Sustained neonatal systemic inflammatory response and growth at 12 months corrected age in very preterm infants.

Abstract

Introduction: Sustained systemic inflammatory response (SSIR) during the neonatal period has been associated with poor linear growth in very preterm infants (VPI), with reduced bone mass accumulation and dysfunction of the somatostatin (GH)/Somatomedina (IGF-1) axis at term corrected age (CA). It is unknown whether these alterations persist at 12 months CA.

Objective: To compare growth and body composition at 12 months CA between VPI with and without neonatal SSIR.

Materials and Methods: Prospective study. VPI ≤31 weeks gestation and ≤1.5 kg at birth, with appropriate weight for gestational age were included. Those with factors that could alter growth or inflammation at birth were excluded. Weight, length, and head circumference (HC) were recorded at birth and at 12 months CA. SSIR was defined as mean C-reactive protein (CRP) above the median, determined along with procalcitonin at 7, 14, and 28 days of life. Body composition was assessed by DXA, expressed as percentage of bone mineral content (BMC), fat mass (FM), and lean mass (LM). At 12 months, GH and IGF-1 were measured. Fisher's exact test, Student's t-test, or Mann-Whitney U test were applied as appropriate.

Results: Of the 33 VPI, 16 had SSIR. At 12 months CA, VPI with SSIR showed lower weight z-score (-0.82±1.00 vs -0.07±0.60; p=0.01), length (-1.27±0.36 vs -0.48±0.34; p=0.00), and HC (-0.23±1.51 vs 0.77±1.03; p=0.02). Additionally, they showed lower percentage of BMC (1.81±0.29 vs 2.04±0.23; p=0.01) and LM (65.61±5.55 vs 68.91±1.22; p=0.02), along with higher FM (32.58±5.30 vs 29.05±1.17; p=0.01). IGF-1 levels were lower in the SSIR group (48.20±33.88 vs 79.21±33.96 ng/ml; p=0.01), with no differences in GH (p=0.10).

Conclusion: Neonatal SSIR is associated with persistent linear growth deficit, reduced bone and muscle development, increased adiposity, and reduced IGF-1 at 12 months corrected age in VPI, suggesting a persistent effect of peripheral GH resistance.