56 Chapter 3 Table 3. Multivariable logistic regression for the occurrence of BPD B (SE) p-value Odds ratio (95% CI) Included variables Constant 23.9 (8.0) 0.003 Change in IGF-I (µgram/L per week) -0.5 (0.2) 0.018 0.63 (0.43 – 0.92) Gestational age at birth (weeks) -0.8 (0.3) 0.003 0.44 (0.26 – 0.76) Predominant donor human milk for at least 1 weeka 2.0 (1.0) 0.035 7.6 (1.2 – 50.4) R² = 0.358 (Cox & Snell), 0.498 (Nagelkerke). Model χ² (3) = 26.63, p < 0.001 a Predominant donor human milk for at least one week compared to less than one week predominant donor human milk feeding. Predominant donor milk feeding was defined as at least 60% of total enteral intake consisting of donor human milk. Variables removed in backward regression: IRDS IGF-I: Insulin-like growth factor I, IRDS: Infant respiratory distress syndrome Discussion This study showed that, in particular before 35 weeks PMA, low IGF-I levels and a slower increase in IGF-I increased the odds of BPD in preterm infants. IGFBP-3 showeda similar pattern, butwasn’t significant inmultivariableanalysis. Gestational age and donor human milk consumption were significant confounders in the association between IGF-I and the occurrence of BPD. In line with our findings, other studies have shown that preterm infants with BPD have lower postnatal IGF-I levels and a slower increase in IGF-I, whichwas associated with an increased risk of developing BPD. 16-18 Also, in cases of intrauterine growth restriction IGF-I levels are decreased and the odds of BPD increase. 19 20 Previous research has suggested that IGF-I levels are a representation of the grade of infant immaturity, and the link between IGF-I and BPD may be an indirect connection 17. However, after adjustment for gestational age and other potential confounders, which significantly differed between infants with and without BPD, the association remained significant. This makes a functional direct mechanismmore plausible. Potential pathways through which IGF-I influences the occurrence of BPD A number of factors may play a role in the association between IGF-I and the occurrence of BPD. IGF-I signaling influences the development and differentiation of several types of lung cells 5. Lower IGF-I could therefore arrest lung development. Furthermore, IGF-I is known to be an important factor in the lung injury and repair process. During lung injury, IGF-I increases the proliferation of lung fibroblasts and enhances collagen products 16 21. In addition, pre-and postnatal inflammation contributes to lung injury and subsequently to the development of BPD. It has been shown by previous studies that the incidence of BPD, independently increases with postnatal sepsis due to increased oxidative stress, inflammation
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