Abberations in circulating components of the GH-IGF-I axis may be causally linked to the delay in somatic and bone growth observed in infants treated with dexamethasone (DEX) to manage chronic lung disease. However, the changes in plasma IGF-I and the IGFBP profile in infants who receive steroids postnatally have not been characterized. We investigated the ontogeny of the GH-IGF-I axis and biochemical markers of bone turnover, and monitored growth in very low birth weight infants (n=17; BW=782±185 g; GA=25.4±1.3 wk) who were followed from the start of DEX treatment(10-33 d postnatal age) until term corrected age. Plasma and urine samples were obtained prior to first DEX dose (pre-DEX), after 10 days of DEX (during DEX) and 10 days after completing DEX (post-DEX). Daily weight and nutrient intakes, and weekly length growth were monitored. Bone mineral content (BMC) was evaluated using dual energy x-ray absorptiometry (HologicQDR1000W) at term corrected age. Plasma IGF-I and osteocalcin were significantly higher(p<0.001) post-DEX compared to both the pre and during DEX values. Mean urinary N-telopeptide (NTX) during DEX was significantly lower (p=0.01) compared to pre and post-DEX. Plasma IGFBP-3 was higher (p<0.001) during and post-DEX compared to baseline. Plasma IGFBP-2 was unchanged during the study. Length growth velocity was higher (p=0.003) from the end of DEX until term age compared to during DEX while weight growth velocity was similar during both time periods. However, at term, 65% and 94% of infants remained at or below the 5th percentile for weight and length, respectively. Nutrient intakes were similar during and post-DEX. BMC was lower than reference values for infants born at term (18±2 vs. 22±2 g/kg body weight) (FASEB J 1994;8:A 1604). In summary, changes in plasma IGF-I, IGFBP-3 and osteocalcin were comparable to the developmental changes reported in the literature for non-steroid treated preterm infants; however, lower NTx during DEX was likely DEX-induced. Reduced circulating IGF-I, IGFBP-3, osteocalcin and NTx during early life may explain the low BMC and growth delay in the presence of adequate nutrient intake.
