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Editor—The paper by Ogiharaet al 1 adds to our understanding of the pathogenesis of chronic lung disease (CLD) associated with high plasma concentrations of aldehyde lipid peroxidation products on the first day of life in preterm infants, a common complication of neonatal intensive care. Specifically, plasma concentrations of heptanal ⩾500 nM, 2-nonenal ⩾150 nM, and 4-hydroxynonenal (HNE) ⩾200 nM were associated with odds ratios for the development of CLD of 6.0, 16.0, and 32.0, respectively. The authors point out that HNE might induce the expression of fibrogenic cytokines, such as transforming growth factor β, as well as an increased transcription and synthesis of collagen.1
Two distinct clinical forms of CLD have been described.2Chest x-ray pictures of infants with CLD type 1 show diffuse bilateral haziness without evidence of emphysema whereas the radiographic findings in infants with CLD type 2 are more consistent with the classic appearance of Northway’s stage 4 disease.3 Histologically, CLD type 1 is characterised by marked interstitial fibrosis without airway lesions. In contrast, marked airway lesions and alveolar emphysema occur in CLD type 2.4 Air leaks frequently precede the development of CLD type 2,2 suggesting that volutrauma has an important role in its pathogenesis. Oxygen free radical induced injury, on the other hand, might be more important in the development of CLD type 1.
Perhaps the authors could provide more information on the radiographic and clinical presentation of CLD patients in their study? A predominance of CLD type 1 would further support the contention that free radical induced lipid peroxidation products can cause fibrotic changes in lungs of preterm infants.
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