Presented at the Neonatal Society 2001 Summer Meeting.
Harding D1, Montgomery H2, Dhamrait S2, Humphries S2, Whitelaw A1, Marlow N4.
1 Division of Child Health, University of Bristol, UK
2 Department of Cardiovascular Genetics, The Rayne Institute, University College London, UK
3 AcademicDivision of Child Health, Queen’s Medical Centre, Nottingham, UK.
The ACE gene is polymorphic (DD/ID/II). The absence (deletion, D) rather than the insertion (insertion, I) of a 287 base pair fragment is associated with higher tissue and plasma ACE activity, less efficient metabolic and cardiac performance and lower VO2max. We hypothesised that DD genotype would be associated with worse perinatal cardio-respiratory stability.
ACE genotype was determined from DNA extracted from the Guthrie cards of 194 preterm infants. All were born at 23 – 32 weeks gestation and had participated in a prospective outcome study. Perinatal variables were examined for association with ACE DD genotype. Primary analysis was performed on the whole group and secondary analysis by gestational age groups.
In the whole study group there was a trend in the DD patients towards worse acute perinatal indices (foetal distress, worse base excess and minimum and maximum O2 requirement in the 1st 12 hours of life, p=0.09 – 0.049). DD infants > 29 weeks adapted significantly worse than ID/II patients (foetal distress, DD 18 [45%], ID/II 27 [25%] p=0.017: worse BE in 1st 12 hours, DD -4.8 (SEM + 0.2), ID/II -2.9 (SEM + 0.1), p=0.014: Min. fiO2 in 1st 12 hours, DD 0.34 (SEM + 0.03), ID/II 0.28 (SEM + 0.01), p=0.009: Max. fiO2 in 1st 12 hours DD 0.43 (SEM + 0.02), ID/II 0.035 (SEM + 0.01), p=0.015: blood pressure support in 1st 12 hours, DD 12 [30%], ID/II 15 [14%] p=0.032).
The ACE I/D polymorphism may influence the condition of preterm infants in the perinatal period.