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Response

Journal of Perinatology volume 24, page 801 (2004)Cite this article

We appreciate the comments of Drs. Cooke, Drury, Beresford and Shaw regarding our recently published investigation.1 They also compared the 105 ile/ile polymorphism of the glutathione-S-transferase-P1 (GSTP1) gene in premature newborns with chronic lung disease (CLD). As they described for their study of 174 Caucasian infants, the distribution of the GSTP1 genotypes did not differ between control premature newborns and those who developed CLD (p=0.09). Comparatively, we found a significant difference in the distribution of GSTP1 genotypes (p<0.05) with the CLD cases less likely to possess the more efficient val/val homozygote genotype (OR 0.21, 95% CI: 0.045–0.95, p=0.04).

When compared with our control sample, the distribution of GSTP1 genotypes in Cooke et al.'s control group approached, but did not reach statistical difference (p=0.07). However, the two patient populations did differ in several important aspects. As mentioned, the control group for Cooke's evaluation contained “similar” premature newborns, raising the possibility that the distribution of the GSTP1 polymorphism is altered in all premature newborns. While the majority (∼90%) of our patient population was African American, Cooke's population was 100% Caucasian. Furthermore, the percentage of val/val homozygotes in our control sample (23%) was significantly higher than the 10% val/val homozygotes found in the control group of Cooke et al. (p=0.04).

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References

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Authors and Affiliations

  1. Emory University School of Medicine, Pediatrics: Neonatology, 2040 Ridgewood Drive, Atlanta, 30322, GA, USA

    Theresa W Gauthier MD, Martha H Manar MD, Milton R Brown PhD & Lou Ann S Brown PhD

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  1. Theresa W Gauthier MD
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  2. Martha H Manar MD
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  3. Milton R Brown PhD
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  4. Lou Ann S Brown PhD
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Gauthier, T., Manar, M., Brown, M. et al. Response. J Perinatol 24, 801 (2004). https://doi.org/10.1038/sj.jp.7211169

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