UNLABELLED: Bronchopulmonary dysplasia (BPD) remains as a major and increasing burden in Egypt. RATIONALE: To determine whether alleles of TNFα-238G > A affect the risk of BPD or the severity of BPD in preterm infants in Egypt. STUDY DESIGN: We prospectively genotyped 220 premature neonates (birth weight <1,500 g and gestational age 26-32 weeks) for the -238 polymorphism, and assessed the clinical risk factors for BPD in our study populations. Infants with BPD were mechanically ventilated. RESULTS: Infants who developed BPD (n = 120) had a younger gestational age (31.0 ± 2.1 weeks vs. 34.3 ± 1.5 weeks) and lower birth weight (1,490 ± 360 g vs. 1,880 ± 520 g) than infants who did not develop BPD (n = 100). Results of antenatal steroid supplementation, surfactant therapy, or sepsis might affect the genetic modulation of BPD. The -238G > A polymorphism was associated with a twofold risk of BPD (OR = 2.86; 95% confidence interval, 1.35-3.83). Despite the dominance of the G allele in the Egyptian population, the -238A allele was more common among infants with BPD (23%) than among infants without BPD (15%). The A allele occurred less often in infants with mild BPD (9%) than in infants with severe (39%) or moderate (52%). The AA genotype occurred in 15% of cases but in none of the controls. CONCLUSION: The TNFα -238G > A polymorphism-particularly the presence of an A allele-should be evaluated as a biomarker to predict the clinical outcome of preterm infants with BPD in Egypt. Even the presence of one copy of this mutant allele appears to be sufficient to influence the severity of disease.
UNLABELLED: Bronchopulmonary dysplasia (BPD) remains as a major and increasing burden in Egypt. RATIONALE: To determine whether alleles of TNFα-238G > A affect the risk of BPD or the severity of BPD in preterm infants in Egypt. STUDY DESIGN: We prospectively genotyped 220 premature neonates (birth weight <1,500 g and gestational age 26-32 weeks) for the -238 polymorphism, and assessed the clinical risk factors for BPD in our study populations. Infants with BPD were mechanically ventilated. RESULTS:Infants who developed BPD (n = 120) had a younger gestational age (31.0 ± 2.1 weeks vs. 34.3 ± 1.5 weeks) and lower birth weight (1,490 ± 360 g vs. 1,880 ± 520 g) than infants who did not develop BPD (n = 100). Results of antenatal steroid supplementation, surfactant therapy, or sepsis might affect the genetic modulation of BPD. The -238G > A polymorphism was associated with a twofold risk of BPD (OR = 2.86; 95% confidence interval, 1.35-3.83). Despite the dominance of the G allele in the Egyptian population, the -238A allele was more common among infants with BPD (23%) than among infants without BPD (15%). The A allele occurred less often in infants with mild BPD (9%) than in infants with severe (39%) or moderate (52%). The AA genotype occurred in 15% of cases but in none of the controls. CONCLUSION: The TNFα -238G > A polymorphism-particularly the presence of an A allele-should be evaluated as a biomarker to predict the clinical outcome of preterm infants with BPD in Egypt. Even the presence of one copy of this mutant allele appears to be sufficient to influence the severity of disease.
Authors: Felix Blume; Holger Kirsten; Peter Ahnert; Trinad Chakraborty; Arnd Gross; Katrin Horn; Mohammad Reza Toliat; Peter Nürnberg; Eva-Maria Westenfelder; Wolfgang Goepel; Markus Scholz Journal: Pediatr Res Date: 2021-08-31 Impact factor: 3.953