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Lung Growth and Development after Preterm Birth

Further Evidence

While we agree with the interpretation and general message of the recent editorial by Jobe (1), which proposed that the relative reduction in airway function during the first year of life in preterm infants recovering from chronic lung disease of prematurity might represent the additive adverse effects of very preterm birth plus bronchopulmonary dysplasia, we should like to point out that his suggestion that Hofhuis and colleagues (2) were the first to note such deterioration is not strictly true. The publication by Hofhuis and colleages was in fact preceded by that from Hoo and colleages (3), who showed that airway function may deteriorate during the first year of life in infants born prematurely in the absence of any neonatal disease or therapy. This provides further evidence regarding the importance of prematurity per se on subsequent lung growth and development and for Jobe's proposal that such infants may be "functionally growing out of their airways." Preliminary findings from Hannover (4) have reported similar findings.

Given the potential clinical significance of these findings, we have collated recent data from preterm infants with and without chronic lung disease of prematurity, from three centers in Germany, Britain, and the Netherlands. As can be seen from Figure 1 , these suggest a similar decrement in airway function at one year of age, irrespective of prior disease severity or mode of treatment. While these findings need confirmation in a larger prospective study, they emphasize the importance of sequential measurements and of using an appropriate control group when interpreting long-term effects of respiratory disease or management in the neonatal period. Mechanisms underlying these observations remain speculative, but may include the fact that maturation, dimensional growth, and alveolar septation occur out of phase following preterm delivery, thereby resulting in airways that are more compliant, smaller, and/or have fewer alveolar attachments. Hence, pulmonary changes in preterm infants may be characterized by an arrest in both lung and airway development. This adds concern to the possibility that chronic lung disease of prematurity may be associated with subsequent chronic obstructive pulmonary disease in later life (5). In conclusion, there is growing evidence that reduced lung and airway function following preterm delivery may be related to developmental changes as much as to initial disease severity or to treatment effects. Improved antenatal care and avoidance of prematurity may be as important for future lung health as further improvements in neonatal ventilation strategies.

View larger version (23K): [in this window] [in a new window]   Figure 1. Development of maximal expiratory flow at functional residual capacity (maxFRC) as a measure of airway function in two groups of infants born prematurely, who were ventilated and developed CLD (2, 4), (mean [SD] gestational age of 27 ± 2 and 28 ± 2 weeks, respectively) or who had no respiratory disease (GA = 33 ± 2 weeks) (3). maxFRC was measured on at least two occasions during follow-up and is expressed in standard deviation scores (Z-scores) based on equations published by Hoo and colleaues (6).

^a Medizinische Hochschule Hannover, Hannover, Germany
^b Institute of Child Health, London, United Kingdom
^c Erasmus University, Rotterdam, The Netherlands

REFERENCES

1. Jobe A. An unknown: lung growth and development after very preterm birth. Am J Respir Crit Care Med 2002;166:1529–1530.[Free Full Text]
2. Hofhuis W, Huysman M, Van der Wiel E, Holland WP, Hop WC, Brinkhorst G, de Jongste JC, Merkus PJ. Worsening of maxFRC in infants with chronic lung disease in the first year of life. A more favourable outcome after High-Frequency ventilation. Am J Respir Crit Care Med 2002;166:1539–1543.[Abstract/Free Full Text]
3. Hoo A, Dezateux C, Henschen M, Costeloe K, Stocks J. Development of airway function in infancy after preterm delivery. J Pediatr 2002;141:652–658.[CrossRef][Medline]
4. Süßmuth S, Bahr A, Hoo A, Poets C, Gappa M. Longitudinal assessment of lung function in sick preterm infants with and without chronic lung disease (CLD). Eur Respir J 2001;18:359s.
5. Eber E, Zach M. Long term pulmonary sequelae of bronchopulmonary dysplasia (chronic lung disease of infancy). Thorax 2001;56:317–323.[Free Full Text]
6. Hoo A, Dezateux C, Hanrahan J, Cole T, Tepper RJS. Sex-specific prediction equations for Vmax(FRC) in infancy: a multicenter collaborative study. Am J Respir Crit Care Med 2002;165:1084–1092.[Abstract/Free Full Text]

Gappa and Merkus point out that others have reported a deterioration in max FRC prior to the report of Hofkuis and coworkers (1). I was in error to say that was the first report of deterioration of max FRC in preterms in the first year of life (2). However, I was not far wrong based on the publication dates of other similar observations. The number of recent publications reflects an appropriate interest in exploring clinically how the preterm lung develops. Hofkuis and colleagues did evaluate very small preterms with a history of bronchopulmonary dysplasia. The composite figure provided by Gappa and Merkus is helpful and clearly points out that prematurity per se may be a more important contribution to the decrease in max FRC at 1 year of age than the superposition of bronchopulmonary dysplasia.

Alan H. Jobe

Cincinnati Children's Hospital Cincinnati, Ohio

REFERENCES

1. Hofhuis W, Huysman MW, van der Wiel EC, Holland WPJ, Hop WCJ, Brinkhorst G, de Jongste JC, Merkus PJFM. Worsening of maxFRC in infants with chronic lung disease in the first year of life: a more favorable outcome after high-frequency oscillation ventilation. Am J Respir Crit Care Med 2002;166:1539–1543.
2. Jobe A. An unknown: lung growth and development after very preterm birth. Am J Respir Crit Care Med 2002;166:1529–1530.

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