Schreiner Felix, Stutte Sonja, Bartmann Peter, Gohlke Bettina, Woelfle Joachim
Pediatric Endocrinology Division, Children's Hospital, University of Bonn, Adenauerallee 119, 53113 Bonn, Germany.
J Clin Endocrinol Metab. 2007 Nov;92(11):4489-93. doi: 10.1210/jc.2007-0956. Epub 2007 Aug 21.
Preterm infants with very low birth weight frequently exhibit impaired longitudinal growth during the first years of life. Recently, the d3-isoform (genomic deletion of exon 3) of the GH receptor (GHR) has been linked to an increased responsiveness to GH.
Our objective was to test whether the GHRd3 isoform is associated with postnatal catch-up growth in very low birth weight preterm infants.
We compared the postnatal growth pattern of 77 otherwise healthy preterm infants (mean gestational age, 28.5 wk; range, 23-35 wk) with a birth weight below 1500 g (mean birth weight, 941 g) to their GHR exon 3 genotype, which was analyzed by multiplex PCR. On examination, mean age of the children was 6.0 yr (range, 4.2-8.0 yr).
Children homozygous or heterozygous for the GHRd3 allele showed a significantly higher rate of postnatal catch-up, compared with those homozygous for the full-length allele.
Our results define the GHR exon 3 genotype as a predictor for the postnatal growth pattern of very low birth weight preterm infants. Those who carry at least one GHRd3 allele are more likely to catch-up.