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Glutathion-S-Transferase P1 polymorphisms association with broncopulmonary dysplasia in preterm infants
P Karagianni1, D Rallis1, L Fidani2
12nd NICU and Neonatology Department, Papageorgiou General Hospital, Aristotle University of Thessaloniki, Greece.
Insights
This study investigated glutathione-S-transferase P1 (GSTP1) gene polymorphisms in relation to bronchopulmonary dysplasia (BPD) in preterm infants. Results indicate no significant association between GSTP1 polymorphisms and BPD development or severity.
Area of Science:
- Neonatal Medicine
- Genetics
- Respiratory Medicine
Background:
- Oxidative stress is implicated in bronchopulmonary dysplasia (BPD) pathogenesis.
- Glutathione-S-transferase P1 (GSTP1) is a key antioxidant enzyme with identified polymorphisms.
- Understanding genetic predispositions like GSTP1 polymorphisms is crucial for BPD research.
Purpose of the Study:
- To investigate the potential association between GSTP1 gene polymorphisms and the risk of developing BPD.
- To determine if GSTP1 polymorphisms correlate with the severity of BPD in preterm infants.
Main Methods:
- A prospective case-control study was conducted.
- GSTP1 genetic polymorphisms were analyzed in 28 preterm infants with BPD and 74 controls (preterm infants without BPD and healthy term infants).
Main Results:
- The homozygous ile isomorph of GSTP1 was predominant across all groups.
- No significant differences in GSTP1 genetic distribution were observed between BPD cases and controls.
- GSTP1 polymorphisms were not found to be associated with the development or severity of BPD.
Conclusions:
- This study did not find evidence supporting an association between GSTP1 polymorphisms and BPD.
- Further research may be needed to explore other genetic factors in BPD pathogenesis.
Background:
Oxidative stress, characterized by the excretion of pre-oxidative and anti-oxidative proteases, has a key role in the pathogenesis of bronchopulmonary dysplasia (BPD). One of the many host anti-oxidant enzymes is glutathione-S-transferase P1 (GSTP1), with three polymorphic alleles having been identified: homozygous ile, heterozygous ile/val and homozygous val isomorph. The aim of this study was to examine the genetic predisposition to BPD in the GSTP1 polymorphisms.
Methods:
A prospective case-control study was carried out in the 2nd Neonatal Intensive Care Unit of Aristotle University in Thessaloniki, Greece during 2008. The genetic polymorphisms of GSTP1 in 28 preterms <32 weeks gestational age (GA) with BPD compared to 74 controls (33 preterms without BPD and 41 healthy terms) were examined.
Results:
The homozygous ile isomorph was predominant in all groups (preterms with BPD: 82%, preterms without BPD: 70%, healthy terms: 78%), followed by the heterozygous ile/val (14%, 18% and 20% respectively) and the homozygous val isomorph (4%, 12% and 2% respectively). The homozygous ile isomorph was also identified in the majority of preterms with mild (80%), moderate (100%) and severe (73%) BPD. The GSTP1 genetic distribution did not differ between the groups and GSTP1 polymorphisms were not associated with the severity of BPD.
Conclusions:
This study could not confirm an association between GSTP1 polymorphisms and the development of BPD or the severity of the disease.
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