). Low secretor phenotype was associated (P < .05) with NEC, and non-secretor genotype was associated (P = .05) with gram negative sepsis. Secretor status remained significant after controlling for multiple clinical factors. Conclusions Secretor genotype and phenotype may provide strong predictive biomarkers of adverse outcomes in premature infants. (J Pediatr 2011; 158: 745-51).
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available