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NEONATAL SOCIETY ABSTRACTS

Longitudinal evaluation of lung growth 21 years after preterm birth

Presented at the Neonatal Society 2003 Summer Meeting (programme).

Narang I1, Rosenthal M1, Cremonesini D1, Silverman M2, Bush A1 (introduced by Dr M Rosenthal)

1 Department of Respiratory Paediatrics, Royal Brompton Hospital, Sydney Street, London, UK
2 Department of Child Health, Leicester Royal Infirmary, Leicester, UK

Background: There are limited longitudinal data on lung function in adulthood of low birthweight, preterm (LBP) babies. It has been hypothesised that there is alveolar-capillary hypoplasia secondary to prematurity, oxygen therapy and positive pressure ventilation. A cohort of LBP babies (all < 2.0kg) were recruited into a follow up study between 1979 and 1980. Full data exists on their neonatal course. These subjects (n=130) were assessed between 7 and 9 years of age. There was evidence of increased airway hyperresponsiveness (AHR) (1) and airways obstruction (2) when compared to controls. Birthweight was an independent predictor of airflow obstruction and overall, low birthweight children who had received any neonatal treatment had poorer airway function than those who had not.

Aim of this study: To assess lung growth in this original cohort at 21 years of age, to determine whether abnormalities persisted or whether there is evidence of catch up lung growth.

Methods: 60 LBP subjects were compared to 50 controls (C), of normal birthweight and gestation. Cardioventilatory variables including alveolar-capillary surface area, the latter using the transfer of carbon monoxide (Dlco) as a surrogate, were assessed both at rest and during an incremental exercise test using a respiratory mass spectrometer and a cycle ergometer. Spirometry and methacholine challenge testing (MCT) were also performed.

Results: The median age of LBP and C were 21.6 and 23.3 years respectively. The median % predicted values for forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and mid expiratory flow between 25 and 75% of FVC, (MEF25-75) in the LBP group were 93.0, 97.0, and 77 respectively and in the C group they were 93.5, 95.5 and 83.5 respectively. Birthweight and neonatal treatments were no longer predictors of any spirometric abnormality in the LBP group. MCT showed that 11% of the LBP group and 5% of the C group had evidence of increased AHR. There were no statistically significant differences between the 2 groups for any spirometric measurements or AHR, p>0.05. At 9 minutes of exercise, the Dlco in the LBP and C were 6.3 and 6.4 mmol/min/KPA/m2 respectively. There was no difference between the 2 groups, p>0.05. Similarly, there were no differences in the cardioventilatory variables measured at rest or any exercise stage.

Conclusion: There is evidence of catch up growth and normalisation of lung function in adulthood. Furthermore, there was normal recruitment and distension of the alveolar-capillary bed during exercise testing, implying no alveolar-capillary hypoplasia. By adulthood, birth factors were no longer predictive of lung function in this cohort.

References
1. Chan KN, Noble-Jamieson CM, Elliman A, Bryan EM, Aber VR, Silverman M. Airway responsiveness in low birthweight children and their mothers. Arch Dis 1988, 63:905-910.
2. Chan KN, Noble-Jamieson CM, Elliman A, Bryan EM, Silverman M. Lung function in children of low birthweight. Arch Dis Child 1989; 64:1284-1293.

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